The following analysis presents the next Americas flu outbreak challenge. The influenza pandemic that was reported in the last two years shook the entire globe with many people hospitalization cases reported in the United States. Many people lost their lives to the disease, and it was estimated that more than 1,280 children died (CDC 1). As a result of this pandemic, both the leading medical professionals and public health experts will make a public gathering in Washington, DC on 21 September to educate Americans on the impact of influenza and carry out immunization campaigns. This will help in reducing flu cases during the influenza season. In an attempt to shed some light on the 2011-2012influenza outbreak, the following research presents a discussion on seasonal flu.
Overview
The toll taken by flu in every season cannot be predicted with some levels of accuracy. Therefore, medical experts and public health professions advise that people who are over six months should be vaccinated every year in order to reduce the effect of the illness.
Seasonal Influenza Outbreak
According to research findings, flu viruses cause the seasonal influenza illness. This is a respiratory disease that is contagious in nature. And, it has been statistically proven that about 5 to 20 percent of those people who reside in the United States get the influenza infection every year. This is a matter of public health concern that requires urgent medical intervention, policy formulation and implementation. Recent research findings ascertain that cases of flu season are often common in the months of January and February (CDC 1). As a matter of an urgent intervention, flu vaccine can be the best influenza protection. This will help in protecting against flu complications, which include, but not limited to dehydration and pneumonia, among others. Seasonal influenza illnesses can last for more than one week, and in certain cases the duration lasts up to two weeks.
As discussed earlier, seasonal influenza illness is transmitted from the infected person to another individual through contact. This contagious respiratory disease causes mild and severe infections. According to healthcare reports, flu has been found to cause death (CDC 1). This deadly illness is frequent in the US during the winter seasons when the temperatures are extremely cold, and the peak is usually in the months of January and February. However, there are seasonal flu cases, which have been reported during the months of October and May. The research findings of the healthcare experts and medical professionals ascertain that the seasonal flu can be spread through sneezing. In fact, coughing contributes a lot to its spread. When such germs from influenza infected person land in ones nose or mouth, he/she stands a high risk of getting the infection. Seasonal flu complications are common among various groups of people. These groups include seniors of between 65 years and above, children who are below 2 years and people who are suffering chronic health illnesses (CDC 1).
In sum, the best way to protect someone from seasonal flu outbreak infections is to keep oneself healthy by observing daily healthcare steps. Some of the common seasonal flu complications include dehydration, bacteria pneumonia, sinus and ear infection. Often, people with chronic health illnesses are mostly affected and their conditions become worse. And, as discussed earlier, those people who get seasonal flu infection can last with it for two weeks. People whose immune systems are weak and children take a long time to heal from this contagious illness.
Work Cited
Center for disease Control and Prevention (CDC). America2s Next Flu Challenge. CDC Online Newsroom, 2011. Web.
The group case study involves analysis of preparedness plan and challenges of an influenza pandemic on a developing nation. The infectious disease has undergone extensive studies in collaboration with CDC leadership. The leadership in the management of influenza pandemic is vital for efficient mitigation. Leaders in the healthcare infrastructure have great responsibility in training personnel, planning the mitigation intervention, and strengthening core capacities through financial support from donors. Challenges are inevitable in the mitigation process, and the success of the preparedness plan depends on the leadership qualities. Transactional and transformational leaders have important aspects of management that influence the achievement of the mitigation intervention. Poor leadership contributes immensely to the general failure of the preparedness plan of an influenza pandemic.
CDC Director, Crisis Response
The group case study involves analysis on the level of preparedness of influenza pandemic in a developing nation. The nation faces major challenges within the healthcare system and the individuals within it, which include lack of medical infrastructure and trained personnel to cope with the influenza pandemic (Danforth, Doying, Merceron, & Kennedy, 2010). Being the director of CDC, I have the mandate of training more personnel on the development of preparedness plan that mitigates the social and health effects of the people (Osterholm, 2005). The training process makes use of available plans from developed nations or adopts a similar approach in the mitigation process. The adoption of the plans from the developed nation may encounter some challenges due to limited infrastructure, technical expertise, and funds (Danforth et al., 2010). The delay in the mitigation process may result to increase in morbidity and mortality rate. To address these challenges, the newly trained team will participate in a feasible approach that involves non-pharmaceutical interventions. The non-pharmaceutical interventions include isolation, social distancing, quarantine, and personal hygiene. Further assistance from the national government will be essential for implementing the pharmaceutical intervention (Nahavandi, 2014).
Transformational and Transactional leaders
Leadership is essential in the management of pandemic influenza outbreak (Leadership-Central, 2011). A transformational leader may motivate the healthcare personnel in the mitigation intervention of the influenza pandemic through active participation in the identification of social factors that facilitate the fast spread of the disease (Lindebaum & Cartwright, 2010; Weberg, 2010). Some of the social factors that need critical evaluation are the nature of housing, the population density of the endemic region, nutritional status of the people, and the co-existence of the medical conditions. The intervention of the transformational leader will influence the development of feasible mitigation strategies (Laureate Education, 2012; Gupta, 2009). A transactional leader may influence the outcomes of intervention through monetary reward of the trained personnel upon successful mitigation of the influenza pandemic. However, the transactional leader may not manage to solve technical problems that the trained team may face in the field due to lack of active participation in the mitigation process. The transactional leader may lack an understanding of the failure of the mitigation intervention (Laureate Education, 2012; Melvyn, Hamstra, Yperen, Wisse, & Sassenberg, 2011).
Poor Leadership
Poor leadership may contribute to inefficiency in the mitigation process on influenza pandemic. Pandemic planning and response to influenza require ethical consideration in the preparedness planning process (Leadership Champions, 2008). A misinformed leader may lack the understanding of the crisis in the mitigation process and value-based research for pandemic influenza. For example, logistical challenges are evident in the majority of pandemic diseases, hence the need for addressing them before embarking on the preparedness plan (Nahavandi, 2014). A bad leader may shortfall the need for detecting, controlling and preventing the spread of influenza virus. The inefficiency in handling the influenza pandemic may have a link on the lack of expanded knowledge on the infectious disease leading to poor surveillance. Additionally, The leader may lack an interest in seeking collaboration from other health facilities and support from donors (Leadership-Central, 2011).
References
Danforth, E., Doying, A., Merceron, G., & Kennedy, L. (2010). Applying Social Science and Public Health Methods to Community-Based Pandemic Planning. Journal of Business Continuity & Emergency Planning, 4(4), 375-390.
Gupta, A. (2009). Transformational Leadership: Practical Management-Designing a Better Workplace. Web.
Lindebaum, D., & Cartwright, S. (2010). A Critical Examination of the Relationship Between Emotional Intelligence and Transformational Leadership. Journal of Management Studies, 47(7), 1317-1342.
Melvyn, R. W., Hamstra, N. W., Yperen, V., Wisse, B., & Sassenberg, K. (2011). Transformational-transactional leadership styles and followers regulatory focus. Journal of Personnel Psychology, 10(4), 187-186.
Nahavandi, A. (2014). Current Era in Leadership: Inspiration and Connection to Followers. In, The Art and Science of Leadership (pp. 178-210). Upper Saddle River, NJ: Pearson.
Osterholm, M. T. (2005). Preparing for the Next Pandemic. New England Journal of Medicine, 352(18), 1839-1842.
Weberg, D. (2010). Transformational Leadership and Staff Retention: An Evidence Review with Implications for Healthcare Systems. Nursing Administration Quarterly, 34(3), 246-258.
Influenza (flu) is a contagious respiratory disease caused by the influenza virus that affects respiratory organs, including the nose, throat, and lungs. The illness can cause mild to severe complications and it is primarily spread through the transfer of respiratory fluids from an infected person to a healthy person during coughing or sneezing. The influenza virus exists in four main forms, namely Type A, Type B, and Type C and Type D. Types A and B are the most common and account for the highest number of illnesses and outbreaks globally.
The Centers for Disease Control and Prevention (CDC) has reported that the virus mutates quickly. In that regard, new vaccines are produced annually to combat viral mutations. The main treatment and prevention methods for influenza include the administration of antiviral drugs and the maintenance of proper hygiene.
Disease Description
Causes
Influenza is caused by the influenza virus that exists in three main types that have varying virulence levels. Types A and B are the most virulent while Types C and D are the least virulent (Wang & Tao, 2016). A strains virulence determines whether the symptoms are mild or severe. Type D viruses affect animals and any evidence of infecting humans has not been found.
Mode of Transmission
Flu is transmitted through droplets of respiratory secretions that are released when an infected person coughs or sneezes. This can occur through various routes that include hand-to-nose contact, direct transmission, and hand-to-mouth contact (Wang & Tao, 2016). When the droplets are released, they are transported to the mouths and noses of healthy people, and thereby trigger the infection process. In rare cases, the illness is spread through contact with a surface or object that harbors the virus and then touching ones mouth, nose or eyes.
Symptoms
The symptoms of flu are usually observed 1 to 4 days after coming into contact with the virus and they linger for approximately a week. They range from mild to severe, depending on the virus type. The most common signs include fatigue, chills, body aches, sore throat, fever, cough, runny and stuffy nose, and headache ( Flu symptoms and complications, 2018). Others include cold sweats and shivers, nasal congestion, sneezing, petechial rash, and gastrointestinal symptoms such as vomiting, diarrhea, and nausea ( Flu symptoms and complications, 2018). Emergency warning signs include extreme vomiting, chest pain, dizziness, shortness of breath, and cyanosis.
It is important to note that these symptoms might vary from person to person. The symptoms of common cold and flu are similar during the early stages of infection. Therefore, physicians need to examine patients thoroughly to avoid misdiagnosis.
Complications
Complications might arise if influenza is not diagnosed and treated early enough. The illness can either worsen other conditions or progress to more serious illnesses. Common complications include dehydration, ear infections, bacterial pneumonia, and sinus infections ( Flu symptoms and complications, 2018). Flu can also worsen chronic medical conditions that include asthma, diabetes, and heart failure. Other complications associated with the illness include myocarditis, myositis, and heart attacks ( Flu symptoms and complications, 2018). Influenza complications are common among children aged between 6 months and 4 years, with compromised immune systems, pregnant women, and adults over the age of 65 years.
Treatment
Influenza antiviral drugs are the most common form of treatment used in the treatment of flu. These drugs are grouped into two classes, namely neuraminidase inhibitors and M2 protein inhibitors (Wang & Tao, 2016).
Examples of neuraminidase inhibitors include zanamivir, oseltamivir, peramivir, and zanamivir. These drugs have been shown to eradicate certain symptoms. However, they do not eliminate the risk of developing complications. The M2 inhibitors stop the replication of the influenza virus (Wang & Tao, 2016). They are effective against Type A virus. Physicians recommended the intake of fluids, adequate rest, and the avoidance of alcohol and tobacco for influenza patients. In certain cases, physicians recommend the use of painkillers to alleviate symptoms such as muscle aches, headache, and other body aches (Wang & Tao, 2016).
Demographic of Interest
Vaccines and antiviral medicals are available for the treatment and prevention of influenza. However, the illness exerts a significant toll on global morbidity and mortality. Statistics released by the World Health Organization (WHO) and the CDC show that approximately 15 percent of the United States population contracts influenza every year and the illness causes about 500,000 deaths annually (Wang & Tao, 2016). Between 3 and 5 million cases of severe influenza are reported annually around the world, with the majority of cases found in developing countries (Fischer, Gong, Bhagwanjee, & Sevransky, 2014).
In the US alone, the mortality rate is roughly 36,000 deaths (Wang & Tao, 2016). The illness is most prevalent among the elderly, children, individuals with chronic medical conditions, and pregnant women ( Influenza, 2018). In addition, individuals with weak immune systems are at high risk of contracting the disease. Increased exposure places health care workers and health care practitioners are at high risk of infection because of their interactions with patients. Seasonal epidemics are common during winter in temperate climates (Wang & Tao, 2016). However, epidemics have been reported throughout the year in tropical regions.
Reporting
Influenza is a reportable disease. However, only the total number of cases is reported. Health care providers are required to report to the CDC when the disease is diagnosed by physicians or laboratories within one hour (Wang & Tao, 2016).
Health Determinants
The determinants of health comprise the social, environmental, economic, and behavioral factors that affect the health of individuals and communities. The state of the environment, how people behave, their access to health care services, genetics, and education level have an impact on the health of individuals (Wang & Tao, 2016). The health determinants of influenza include the environment, behavior, and economic factors. The influenza virus thrives in cooler regions. Therefore, higher rates of incidence are reported in tropical regions. Behaviors such as coughing and sneezing with an open mouth as well as poor hygiene increase the risk of contracting the illness (Wang & Tao, 2016).
Economic factors such as trade and travel enhance the transmission of flu around the world. Moreover, economic constraints increase the severity of the disease in developing countries because of the lack of access to health care services (Wang & Tao, 2016). A poor health system plays a key role in the development of the disease because outbreaks progress to epidemics due to a lack of disease-control resources.
The Epidemiologic Triangle
The epidemiologic triangle is made up of three elements: host, agent, and environment. Each of these elements plays a distinctive factor in the development of influenza.
Host
Human beings are the primary host for influenza. Individuals with compromised immune systems are the most suitable hosts as the illness can progress from mild to severe quickly. Animals and birds are also hosts. For example, strains such as H1N1 and H5N1 are found in birds and animals respectively. In 2009, a new strain of H1N1 influenza from pigs infected humans and caused more than 200 million infections (Wang & Tao, 2016). That was the first influenza pandemic to occur in the 21st century since the 1918 outbreak that had a mortality rate of 2-2.5% (Wang & Tao, 2016).
Agent
The agent for influenza is the influenza virus that is transmitted from infected to healthy individuals through tiny droplets of respiratory fluids. These droplets are released when talking, coughing, or sneezing. The virus has several strains due to the high rate of mutation. The emergence of a new strain of Type A virus can be the cause of an epidemic.
Environment
The key environmental factors that influence the development of influenza include climate, the presence of animal carriers, and sanitation. As mentioned earlier, the influenza virus thrives in cooler climates. Individuals who come into contact with carrier animals become highly susceptible to infection (Wang & Tao, 2016). A common source of infection is objects and surfaces. The virus can be transmitted from surfaces to healthy individuals through physical contact. Therefore, it is important to keep the environment clean.
The Role of a Community Nurse
The primary role of a community nurse in the control of influenza is the investigation and reporting of the incidence of the illness in the community. For example, a nurse is responsible for collecting data regarding the number of cases reported and the most affected group. The data is then forwarded to the organizations that are responsible for the prevention, control, and eradication of influenza.
Another role of the nurse is to augment research activities by supplying data that is used in risk assessment and the determination of the efficacy of various disease control strategies. Moreover, the data is used to evaluate the effectiveness of treatment remedies and prevention methods. Community health nurses also conduct patient follow-up to ensure that treatment instructions are followed and evaluate the recuperation process. Awareness creation is an important action in the control and prevention of diseases. Community health nurses educate the public regarding the proper control and prevention of influenza (Wang & Tao, 2016).
They share the information that they collect with the public through workshops and campaigns. The main goal of awareness is to sensitize people about the risks of influenza, causes, symptoms, treatment, and prevention. The nurses also educate the people regarding the importance of vaccination and the various ways through which infection can occur.
Responsible Organization
Families Fighting Flu, Incorporated (FFF) is an organization that fights influenza. It is a national nonprofit organization that raises awareness regarding influenza and the importance of vaccination ( Families Fighting Families, 2013). It was founded in 2004 and comprises health care practitioners and families that have lost love to the disease or that have experienced a case of severe illness ( Families Fighting Families, 2013).
Members of the organization share their experiences with influenza to raise awareness and receive support from the organization to ensure that other people do not undergo similar experiences. In addition, the organization aims to urge the CDCs Advisory Committee on Immunization Practices (ACIP) to adjust current immunization recommendations to include older children ( Families Fighting Families, 2013).
The mission of FFF is to save lives and reduce hospitalizations by preventing the spread of influenza. The organization uses funds from donors to educate the public and finance advocacy programs ( Families Fighting Families, 2013). Every year, FFF organizes a campaign to fight influenza to prevent childhood illness and death through education and vaccination.
Influenzas Global Implication
According to the WHOs statistics, between three and five million cases of severe illness are reported annually. Moreover, the illness is responsible for between 250,000 and 500,000 deaths every year. In that regard, the illness causes loss of life and increases the cost of health care. Influenza control and prevention present a significant healthcare burden through hospitalizations and treatment. There is also economic loss due to employee absenteeism ( Influenza, 2018). The impact of influence is more severe in developing countries due to the scarcity of resources for the treatment and control of the illness. In such countries, there is poor health care infrastructure, shortages of health care providers, and vulnerable populations have limited access to antiviral mediations Fischer et al., 2014).
Conclusion
Influenza is a viral respiratory disease that is caused by the influenza virus. Human beings are the primary hosts of the influenza virus that exists in three types, namely Type A, B, C, and D. Types A, B, and C are found in humans while type D is found in animals. The symptoms of infection range from mild to severe, and they include headache, runny nose, sweat and chills, sore throat, muscle aches, and coughing.
These symptoms are observed two days after infection as the incubation period of the virus lasts approximately 24 hours. If the illness is not diagnosed and treated early, it might lead t complications that include asthma, viral pneumonia, secondary bacterial pneumonia, sinus infections, and cardiovascular problems. Treatment of influenza involves the administration of antiviral drugs such as zanamivir, oseltamivir, peramivir, and zanamivir. Several factors, including poor hygiene, behavior, and access to health care services influence the development of the illness. Influenza has a greater impact in developing countries than in developed countries.
References
Families Fighting Families (FFF). (2013). Web.
Fischer, W. A., Gong, M., Bhagwanjee, S., & Sevransky, J. (2014). Global burden of influenza: Contributions from resource limited and low-income settings. Global Heart, 9(3), 325-336.
In the article titled, Influenza Preparedness in Low-resource Settings: a Look at Oxygen Delivery in 12 African Countries, Belle, Cohen, Shindo, Lim, Velazquez-Berumen, and Ndihokubwayo (2010) investigate the preparedness of 12 African countries healthcare systems for influenza outbreaks. Belle et al. (2010) assert that while influenza is a serious threat to many populations in these countries, the few resources at the disposal of many healthcare resources pose an even greater risk in the event of an influenza outbreak. According to Belle et al. (2010), many healthcare facilities in countries that are being studied are inadequate. They experience even more challenges in terms of the accessibility of healthcare for patients. The situation even makes the risk even higher.
Analysis
The key strength of the article lies in its wide scope of reporting, which covers 12 African countries whose populations are at risk of influenza. Further, through the assistance of the World Healthcare Organization (WHO), it is evident that the credibility of the data and findings is affirmed. Belle et al. (2010) use survey method to take stock of the available resources such as the availability of oxygen and the associated infrastructure across 231 health centers. The survey effectively gives a snapshot of the level of preparedness of the healthcare systems for outbreaks of Influenza. The weakness of the article is that it makes important recommendations that relate to more investments in critical infrastructure in the countries survey, yet it does not adequately deal with the challenge of accessing funds. This challenge is the main hindrance to these proposed investments. Further, its focus on only one disease, namely influenza, leaves a lot to be discovered concerning the preparedness levels of healthcare facilities for other diseases.
Key Elements
The key idea that is presented in the paper is the lack of adequate preparedness in terms of addressing some illnesses such as influenza in resource-limited healthcare facilities. The findings of the research from the survey clearly show how resource-limited the health facilities are. This issue is a major concern that should be addressed to increase the preparedness of health care facilities in the countries that are mentioned in the study.
Reflection
The findings of the research indicate that only 43.8% of the healthcare facilities surveyed have an uninterrupted supply of oxygen, which is highly worrying. Further, only 24.6% of the hospitals have an operational air gadget while only 35.1% of them are connected to power. These trends show the dire need for more resources to be dedicated to improving critical infrastructures that can help healthcare facilities to handle healthcare emergencies such as influenza outbreaks. The future implications of this study are several. Firstly, there is a need for more research to be done on other diseases to ensure that the interventions that will be put forward will cater to a larger scope of diseases. Lastly, there is the need for prioritization to be done to guide proper utilization of the limited resources to provide the critical and much-needed resources to address emergency needs in the event of disease outbreaks in regions where healthcare institutions operate in resource-limited environments.
Reference List
Belle, M., Cohen, J., Shindo, N., Lim, L., Velazquez-Berumen, A., & Ndihokubwayo, B. (2010). Influenza preparedness in low-resource settings: a look at oxygen delivery in 12 African countries. The Journal of Infection in Developing Countries, 4(7), 419-424.
The Y2K bug was a programming issue caused by a shortcut that displayed the last two digits of the year instead of the full-four numbers (Uenema). There was an assumed possibility that banks would run into significant problems. There were a multitude of other concerns over the bug, and the atmosphere caused individuals to react in unconventional ways. It would be possible to conduct interviews or surveys with people who were 18-65 during the Y2K bug incident. For a broad collection of data, a detailed survey listing precautions and reactions to the Y2K bug that are known would be distributed to a focus group. There should be an option to respond to open-ended questions due to the social-psychological nature of the research. Furthermore, microchipping pets is a highly debated topic of the current day. It is a similar technological issue and people’s opinions about it can be gathered through surveys and interviews as well.
The Nebraska State Capitol and the Spanish flu pandemic of 1918 are both rooted in the past and will have no available people to interview. As such, it would be vital to conduct an analysis of previously collected information, namely, research primary or secondary sources. Most of the data can be gathered through organizations responsible for current knowledge of the two topics, historical writings, and museum resources. The majority of the resources can be found online. However, there are certain downsides to simply analyzing previously collected information, such as being unable to draw meaningful conclusions due to the lack of quantitative data, the inability to eliminate errors or misjudgments of data collected by others, as well as possible insufficient understanding of the data analysis tactics. There are three steps that should be followed for successful data collection. They include the organization of the data samples, summarizing the categories of the data, and evaluation that leads to measurable results.
Work Cited
Uenema, Francine. “20 Years Later, the Y2K Bug Seems Like a Joke—Because Those Behind the Scenes Took It Seriously.” Time, Web.
NK cells were first discovered in 1975 as lymphocytes of the innate immune system that can kill leukemia cells in vitro without previous sensitization:
Since then, NK cells have been revealed to play an important role in the early defense against certain viruses, microbial infections and cancer
Recently, NK cells have been implicated in the regulation of adaptive immune responses following an inflammatory response through the elimination of specific antigen-activated T cells
In contrast to T and B cells, NK cells do not express rearranged antigen-specific receptors. This is because an alternative NK effector function is tightly controlled by the combination of signals received through germ-line-encoded receptors with inhibitory
Activating functions that can recognize ligands on their cellular targets.
Inhibitory receptors, such as the inhibitory Ly49, killer cell immunoglobulin-like receptors (KIRs), leukocyte immunoglobulin-like receptors (LILRs) and CD94-NKG2A receptors, bind to self-MHC class I, or MHC class-I like molecules and signal through immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in their cytoplasmic tail. Some of the transformed and virus-infected cells tend to down-regulate normal expression of MHC class-I in order to avoid recognition by CD8+cytotoxic T lymphocytes and that makes them super susceptible to NK cell-mediated killing. Activating NK receptors, such as NKG2D, KIR2DS2 and CD94-NKG2C are structurally related to inhibitory receptors but lack ITIMs. They also associate with signaling molecules such as DAP12, CD3ζ, or FcRγ, which signal through immunoreceptor tyrosine-based activating motifs (ITAMs), located in its cytoplasmic tail (5). Additionally, NK cells also express the low-affinity Fc receptor (CD16), thus enabling them to detect antibody-coated target cells and exert antibody-dependent cellular cytotoxicity (ADCC) (6).
NK cells kill their target cells by either of two mechanisms that require direct cell-cell contact. In the first pathway, cytoplasmic granule toxins are known as perforin (pore-forming protein) and granzymes (serine proteases) are secreted by exocytosis and together they induce apoptosis of the target cell. The second pathway, apoptosis via Fas/Fas ligand (FasL) interactions involves the engagement and aggregation of Fas-expressing target cells by its cognate ligand, FasL, which is expressed on NK cells’ cell membrane, resulting in apoptosis of the target cell (7).
Furthermore, upon stimulation, NK cells can secrete potent levels of cytokines especially interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), IL-10, IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and chemokines such as CC chemokine ligand 3 (CCL3), CCL4 and CCL5 (8). Studies have also demonstrated a critical role of several cytokines in the induction of NK-cell cytotoxicity. These include interleukin-12 (IL-12), IL-18, IL-15, and type I interferons (9).
Studies have shown that IL-12 release by mature DCs leads to the production of IFN-g by NK cells, which increases the surface expression of MHC class I and MHC class II on surrounding cells enhance their recognition by cytotoxic T cells. Moreover, IFN-g further activates macrophages, dendritic cells, and enhances Th1 activation and polarization by inducing T-bet expression (10, 11).
Missing-self hypothesis
A hypothesis proposed by Klas Kärre and collaborators suggests that the absence or altered expression of MHC class I molecules on the cell surface of transformed or virus-infected cells renders these cells significantly susceptible to NK cell cytotoxicity. This observation led to the “missing-self” hypothesis, which proposed that NK cells recognize and destroy cells lacking normal expression of MHC-I molecules on the cell surface, due to an absence of an inhibitory signal that is received through inhibitory receptors that recognize and bind to ‘self’ MHC class I molecules. Thus, cells that express the normal level of host MHC class I molecules are protected from NK cells cytotoxicity (12). The missing-self hypothesis is supported by finding that transformed and viral infected cells usually tend to down-regulate MHC class I surface expression on its host (13), thus making them susceptible to NK cells attack (14). Transfecting MHC class I demonstrated an important validation of the “missing self” hypothesis- deficient target cells with MHC class I gene encoding Dd, Kb, and Kk. As a result, these cells become protected from lysis by NK cells (15). Further support for the “missing self” hypothesis demonstrated by typical rejection of allogeneic donors of MHC class I deficient bone marrow cells by wild-type mice was confirmed to be NK cell-mediated (16). The capability of an NK cell to recognize the lack of self-MHC class I expression on targets cells was linked to Ly49 inhibitory receptors. In 1989, Yokoyama and his colleagues identified an inhibitory receptor called Ly49 that is expressed on a subset of NK cells and that would be responsible for blocking NK cell activation. They purified and compared Ly49+ NK cells with Ly49- NK cells. They found a considerable number of target cells from H-2d and H-2k backgrounds, which were very susceptible to killing by the Ly49- NK cell subsets but were not killed by the Ly49+. Interestingly, mAb against Ly49 or the a1 and a2 domains of the H2Dd molecule was able to restore the killing of resistant target cells by Ly49+NK cells. Suggesting that interactions between MHC class I, and Ly49 inhibitory receptor will transmit an inhibitory signal that will turn off NK cell activation (17).
Human NK cells
Human NK cells constitute approximately 10% of the peripheral blood lymphocytes. They can be divided into two subsets based on their cell surface density of CD56. The majority of NK cells are CD3– CD56dim cells, which express high levels of CD16 (the FcgRIII), have greater cytolytic activity, play a key role in natural and Ab-mediated cell cytotoxicity, have an immunoregulatory function, and makeup around90% of circulating NK cells. On the other hand, 10% of NK cells are CD56bright cells, which express low or no levels of CD16, and produce abundant cytokines (e.g., IFN-g). Therefore, the traditional phenotype of human circulating NK cells are CD3–CD16– CD56 dim or CD3–CD16+ CD56 bright (18, 19).
A balance between opposite signals delivered by the MHC class I–specific inhibitory receptors is responsible for the regulation of the effector function of NK cells. The inhibitory receptors are specific for HLA class I consist of three structurally distinct families: the killer cell Ig-like receptors (KIR), immunoglobulin-like transcripts (ILTs), and the killer cell lectin-like receptors (KLR) (20). Interestingly, KIR receptors were reported to be expressed on a considerable fraction of CD56dim CD16+ NK cells, where the CD56bright CD16– NK subset expresses uniformly CD94/NKG2A and lacks KIR receptors. Both NK cell subsets express the activating receptors NKG2D, which recognizes the MHC-class-I-related molecules MICA and MICB, as well as the natural cytotoxicity receptors (NCRs) NKp30 and NKp46 (21, 22).
The tissue distribution of these two major NK cell subsets depends on the distinct expression of chemokine receptors. CD56dim CD16+ cytotoxic NK cells can be attracted from blood to peripheral tissues by several chemokines released during inflammatory responses because of the expression of CXCR1 and CX3CR1. In contrast, CD56bright CD16– cytokine secreting NK cells express CD62L and CCR7, the receptor for CCL19 and CCL21 chemokines, which allow its migration from the bloodstream into lymph nodes (23).
Murine NK cells
Murine NK cells were initially characterized as a population of lymphocytes expressing the NK1.1 antigen. However, later on, NK1.1 was found to be only expressed in a few mouse strains, such as C57Bl/6 (B6), NZB, CE, FVB, and Swiss outbred mice, but not BALB/c, CBA, C3H, or 129 mice (24). Mouse NK cells are identified by the lack of CD3-TCR complex and by the expression of CD49b (DX5), CD11b, CD27, CD127, and NKp46 (25). Therefore, in NK1.1− mouse strains NK cells are commonly identified using a monoclonal antibody (DX5) that recognizes CD49b, despite its expression on some activated T cells, platelets, and basophils (26). Interestingly, NKp46 were shown to be conserved between human, all strains of mice tested, and in three species of monkey. This made it the only unifying marker for NK cells across mammalian species, which would be defined as a true NK-specific marker however it was shown to be expressed by a very small subset of human and mouse T lymphocytes, including NKT cells (27, 28).
Many NK cells receptors that have been shown to activate or inhibit NK cell function, such as those belonging to theNKRP1, NKG2 and Ly49 families are encoded in the NK gene complex (NKC) that is located on chromosome 6 in mouse and chromosome 12p13.1 in human. Resistance or susceptibility of certain mouse strains to MCMV was linked to a mouse gene named Ly49H that is located in the NKC region. C57BL/6 mice, which express the Ly49H allele, are resistant to MCMV, whereas BALB/c mice, lacking Ly49H, are highly susceptible to MCMV infection (29). Many studies have shown that NKC appears to be a highly polymorphic region. Allelic variability of various NKC loci has been demonstrated in inbred mice and that involved in NK cell education (30).
NK cell receptors
General properties of NK cell receptors
NK cells express a variety of activating and inhibitory receptors including Ly49 or KIR, NKG2D, CD94–NKG2 heterodimers as well as natural cytotoxicity receptors. These receptors use opposing signaling motifs to inhibit or stimulate the activation of NK cells, with the negative signal mediated by MHC class I-specific inhibitory receptors being dominant over the activating signals. Inhibitory receptors allow NK cells to survey tissues for normal MHC class I expression and protect healthy cells from inappropriate NK cell-mediated killing (31).
Most NK cell inhibitory receptors such as inhibitory Ly49 family, KIR family, and CD49/NKG2A, signal through a common mechanism that is operating through immunoreceptor–tyrosine-based inhibitory motifs (ITIMs) which is present in their cytoplasmic tail. ITIMs motifs is consisting of Ile/Val/Leu/Ser-x-Tyr-x-x-Leu/Val (where ‘X’ represents any amino acid), the tyrosine residues in the ITIMs are critical elements for mediating inhibitory function. Ligation of these inhibitory receptors with its equivalent MHC-class I molecules leads to tyrosine phosphorylation of ITIMs motifs. Phosphorylated tyrosines in the ITIMs serve as docking sites that lead to recruitment of protein tyrosine phosphatase, Src homology region 2-containing protein tyrosine phosphatase (SHP)-1, to phosphorylated ITIMs. Recruited (SHP)-1 leads to disruption of activating responses (32).
Unlike the inhibitory receptors that contain an inhibitory motif in their cytoplasmic tail, most of activating NK cell receptors do not contain cytoplasmic domains capable of transducing signals. Instead, activating receptors signals is mediated by the association of the activating receptors with activating transmembrane adaptor proteins, such as DAP10 and DAP12, that contain an immunoreceptor tyrosine-based activation motif (ITAM), defined by the sequence (D/E)XXYXX(L/I)X6–8YXX(L/I). Engagement of these receptors leads to the phosphorylation of the ITAM tyrosine residues by Src family kinases. This leads to recruitment and activation of spleen tyrosine kinase, also known as Syk, ultimately leading to NK cells activation (33).
CD94/NKG2
Structurally CD94 and NKG2 belong to type II integral membrane glycoproteins that contain an extracellular C-type carbohydrate recognition domain. The CD94 protein were shown to be covalently assembled with distinct members of the NKG2, forming functionally distinct heterodimers. These receptors are expressed predominantly on NK cells and a subset of CD8+ T cells. This receptor varies in function as an inhibitor or activator depending on which type of NKG2 is expressed, activating (NKG2C, NKG2E/H) or inhibitory (NKG2A/B) isotypes (34). The ligand for CD94/NKG2 is a non-classical MHC I molecule, Qa1, in mouse and its homolog, HLAE, in human. HLA-E and Qa-1b molecules bind to peptides derived from the leader sequences of other MHC-I molecules (35).
NKG2A molecules present longer cytoplasmic tails containing ITIMs motifs in their cytoplasmic domains. Engagement of CD94/NKG2A with its ligand results in the inhibition of NK cell cytotoxicity (36). On the other hand, NKG2C and NKG2E have short intracellular regions and lack ITIM or ITAM motifs. These were found to be associated with the DAP12 for proper expression and initiation of activating signals (37). Although the activating CD94-NKG2C and CD94-NKG2E bind to the same ligand, their affinity for non-classical MHC-I molecule is much lower than the affinity of CD94-NKG2A (38). Interestingly, CD94-NKG2E plays an important role for NK Cell-Mediated Resistance to the Orthopoxvirus ectromelia virus (39). Moreover, NKG2C were also found to be able to recognize and kill of HIV-infected cells. During HIV infection the expression of the NKG2C receptor on NK cells as well as its ligand was shown to be unregulated, which could indicate its protective role during HIV infection (40).
NKG2D
NKG2D is a type II transmembrane protein that is a member of the C-type lectin family. NKG2D gene exists within the NK gene complex on human chromosome 12 and mouse chromosome 6. Although the NKG2D gene is located next to the other NKG2 genes in the NK gene complex, NKG2D displays only limited sequence homology to other NKG2 family members and it does not form heterodimers with CD94. NKG2D is expressed as a homodimer and signals through association with an adaptor protein, DAP10 in humans, and DAP10 and DAP12 in mice, which also help in stabilizing its surface expression. NKG2D is constitutively expressed on all NK, subsets of T cells, activated CD8+T and macrophages (41).
Several ligands have been identified for human NKG2D, including major histocompatibility complex class I chain-related molecules A and B (MICA and MICB) and UL-16 binding proteins (ULBP-1, -2, -3, -4, and -5), whereas mouse NKG2D bind to Rae-1α, Rae-1β, Rae-1γ, Rae-1δ, Rae-1ε, and histocompatibility antigen 60 (H60). Those self-molecules have been shown to be expressed in response to several stress conditions such as viral infections and DNA damage. Engagement of NKG2D with one of these self-molecules activates NK cell cytotoxicity and induces cytokine production (42).
In vivo and in vitro studies have demonstrated that mice were successfully able to eliminate tumor cells expressing NKG2D ligands. In human cancer patients, NKG2D ligands are constitutively expressed in multiple types of tumors, including AML (acute myeloid leukemia), ALL (acute lymphatic leukemia), CML (chronic myeloid leukemia), and CLL (chronic lymphatic leukemia) (42).
NKp46
One important family of activating receptors that are expressed on NK cells is the natural cytotoxicity receptors (NCRs) which include NKp30, NKp44 and NKp46. NKp46 is a type I transmembrane glycoprotein with 2 extracellular C2-type Ig-like domains and contains a charged amino acid in their transmembrane domain which associates with ITAM-bearing adaptor molecules CD3ζ and/or FcεRIγ. NKp46 has been shown to be expressed in both human as well as mice NK cells. Indeed, NKp46 is considered a major NK lysis receptor and plays a dominant role in the activation of NK cells against various targets furthermore is involved in the clearance of both tumor and virus-infected cells (43). Interestingly, Hemagglutinin molecules of influenza virus and the haemagglutinin–neuraminidase of parainfluenza virus were identified as the first specific NKp46 ligands (44). Although NKp46 receptors can recognize and kill tumor cells, however, the nature of these ligands is still unknown (45).
Mice lacking the NKp46 receptor fail to clear the influenza virus and do not survive the infection. A recent study has demonstrated that NKp46high NK cells were more efficient at controlling HCV-infected hepatocytes than NKp46low NK cells (45).
Killer immunoglobulin-like receptors (KIRs)
KIRs are typed I transmembrane glycoproteins that are expressed predominately on NK cells and small subsets of T cells. KIRs are named based on their extracellular domain (2D and 3D), which reflects the number of immunoglobulin-like domains. Moreover, KIRs consist of both inhibitory and activating receptors, activating KIRs are characterized by their short cytoplasmic tail, whereas Inhibitory KIRs have a long cytoplasmic tail. The only exception is KIR2DL4, which is activating receptor with a long cytoplasmic tail (46)KIR gene family contains 15 genes and 2 pseudogenes with substantial allelic diversity of many of these genes that are closely linked on human chromosome 19q13.4 within the leukocyte receptor complex (LRC). Each KIR gene was shown to encode either an inhibitory or an activating KIR (47).
Studies of KIRs genotype demonstrated variations in the KIRs gene content depending on the individual. Based on the genetic diversity and allelic polymorphism of KIRs at the level of the locus, two main KIRs haplotypes can be distinguished: A and B. Generally, A haplotypes have encoded mostly for inhibitory KIRs (KIR2DL1, KIR2DL3, KIR3DL1, KIR3DL2, and KIR3DL3) and include KIR2DS4 and KIR2DL4 as the only activating KIRs, whereas B haplotypes are defined by the presence of one or more of the following genes: KIR2DL5, KIR2DS1, KIR2DS2, KIR2DS3, KIR2DS5, and KIR3DS1, most of which are activating. Only three common genes (called framework) are shared by all haplotypes KIR3DL3, KIR2DL4, and KIR3DL2 (48-50).
Ligands for several KIRs have been defined, and every receptor appears to recognize a set of classical HLA class I molecules. The inhibitory KIRs contain ITIM motifs in their cytoplasmic domains and they interact with MHC class I molecules with various allelic specificity. For an instant, KIR2DL receptors were found to recognize predominantly the HLA-C alleles, whereas The KIR3DL2 receptors bind HLA-A3 and HLA-A11. On the other hand, activating receptors possess a lysine residue in their transmembrane domain allowing for association with DAP12, a molecule that possesses an immunoreceptor tyrosine-based activating- motif (ITAM). Excluding, KIR2DL4 that has a long cytoplasmic tail, was found to be associated with FcεR1γ, adaptor molecules containing the ITAM, to transduce an activating signal (51-53). Interestingly, some pairs of activating and inhibitory receptors, such as KIR2DS1 and KIR2DL1, recognize the same ligand (HLA-C), however activating KIR interact with HLA class-I molecules with lower affinity than their inhibitory counterparts (54).
Ly49 family
Ly49 family members are type II transmembrane glycoproteins with extensive homology to C-type lectin superfamily, structurally characterized as disulphide-linked homodimers. Ly49 genes are encoded in the NK gene complex on mouse chromosome 6. The Ly49 receptors are extremely polymorphic, with variations in gene number that exist in multiple allelic forms. Mapping experiments and complete sequencing of this locus of the Ly49 gene cluster using different inbred strain genomes (C56BL/6, 129/J, BALB/c, and NOD mice) showed distinct numbers of Ly49 genes in each mouse strain. For an instant, The C56BL/6 (B6 mice) Ly49 cluster is composed of two activating receptors (Ly49d, h), eight inhibitory receptors (Ly49q, e, f, i, g, j, c, a), and five pseudogenes that do not code for any functional proteins. In contrast, the 129-Ly49 cluster is composed of three activating receptors (Ly49r, u, p), nine inhibitory receptors (Ly49q1, e, v, ec2, s, t, i1, g, o), and seven pseudogenes (55). The majority of the Ly49 receptors are expressed by mature NK cells with an exception for Ly49E, Ly49B, and Ly49Q. Ly49E is expressed on fetal NK cells then disappears on mature NK cells. On the other hand, Ly49B and Ly49Q are not expressed completely by NK cells, although they are located on the same Ly49 gene complex (56).
Although mouse Ly49 receptor families are not structurally related to human KIRs, the Ly49 family members were demonstrated to be functionally equivalent to human KIRs. The ligands for Ly49 receptors have been demonstrated to be either major MHC-class I molecules or MHC-class I related molecules that are expressed by pathogens upon infection. Individual Ly49 receptors can recognize several, but not all, polymorphic MHC class I alleles. For example, Ly49A can recognize and bind to H2-Dd, H2-Dk, and H2-Dp, but not to H2-Db, H2-Ld, or H2-Kb. and that makes Ly49A not functional in B6 mice, which express only two types of MHC-class I molecules (H2-Kb and H2-Db) (57). Nevertheless, both Ly49C and Ly49I are extremely functional in B6 mice since they are able to recognize and bind to the H2-Kb molecule. If a target cell does not express the specific MHC I molecule that would be recognized by the available inhibitory Ly49 receptors on a given subset of NK cells will be lysis (58).
Inhibitory Ly49 receptors
The inhibitory Ly49s, such as Ly49A, Ly49C, Ly49I, and Ly49G, contain ITIMs in their cytoplasmic domains that become phosphorylated in response to receptor ligation with its MHC class I ligand on the target cell. This results in tyrosine phosphorylation of the ITIM, leading to recruitment of SHP-1 phosphatase, which results in dephosphorylation and deactivation of signaling proteins, the nucleotide exchange factor VAV1, involved in the NK activation cascade, thus blocking NK activation signals as consequence inhibit NK cells cytotoxic function (59).
Many tumors have been shown to express sufficient levels of self-MHC class I that in turn are recognized by Ly49 inhibitory receptors, thus making them able to escape lysis by NK cells. For example, In H2b strains of mice (B6 or 129 mice) the tumors bearing MHC H2b will grow smoothly without being killed by NK cells because of the strong interaction between the Ly49 inhibitory receptors (Ly49 C and I) and the tumor. However, blockade of Ly49C and I inhibitory receptors using F(ab’) 2 fragments of the 5E6 monoclonal antibody(mAb) resulted in increased cytotoxicity against these types of tumors and decreased tumor cell growth in vitro and in vivo (60).
Attempting to evade T-cell recognition, transformed and virally infected cells tend to down-regulated MHC class I from the surface of infected cells. This induces NK-mediated target cell lysis because of loss of inhibitory signals via self-MHC–recognizing receptors which induce NK cell cytotoxicity (61).
Activating Ly49 receptors
Activating Ly49, receptors lack ITIM sequences. Rather, their cytoplasmic domain is associated with ITAM-containing adaptor molecules, such as DAP12. Upon engagement of an activating Ly49 receptor, the ITAMs of the associated DAP12 become phosphorylated most likely by Src family kinases (including Lck, Fyn, Src, Yes, Lyn and Fgr), leading to the recruitment of protein tyrosine kinases ZAP-70 or Syk, which in turn initiates a cascade of signaling events leading to NK activation. It comes into sight that, when NK cell engages with healthy cells that express the normal level of MHC class I, inhibitory receptor signals are dominant over activating receptor signals by recruiting tyrosine phosphatases such as SHIP-1 to dephosphorylate appropriate kinases, preventing auto aggression and thus maintaining NK self-tolerance (62, 63).
NK cells from C57BL/6 mice express activating Ly49D receptors that are capable of recognizing and killing target cells that express MHC class I molecule, H-2Dd. Ly49D+NK cells in B6 mice play an important role in the rejection of bone marrow cells that were obtained from Balb/c mice, which express normally H-2Dd class I molecules. Additionally, Depletion of the Ly49D+NK subset resulted in increased engraftment of bone marrow cells in recipient mice (64). Interestingly, Ly49D was also shown to recognize MHC class I like molecule, Hm1-C4 that is normally expressed by Chinese hamster ovary (CHO) cells. Thus, make these cells to be extremely susceptible to lysis by Ly49D+ NK cells. Correspondingly, lysis of this target cell can be specifically inhibited using an antibody against Ly49D receptors to block the interaction between the receptors and its ligand (65, 66).
Several types of Ly49 activating receptors (Ly49H, Ly49P, Ly49I) were found to bind to viral MHC class I like molecules. Interestingly, both the Ly49H activation receptor (express in C57BL/6 (B6) mouse) and Ly49I inhibitory receptor (express in 129/J mouse) bind specifically to m157, and MCMV-encoded glycoprotein with an MHC class I-like homology. The binding of the Ly49H receptor to m157 makes B6 mice resistant to MCMV infection, whereas 129 mice are not. Moreover, Ly49h-deficient C57BL/6 mice were shown to be suitable for the MCMV infection. On the other hand, although BALB /c mice are susceptible to MCMV infection, BALB/c-Ly49H transgenic mice become resistant to the infection. That demonstrates the important role of activating Ly49 receptors during viral infection (67, 68).
Influenza A virus
General future and classification
The influenza viruses are classified as members of the Orthomyxoviridae family, which are defined as enveloped viruses with a segmented, negative single-stranded RNA (ssRNA) genome that contains 7–8 gene segments. Based on the antigenic character of influenza virus nucleoproteins, influenza viruses are divided into three types, influenza A, influenza B and influenza C viruses. Influenza A and B virus contain 8-gene segment whereas influenza C virus contains 7-gene segment. Structurally, unlike Influenza A and B which express two surface glycoproteins the hemagglutinin (HA) and neuraminidase (NA), the Influenza C virus expresses only a single glycoprotein, the haemagglutinin-esterase-fusion (HEF) protein, providing both of HA and NA functions (69, 70).
Influenza C viruses can cause only mild upper respiratory tract infections. However, influenza A and B viruses can cause human illness including upper and lower respiratory tract infection, and pneumonia. Influenza A can spread among both humans and animals including pigs, horses, mink, marine mammals, and birds, and are associated with the major human pandemics. Whares influenza B and C affects predominantly humans, however, it has been also isolated from seals and pigs, respectively (69, 70). Influenza A viruses are further classified based on genetic and antigenic differences in their HA and NA surface glycoproteins into many different subtypes. To date sixteen subtypes of HA (H1–H16) and 9 antigenic subtypes of NA (N1–N9) have been identified, all of which have been isolated from avian hosts. Theoretically, 144 possible different combinations of HA with NA protein could be found, over one hundred subtype combinations have been identified in birds so far (71, 72). Human influenza viruses of the subtypes H1N1 and H3N2 are the major cause of annual epidemics every year in the human population. Additionally, avian viruses H5N1, H7N7, H9N2, and H7N3 were also reported to infect humans (73).
Biology and life cycle of influenza A virus
The influenza A viruses are highly polymorphic and could be visualized as spherical or filamentous. Additionally, it is an enveloped virus with the outer layer composed of a plasma membrane obtained after its budding from an infected host (74). The influenza A virus genome enclose eight negative single-stranded RNA, that encode for HA, NA, viral matrix protein (M1), integral membrane protein (M2), nucleocapsid protein (NP), the RNA polymerase complex (PA, PB1, and PB2), and nonstructural proteins (NS1 and NS2) (Figure 1). Each genome segment is packaged in the virus in complex with the nucleoprotein (NP) and associated with the viral polymerase complex to form viral ribonucleoprotein complexes (vRNPs) (75). HA mediates influenza viral attachment and fusion to the target cell membrane by binding to sialic acids residues that are expressed on the target cell. Therefore, HA has an important role in determining host tropism. Human influenza virus has an HA receptor-binding specificity for sialic acid in a (2-6)-linkage [Neu5Ac (α2-6) Gal], whereas avian influenza virus higher specificity for a (2-3)-linkage [Neu5Ac (α2-3) Gal]. In parallel with these preferential binding properties, human airway epithelial cells were found to express mainly a (2-6)-linkage, and duck trachea and intestine contain mainly a (2-3)-linkage, moreover, In the pig trachea, epithelial cells contain both linkages which explain the capability of human and avian viruses to infect pigs (76, 77). Upon binding to sialic acids on the cell surface of the target cell, the virus is internalized into the endosome by receptor-mediated endocytosis. The lower PH of the endosomes activates the influenza M2 protein to pump in more protons (H+) into the vesicle, which acidifies the viral interior and facilitates the M1 dissociation from RNPs and release of the viral RNP segments into the cytoplasm. The RNPs are then imported into the nucleus, which is the major site for influenza virus transcription and replication. Viral RNA serves as a template for the synthesis of mRNA and cRNA. Newly synthesized HA and NA proteins are transported to the cell surface where they integrate into the cell membrane and initiate the budding event. Later on, the newly synthesized RNPs bind to M1 and that induces their export of the complex from the nucleus to the cytoplasm (70, 78-80). In the cytoplasm, the Interactions between M1 coupled with RNPs and the cytoplasmic domains of HA and NA, which serve as docking sites for M1, trigger the assembly of viral components at the lipid rafts and thus signals for exclusion of host proteins from the budding site. The last stage in the influenza A virus replication cycle is mediated by NA. Cleaving sialic acid residues from viral proteins, that preventing the HA-receptor interaction and aggregation of the new viruses. Consequently, allows the release of newly virions particles from the host cell surface to begin a new round of infection (70, 78-80).
Innate response to influenza virus infections
Both the innate and adaptive immune responses are responsible for host defenses against influenza infection. Although adaptive immune responses including T and B cells are important in clearance and prevention of influenza infection, however, it takes around 5 to 7 days before specific antigen-specific antibody and T cell traffic to the lung. thus during that time period, the innate immune cells including natural killer cells, alveolar macrophages, and dendritic cells (DC) play a critical role in host defense against virus infection by limiting influenza virus replication and enhancing the rapid development of adaptive responses (81). Invading pathogens, such as viruses or bacteria express several distinct ligands, known as pathogen-associated molecular patterns (PAMPs), which are essential for survival and pathogenicity such as Gram-negative outer membrane lipopolysaccharides (LPS), Genomic viral DNA or RNA. These molecular patterns are typically present on the pathogens’ surface or their nucleic acid. The mammalian innate immune system plays an important role in the rapid recognition and elimination of invading microbes through germline-encoded pattern recognition receptors (PRRs) that recognize the molecular signature PAMPs. PRRs can be cell-associated that are expressed intracellularly or extracellularly on the cell surface, such as TLR (Toll-like receptor) family. The stimulation of PRRs leads to the induction of several extracellular activation cascades such as complement pathways and various intracellular signaling pathways, leading to inflammatory responses that are essential for effective clearance of evading pathogens. Most of the innate immune cells express one or more of the PRRs such as macrophages, dendritic cells (DCs), mast cells, neutrophils, eosinophils, and NK cells (82-84).
Influenza A virus primarily infects lung epithelial cells and then spread to nearby epithelial cells and alveolar macrophages. Being a lytic virus, numerous influenza virus particles are released in the extracellular space and that exposes those influenza virus particles to innate PRRs, and by the infected, epithelial cells themselves. Infected lung epithelial cells were shown to detect the influenza virus replicative intermediate double-stranded RNA (dsRNA) using its Toll-like receptor 3 (TLR3), resulting in the production of Type 1 interferon-b (FN-b) (85, 86). Type I IFN (IFN-a and IFN-b) are a major component of the innate immune response that limits influenza viral infections and drives adaptive immune response to the site of infection by enhancing the presentation and recognition of influenza virus antigens. Moreover, IFNs stimulate the induction of several antiviral genes that interfere with influenza virus replication and thus contributing to cellular resistance to influenza virus infection. For example, IFN-induced expression of human MxA protein, which is capable of binding to the RNA polymerase subunit of the influenza virus and that prevent virus replication. Moreover, IFNs enhance significantly NK cell activity leading to NK cells proliferation and production of cytotoxic granules that kill the target cell. Moreover, IFNs enhance DCs differentiation and activation (87-89). Interestingly, DCs are also able to detect and recognize influenza virus single-stranded RNA (ssRNA) using its TLR7 and thus lead to robust induction of type 1 interferons (90).
In the resting state, alveolar macrophages negatively regulate NK cells activity by secreting inhibitory cytokines prostaglandins and transforming growth factor (TGF)-b). Studies have demonstrated that pulmonary NK cells from bronchoalveolar lavage (BAL) or from lung tissue were not able to lyse NK-sensitive target cells. However, incubation of pulmonary NK cells for 24h with IFN-I was enough to restore NK cell activity. Interestingly, NK cells from mice lacking IFN-I receptors were unable to kill MHC-class I deficient cell line (RMAS) in compression to WT NK cells after stimulation with IFN-I, however, both groups were able to recognize and kill another cell line that expresses a ligand for NK cell activating receptors, NKG2D. Thus, demonstrate the ability of NK cells to kill target cells that express stress ligand without previous activation. Moreover, Demonstrates the importance of type I IFNs as an early and critical regulator of NK cell activation and proliferation (91, 92).
Upon influenza virus infection, the infected macrophage produces a high amount of monocyte chemoattractants, particularly the CC chemokines (CCL2), which recruit large numbers of NK cells to the lung within the first few days of infection (93-95). Abundant secretion of IFN-I by activated and infected macrophage and DC augment NK cells cytotoxicity. Furthermore, direct interactions between influenza virus-infected- macrophage or DC with NK cells have strongly stimulated NK cytotoxicity and induction of IFN-g production, which has an important role in macrophages and DCs activation and Th1-type cell proliferation (96, 97).
Role of NK cells during influenza virus infection
Mice and hamsters depleted of NK cells showed increased morbidity and mortality during influenza virus infection, and that demonstrated the important roles of NK cells during influenza virus infection (98). NK cells are recruited to the lung two days after influenza virus infection and peak at day 5, whereas influenza virus peaks within 2 to 3 days after infection and declines significantly by day 5. The protective functions of NK cells during influenza virus infection were further specifically confirmed by the fact that NK cells activating receptor (NKp46) can recognize influenza hemagglutinins on virally infected target cells and this recognition is crucial for protecting mice against lethal doses of influenza virus infection. The binding of NKp46 activating receptor to the influenza virus hemagglutinins on infected cells triggers the NK cell to lyse the infected cell, consequently limiting viral infection and replication (44, 99, and 100). As seen earlier, influenza virus-infected monocytes and dendritic cells robustly enhance NK cells cytotoxicity by producing a high level of type I IFN, and by direct contact. A recent study has demonstrated that influenza virus-infected monocytes and dendritic cells express a high level of stress ligand UL16-binding protein (ULBP)1–3, which is recognized by NK cell activating receptor NKG2D, and that enhances cytolytic activity of NK cells toward influenza virus-infected cell and increased IFNγ production (97, 101). Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis of various tumor cells but not normal cells. Interestingly, influenza A virus infection was shown to induce TRAIL expression on lung NK cells. Interestingly, 4 days post-influenza virus infection TRAIL expression was detected only on NK cells but not on T cells. Blocking of this receptor results in increased virus titer significantly. Therefore, NK cells expressing TRAIL may play an important role in the immune response to influenza A virus infection (102). Additionally, NK cells are able to kill influenza virus-infected cells that are identified by a specific antibody (Ab) that binds to them. The protective function of M2-specific antibodies that recognize and bind to M2 protein expressed on the surface of influenza virus-infected cells depends mainly on the presence of NK cells to confer protection in vivo. NK cells mediate this protection via Antibody-Dependent Cellular Cytotoxicity (ADCC). NK cells express a receptor called CD16 that binds to the Fc portion of the Abs, this binding induces NK cell lytic function and kills the target cell (103, 104).
How influenza viruses can escape NK cell recognition?
In response to NK cell cytolytic potent function, the influenza virus has developed several evasion strategies to escape NK cells recognition. Interestingly, influenza viruses have developed strategy make them able to down-regulated NK cells activating receptors (NKp46) in vitro and in vivo. The study has demonstrated that, incubating influenza virus particles with NK cells resulted in significantly NKp46 down-regulation from the cell surface of NK cells (105). In agreement with this finding, incubation of fresh or IL-2-activated NK cells with influenza virions or hemagglutinin resulted in a significant inhibition in NK cell cytotoxicity toward influenza virus-infected macrophage (106).
Additionally, the influenza virus was found to be able to bind directly to sialic acids residue that is expressed normally on the cell surface of NK cells. As a result, NK cells become extremely susceptible to influenza virus infection, which induces striking NK cell apoptosis. Influenza virus uses clathrin-dependent endocytosis as an entry pathway. Although some influenza viral components have been synthesized, however, no infective virus was produced, abortive infection (85). In vivo infection of lung NK cells by influenza, A virus was also confirmed. NK cells express both sialic acids Alpha-2, 3 and Alpha-2, 6 linkages that facilitate influenza viral binding and entry. Additionally, this infection resulted in significantly lower cytotoxicity of influenza-infected NK cells than uninfected-NK cells against NK cells-sensitive target cells, YAC-1 and RMA/S (107).
As well known, NK cell activity is regulated by a variety of both activating, such as NKp46, and inhibitory receptors, such as inhibitory Ly49 family in mice and KIR in humans. Upon engagement of both activating and inhibitory receptors to a target cell, the outcome is determined by the net balance of signals, which determines whether the NK cell becomes activated to kill the target cell or not (108). Surprisingly, influenza virus infection was shown to induce reorganization and accumulation of MHC class I molecules in the lipid raft microdomains of the infected cell. Leading to increases binding of the NK cell inhibitory receptors, KIR2DL1, therefore NK cell cytotoxicity was significantly decreased (109, 110). Other observations demonstrated that influenza virus infection enhances greatly up-regulation of MHC class I molecules on infected human alveolar epithelial cells, A549 cells, and that would inhibit NK cell cytotoxicity through (111). To our knowledge, there is presently no in vivo infection model to demonstrate that, the influenza virus induces up-regulation of MHC class I on infected epithelial cells. If so, would that inhibit NK cells from targeting infected cells?
The article describes the effects of highly pathogenic avian influenza (HPAI), which is transferred through bird species, such as ducks. As a result of mutations, avian influenza viruses sharply change their biological properties and acquire the ability to overcome the host barrier with direct infection of people bypassing the intermediate host. In addition, they can cause extremely severe clinical forms of the disease, a significant portion of which is fatal.
This movement may also affect humans because the virus may not be species-specific. This determines the need for greater surveillance and control of the infection. The Avian Influenza virus spreads unusually quickly, and this process may not be controlled by traditional methods, such as isolation of patients, quarantine measures, and recommendations for traveling people.
The study analyzes the movement patterns of live ducks, which plays a major role in epidemic prevention approaches. It is stated that developing correct models of the proximity networks of animal movement behaviors can allow epidemiologists to precisely predict the danger zones and the sources of infection (Guinat et al., 2020). The live-duck movements were the main cause of the H5N8 influenza outbreak, which took place in France during 2016 and 2017 (Guinat et al., 2020). Currently, there is no sufficient data on the movement of these birds during the epidemic control.
However, the researchers used a permutation-based approach in identifying the overall contribution of duck relocations. Only the given avian species were studied due to the fact that among all affected species, ducks represented 81.6% (Guinat et al., 2020). The spatial distribution diagrams in the study show that southwest regions were predominantly the most high-risk areas due to a number of live-duck trade communities.
Thus, such sophisticated models can allow experts to take preliminary actions to prevent potential outbreaks. The given novel viruses arise by a number of different mechanisms. These include viral DNA or RNA mutations by physical mutagens, such as x-rays or UV light. In addition, there are natural base changes and errors produced by replicating enzymes (Murray, Rosenthal, & Pfaller, 2015). Environment-specific mutagenic factors directly influence the alteration rate in the areas. Therefore, the mutations lead to the emergence of new virus strains with more pathogenic characteristics.
References
Guinat, C., Durand, B., Vergne, T., Corre, T., Rautureau, S., Scoizec, A….Paul, M. C. (2020). Role of live-duck movement networks in transmission of avian influenza, France, 2016-2017. Emerging Infectious Diseases, 26(3), 472-480.
Murray, P., Rosenthal, K., & Pfaller, M. (2015). Medical microbiology (8th ed.). Amsterdam, Netherlands: Elsevier.
Identified on most occasions as the flu, influenza is a highly contagious viral disease, which mostly affects the respiratory system. Most people presume that the flu only causes the extreme cold. In actual sense, the acute conditions might result in death. The disease is spread through the body fluids released while sneezing or through body contact with the fluids. The flu virus has the ability to change its physical structure. Thus, those with stronger immunity systems might not withstand the different types of viruses circulating in every season. To counter the effect on the vulnerable people, various State Health Agencies, and international communities that deal with health-related issues conduct immunization programs annually to boost the immunity system. Moreover, influenza occurs within the eight weeks of every winter and spring.
Existing Types of Influenza Viruses
Globally, there are only three types of influenza viruses. They include Influenza viruses A, B, and C. Virus type A is mainly hosted by the aquatic birds, and their transmission might result in devastating epidemics among the poultry, thus increasing the vulnerability of the people to the infection (Sherk par. 4). In addition, it causes dangerous symptoms among humans besides being the major infectious human bacteria. Conversely, Virus type B mainly infects human beings. Unfortunately, some domesticated and sea organisms, such as ferret and seal, respectively, are prone to contamination of the virus (Occupational Safety and Health par. 7). The rate of mutation of type B is slower than that of A and does not exhibit variation in the structure. Its immunity occurs only at older ages. Finally, type C of the flu viruses infects the mammals, including humans and pigs.
The Economic Impacts and Rates of Influenza Transmission
With much time taken at workplaces, there is no surprise that they harbor infectious bacteria and viruses. According to the Centre for Disease Control and Prevention (CDC), workplaces transmit approximately 80% of the infectious diseases while workers are shaking hands with the infected people and surfaces (Disease Control and Prevention par. 3). From the business perspective, flu infections may result in draining the level of productivity in the workplace, leading to paralysis of most business activities. As per the study conducted by the National Health Interview Survey, it estimated that nearly 200 million and 75 million days reduction in productivity and absenteeism at workplaces, respectively (Bastien 102).
In America, the infection rate stands between 6% and 21% annually. As a result, many people miss going to work, making the economy lost $12 billion annually. In Canada, the flu virus infects about 10% of the total population annually by seasonal influenza.
Effects of Influenza Transmission at the Workplace
Water fountains offer the channel of influenza transmission from the birds to humans. Notably, birds living in water are the major reservoirs for influenza, type A virus; they transmit the virus through a fecal transmission mechanism. Water fountains offer the birds habitats that harbor influenza viruses. Therefore contact with such surfaces often leads to infections of the flu. Being a highly contagious disease, the infected might accelerate the spread through handshakes, coughing, and touching the office telephones. Water fountains are always good for improving the beautification of the workplace; however, water birds might infect the water with the flu (Centers for Disease Control and Prevention par. 5).
Human contamination is likely to occur while conducting maintenance. As a result, a worker might end up passing the virus to the other workmates through contact methods. The outbreak of the virus in the workplace often affects business activities as the states order quarantine of the affected area to curb the spread of the disease.
Business Shut Down and Cut From International Links
International and various state agencies dealing with health-related issues often monitor the spread of the flu. As a disease that spread fast, it affects many business operations. For example, people shut workplaces in a bid to prevent the spread. Moreover, the disease is becoming an international concern. Outcrop of the disease in the workplace might, therefore, affect international relations of various countries as a precaution of preventing the spread from one state to another. The infected people often take work leave, thereby disorienting some of the business activities (Occupational Safety and Health par. 2).
As the infection spreads, most countries always provide a travel ban on the affected countries. These bans might lead to closure or failure of the business. Flu is a disease that requires monitoring, but waterfowl birds are also difficult to control in the workplaces, especially those with water fountains.
Influenza infection reduces the productivity of the people. Healthy workers always deliver quality works. Therefore, the occurrence of the disease weakens and encourages absenteeism among the employees. Consequently, creating a condition of the reduced labor force in the workplace and increased energy required to conduct the job that was initially done by the absent employees. The costs of curbing the spread of the disease also have an impact on the cost of production (Wilschut, McElhaney, and Palache 45).
With increasing levels of the spread of the flu, especially in the workplace, many organizations globally are taking precautionary measures to prevent the occurrence and spread of the disease. In addition, the professions are also avoiding working on areas prone to the virus, such as the water fountains. These water fountains, as elements of environmental beautification, often require the services of well-trained professionals. Professions are shifting their expertise from servicing and maintaining water fountains to “sustainable” jobs in a bid to prevent contamination with the virus from the water.
Slowing Company Growth
According to the CDC, the cost of managing this pandemic disease has been on the rise, with 15% of the total population being vulnerable to the disease annually in the United States. The economic impact of the flu expected to increase from $71.4 to $166.6 billion without the inclusion of its impact on business activities conducted within the state. Flu infections within organizations always result in damaging business brands. There are businesses specifically designed to construct the water fountains. These businesses might lose customers on the basis that the water fountains harbor the flu viruses. Moreover, the transmission of the virus through the water fountain might discourage those consumers seeking to use the fountain as a source of beautification. As a result, many people are shifting to other methods of beautification, like tree planting and flower gardens.
With a reduced number of people seeking for construction of the water fountains, businesses always opt to lay off some workers in a bid to control the cost of production. Influenza does affect not only individual businesses but also the economic condition of a country. It reduces the amount of taxes affected countries collect, thus contributing to the deteriorating economic conditions globally. Besides laying off the workers after experiencing influenza infection, the states and international communities would be monitoring the activities of the organization in a bid to prevent re-emergence of the virus (Wilschut, McElhaney, and Palache 121). These activities contribute to the decline of the organizational brand image and profitability since the consumers might avoid products and services from such organizations.
Increase in operational cost
The emergence of influenza disease in workplaces increases the organizational cost of operation. Seek leaves due to illness increases the duration of the scheduled projects. In an occurrence of influenza, while the project is on progress, the situation always causes business entities to shut down some of its operations as the infected workers seek medication. These activities often occur at the expense of organizational cost as the projects lag behind the time schedules. Furthermore, seek leaves creates a lot of stress among the works as they struggle to compensate for the lost time and productivity. Sometimes people choose to work on an overtime basis as a method of compensating the lost time with the objective of increasing their overtime bills. Even as the number of sick leaves occurs in many organizations, workers only receive payments for the number of hours they worked; as a result, most people work tirelessly to recover the time lost.
Influenza transmissions reduce labor force participation. The inability of the workers to invest in their areas of profession due to illness reduces their ability to generate economic output. Additionally, the disease transmission reduces the ability of the workers to pay their taxes from incomes as required by the law, thereby contributing to the stagnation of the county’s economic living standards. According to the Commonwealth Fund Biennial, Health Insurance Survey conducted in America in 2013, found that 68.9 million workers took sick days, which accounted for 408 million days of the work. As per the survey, the value of lost wages by the sick workers amounted to nearly $ 48 billion of the economic outcome. Upon realization of the infection, business entities might decide to quarantine the infected worker or give a compulsory sick leave.
Alienation
The transmission of the disease through water fountains in the workplace often reduces the interaction of the business with the public. Moreover, if the disease occurs in a workplace, the rate of infection is always higher, considering the rate of interaction among the employees. The sharing of the working equipment is always a major contributor to the spread of contamination levels. Workers shaking hands and closely chatting often accelerate the rate at which the disease spreads. This increases the number of workers affected with a period leading to reduction or halting of the organizational activities. As a result, the profitability of the organization tends to reduce.
Furthermore, influenza transmission contributes to the economic deterioration of a country’s economic standards as such conditions discourage foreign investors. With more workers becoming ill due to the increasing levels of infections, countries are channeling developmental and project funds to various methods of curbing the spread of the disease. The cost monitoring of the waterfowl birds also reduces the amount which the might have channeled into other projects to prevent human contamination of the disease. Contamination of the influenza viruses might as well contribute to the resignation of many workers for fear of contaminating the disease.
Conclusion
Considering the rates of increasing influenza transmission in the water fountain, organizations are putting measures to decrease the probability of its occurrence within the organization. Moreover, business entities are implementing policies related to Occupational Health and Safety. Influenza reduces the profitability of the businesses and the economy through damaging the organizational brand, reduction in the number of days employees go to work, and the number of revenues the states collect inform of taxes from the workers’ income. Therefore, there is a greater need to control and monitor water fountains.
Works Cited
Bastien, Joseph W. The Kiss of Death: Chaga’s Disease in the Americas. Salt Lake City: U of Utah Press, 1998. Print.
Centers for Disease Control and Prevention. Influenza (Flu), causes, and impact on the people. 2009. Web.
Occupational Safety and Health. Economic consequences of chronic diseases and the economic rationale for public and private intervention. 2005. Web.
Sherk, James. Use and Abuse of the Family and Medical Leave Act: What Workers and Employers Say. 2012. Web.
Wilschut, Jan, Janet McElhaney, and Abraham Palache. Influenza. Edinburgh: Mosby Elsevier, 2006. Print.
The world is grappling with the most recent pandemic caused by a virus called Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2). This coronavirus has triggered fears among Americans as it emerged as a novel disease. May notes that it was evident no one was “immune to the disease caused by the novel coronavirus” right from the time the first case was reported. Several conspiracy theories emerged about how the respiratory illness began, as researchers and experts could not establish the source or carrier of the virus. This is not the first pandemic to occur, as a historical review of world history shows that countries have previously faced a similarly major pandemic, the Spanish flu, of 1918. A critical comparison of two pandemics reveals that both diseases are caused by novel viruses and the US adopted similar containment measures, such as wearing masks and social isolation, although it is apparent that CIVID-19 has been relatively more devastating than the Spanish flue.
The historical background of the two pandemics reveals some differences, although the US responded in almost the same way to both due to the diseases’ shared characteristics. Stronchlic and Champine report that the Spanish flu also called the influenza pandemic of 1918, was caused by the H1N1 virus. On the other hand, a type of coronaviruses called SARS-CoV-2 is the cause of the current pandemic. The origin of the 1918 H1Ni virus remains obscure although it has been shown that World War I soldiers facilitated its spread. According to Webel and Freeman, “soldier mobilization created a situation well-suited to influenza dispersal,” making it difficult to establish the exact origin. However, the world community is confident that COVID-19 started in China, as it was first reported in the country’s Wuhan province. Hence, COVID-19 and the Spanish flu differ in both the causing virus and history of origin.
Like the Spanish flu, COVID-19 has infected and caused many deaths in the US and across the globe. However, a detailed review of the figures reveals that the current pandemic has been more devastating compared to the 1918 influenza, as it has led to over 15 million deaths in less than a year since the initial case was reported (Stronchlic and Champine). The number might continue to rise because the virus has not been contained fully. According to Webel and Freeman, “the Spanish flu killed 50 million people globally, with 675,000 in the United States between 1918 and 1920,” although research shows that the statistic cannot be ascertained. The US and other countries lacked effective reporting channels in 1918, meaning that the severity of the 1918 influenza might not have been documented correctly. Nevertheless, nations were preoccupied with the First World War to the extent that they might have suppressed reports of infections and deaths due to the disease. Even then, it is apparent that the US cannot have underreported the severity by up to several million fatalities.
Both the 1918 influenza and COVID-19 share a common aspect of being novel diseases, although they affected different age groups uniquely. Like the Spanish flu, COVID-19 emerged as a strange disease, meaning human bodies lacked the immunity needed for protection from both viruses. Bristow asserts that the 1918 pandemic affected and killed more healthy persons within the 20-40 age bracket than any other group, much as mortality was still high among people below five years and those above 65 (136). The situation has been different with COVID-19, as the virus is seemingly killing more persons above 65 years than any other age group. Jones notes that older individuals with underlying health conditions, such as high blood pressure and diabetes, are the worst affected cohort. Children and younger healthy adults report mild symptoms, which disappear before they are recognized in some cases. Hence, different from the Spanish flu, COVID-19 is affecting a different population disparagingly, despite sharing the common attribute of being novel viruses.
The US and other world governments adopted similar containment measures to both the 1918 influenza and COVID-19, as the two diseases share a major characteristic of being contagious. Critical measures taken to mitigate both pandemics include restrictions on transportation systems, mandatory social distancing requirements, restrained public meetings, and isolation of identified or suspected cases. According to Stronchlic and Champine, “placing restrictions on transportation; mandating social distancing, and banning public gatherings are among the key measures adopted to combat both plagues.” Besides, people are required to wear facemasks whenever visiting public places, a method that was similarly used during the earlier pandemic. These methods proved effective in controlling the Spanish flu, although the government had to involve the police and other agencies in ensuring the public observed recommended health protocols (Stronchlic and Champine). Ostensibly, authorities are actively involved in compelling citizens to follow COVID-19 containment measures.
In overview, it is apparent that COVID-19 has been relatively more lethal and overwhelming than the Spanish flu of 1918, although it has been shown that the two pandemics resulted from novel viruses. However, the pandemics feature certain stark differences in how they affected communities. The Spanish flu proved deadly among persons within the 20-40 age bracket, whereas COVID-19 has proven to be more devastating among older people, especially those with underlying health conditions. Nevertheless, the current pandemic has led to over 15 million deaths, whereas the earlier influenza pandemic killed about 675,000 US citizens. The US government has since initiated COVID-19 containment measures similar to those adopted earlier in 1918, as the two viruses share critical similarities of being transmissible.
Works Cited
Bristow, Nancy K. “It’s as Bad as Anything Can Be:’ Patients, Identity, and the Influenza Pandemic.” Public Health Reports, vol 125, no. 3, 2010, pp. 134-144, Sage Journals.
Jones, David S. “History in a Crisis – Lessons for Covid-19.” The New England Journal of Medicine, Web.
May, Megan. “Inequality Amplifies African Americans COVID-19 Risk.” The University of North Carolina, 2020. Web.
Stronchlic, Nina, and Riley D. Champine. “How Some Cities ‘Flattened the Curve’ During the 1918 Flu Pandemic.” National Geographic, 2020. Web.
Webel, Mari, and Megan Culler Freeman. “Compare the Flu Pandemic of 1918 and COVID-19 With Caution.” Smithsonian Magazine, 2020. Web.
Pandemics are a source of concern to any society in the contemporary world. They can either be man-made or natural. Regardless of their type, disasters pose a risk to human life and property. Avian flu is one such form of natural disaster that can wreck havoc in the society.
Also known as the avian influenza, the condition is brought about by naturally occurring viruses. The micro-organisms (Type A virus), are usually found in wild aquatic birds, domestic poultry, and other animal and bird species (Centers for Disease Control and Prevention [CDC], 2014).
In this paper, the author reviews two emergency scenarios involving avian flu outbreaks. In the first case, an occurrence of the pandemic in Chicago is analyzed. The parties in command of the response to the outbreak, as well as the coordination of activities of the various state and local agencies are some of the issues addressed in this scenario. In the second case, an outbreak in the larger state of Illinois is outlined.
The author of this paper recommends several epidemic control steps to deal with the issue. The legal authorities involved in the response plan, as well as various factors that determine the success of the proposed plan, are some of the other areas analyzed in this section.
An Emergency Scenario in Chicago, Illinois
The Pandemic
Under normal circumstances, avian flu does not affect humans. However, the virus can cause a serious pandemic if it finds its way into the human population.
Such a case was reported in the 1918 ‘Spanish flu’ epidemic. Healthcare providers in Chicago have noted a growing number of individuals seeking health services as a result of symptoms associated with avian flu. After a careful follow-up, the authorities have determined that an influenza pandemic is developing.
Taking Charge of the Incident
The Illinois Department of Public Health would command the avian flu response initiative. The agency is tasked with the responsibility of addressing health issues in the state.
The Department of Homeland Security (DHS) would be responsible for the coordination and the overall federal response to the avian flu (Homeland Security Council [HSC], 2007). The commanding status of DHS is strengthened through the appointment of pre-designated Principal Federal Officials (PFO), as well as regional PFOs, responsible for the coordination of influenza responses.
Coordinating Resources and Working Together
The management of the federal, state, and local resources determines the effectiveness of the response mechanism. The U.S. Government provides state and local authorities with guidance on the best pharmaceutical and non-pharmaceutical interventions to mitigate the impacts of the pandemic.
The federal and state authorities are expected come up with the best interventional measures to deal with the emergency. On their part, the local authorities play the role of implementing these proposals at the community level. The major role of the federal authorities is to fund the program (HSC, 2007).
The state and local agencies ensure that the hospitals and the emergency departments have the capacity to handle the large number of patients affected by the condition. There are other issues that the two authorities need to deal with. For example, they need to provide healthcare workers with the necessary protective gear.
They should also provide them with the information needed to handle the situation, together with the necessary materials and infrastructure (HSC, 2007). Given this scenario, the state and local authorities would be liable if anything happens to the personnel implementing the relief programs.
Laws, Rules, and Regulations Important for the Response
The Emergency Federal Law Enforcement Assistance would be essential in handling the pandemic. The regulation falls under the Justice Assistance Act of 1984 (HSC, 2007). It calls for maximum assistance from the U.S. Government. Other rules and regulations would be specific to the non-pharmaceutical measures of dealing with the pandemic.
Addressing a Localized Cluster of Phase 5 Pandemic
Recommended Epidemic Control Steps
There are several control measures that can be put in place to deal with an outbreak that is restricted to a Chicago cluster. The primary control strategies for addressing the avian flu pandemic include prophylaxis among the individuals exposed to the virus. The strategy can be achieved through the use of antiviral medications, vaccinations, and the adoption of infection control and social distancing measures (Tyshenko, 2007).
It is not possible to develop a matching vaccine within a short duration to respond to the scenario. As such, social distancing and infection control measures are more appropriate.
Voluntary home quarantines, dismissal of students from schools, isolated treatment for the infected, and other non-pharmaceutical interventions are recommended (Department of Health and Human Services & Centers for Disease Control and Prevention, 2007).
Invoking Legal Authorities to Respond to the Emergency
Such legal authorities as the Public Health Service Act (42 U.S. Code 264), which falls under section 361, may be evoked to help in dealing with the situation.
Applying the laws would facilitate isolation and quarantine efforts by the federal government (CDC, 2014). The act supports the enforcement of measures necessary for prevention of entry and spread of communicable diseases in the country. The federal government, through the various federal agencies, prepares and encourages communities, organizations, and businesses to deal with such outbreaks.
The Centers for Disease Control and Prevention might be forced to exercise its authority under section 42 Code of Federal Regulations (CDC, 2014). The code authorizes the agency to detain, medically examine, and release individuals arriving in the U.S. The persons who are taken through these procedures are those suspected of carrying infections. In most cases, travelers from regions hit by the avian influenza are more likely to carry the virus and infect people in other regions (CDC, 2014).
Factors Affecting the Success of the Proposed Plan
The success of the avian flu response plan would depend on various factors. One of them is the effective coordination of resources between the federal, state, and local authorities.
In addition, enhancing the accountability of the various authorities in carrying out their mandate would facilitate effectiveness in the response initiative. Failure to synchronizing the activities of the assisting personnel would jeopardize the entire process. Organization is very important, regardless of the level of expertise among the personnel or the complexity of the equipment used.
The federal government would be expected to provide the necessary support to the individuals and agencies involved in responding to the emergency. For example, the state’s Department of Public Health should effectively manage, supervise, and control the activities of all the stakeholders involved in the initiative. The major responsibility of local authorities would be to enhance cooperation from members of the public.
Possibilities of Effectively Controlling the Outbreak
Effectual coordination and definition of duties, as indicated above, would help to control the epidemic. Currently, the avian flu pandemic is at phase 5. Under such conditions, the proposed plan is likely to contain the epidemic, making sure that it does not deteriorate to phase 6.
The Adequacy of the Government’s Plan
The national government’s strategy to deal with the outbreak of, together with the efforts made by the Illinois’ Emergency Management Agency, appears adequate enough to deal with the problem. The authorities acknowledge the need for non-pharmaceutical and social distancing measures as immediate responses. For this reason, the efforts seem sufficient enough.
References
Centers for Disease Control and Prevention. (2014). Seasonal influenza (flu): Information on avian influenza. Web.
Department of Health and Human Services, & Centers for Disease Control and Prevention. (2007). Interim pre-pandemic planning guidance: Community strategy for pandemic influenza mitigation in the United States- Early, targeted, layered use of non-pharmaceutical interventions. Web.
Homeland Security Council. (2007). National strategy for pandemic influenza: Implementation plan one year summary. Web.
Tyshenko, M. (2007). Management of natural and bioterrorism induced pandemics. Bioethics, 21(7), 364-369.