Influenza virus is one of the few viruses with capability and history of creating pandemics, having resultant deaths, hospitalizations and interruption of economic and societal activities. They have, hence, been a research interest overtime as to control measures to prevent and manage such outbreaks.
STRUCTURE AND PATHOGENESIS OF INFLUENZA
Influenza virus belongs to the orthomyxovirus family as it has segmented RNA genomes with 8 pieces. Its helical capsid is contained within an envelope, on which are 2 glycoproteins responsible for its antigenicity; namely: Hemagglutinin (HA) and Neuraminidase (NA). HA is responsible for cell surface receptor binding and NA provides entry into the cells of the respiratory epithelium as it degrades the protective layer of the mucus of the respiratory tract. In the respiratory tract, it has an incubation period of 24 – 48 hours, after which the cytokines moving in the blood causes systemic symptoms such as myalgia, fever, headaches, sore throat and cough. Complications can result from bacteria or influenza pneumonia.
CLASSIFICATION AND EPIDEMIOLOGY OF INFLUENZA
Influenza virus is distinguished based on its internal nucleoplasm into types A, B and C. Influenza A has 16 types of HA and 9 types of NA found in aquatic birds but 3 types of HA and 2 types of NA in humans. However, Influenza B is only found in humans. Other animals like swine, horses have also been known to be sources of the Influenza virus so if an animal strain of the virus infects the same cell as a human strain, reassortment of segments of RNA genomes will occur, leading to a new variant of the RNA genomes, capable of causing epidemics in humans as pre-existing immunity of many individuals cannot handle the new variant. Influenza A can undergo antigenic shift hence can cause pandemics and yearly outbreaks. On the other hand, because Influenza B is only found in humans, it undergoes antigenic drifts and not shifts, causing outbreaks that are not as dramatic as Influenza A, occurring every 2-4 years. Influenza C is seen as sub clinical and occurs randomly, however, its research has not been conclusive.
TRENDS IN OUTBREAKS OF INFLUENZA VIRUSES
There has never been a systematic examination of the numerous reported possible outbreaks throughout history. Nonetheless, this study concisely details the events and trends in the occurrence of influenza as stated in various scientific and non-scientific sources. For clarity purposes the outbreaks will be subsequently explained based on the strains of Influenza that have caused human outbreaks.
H1NI INFLUENZA VIRUS
H1NI the cause of one of the fatal pandemics throughout history. The outbreaks caused by this strain has led to the death of more Americans than in the both World Wars and the Asian wars combined. This strain was the cause of the Spanish flu which occurred in 1918 till 1919, although it is uncertain where it originally originated from geographically. During this pandemic, about 500 million people worldwide were affected as well as people in the Arctic and remote Pacific Islands. About 50 million to 100 million people, which makes up at least 3-5% of the world population died, with British India having about 17 million deaths.
In 1977, the Russian flu epidemic was also caused by the H1N1 strain which affected mostly people under the age of 23. Most of the adults were exempt as there was previously a similar widespread strain in 1947 – 1957, which developed their immunity against the Russian flu.
The 2009 novel Swine Originated Influenza Virus (S-OIV) strain resulted into a widespread human Influenza outbreak beginning from Mexico and moving into the US and subsequently quickly spreading to 208 countries by the end of 2009. By this time, the WHO stated that the pandemic was the highest level – Level 6 as millions of cases were recorded worldwide, and the cases increased till they were no longer documented in many countries. There were 9596 deaths globally with 1445 recorded in the US. A decline started by August 2010 and was still declining by 2013. The strain, which did not occur amongst swine and is not transmitted by eating pork, affected majorly young people below 18 who comprised of 60% of all the cases. The symptoms were generally mild but low immunity people experienced fatal symptoms. Apparently, most people globally do not have protective antibodies against the glycoprotein on the envelope of the S-OIV, although they may have developed antibodies against the seasonal strain of H1N1 either any form of exposure to the virus or by immunization.
H2N2 INFLUENZA VIRUS
East Asia experienced a new Influenza A virus (H2N2) in February 1957 which prompted an Asian Flu pandemic. The virus was seen reported first at this time in Singapore and subsequently in Hong Kong in April of the same year as well as in some coasts in the US in mid-1957. The pandemic resulted in 1,100,000 deaths globally with a huge 10% occurring in the US. The death occurrences were a far cry from those caused by H1N1 virus. The H2N2 virus is made up of three genes from an H2N2 virus originating an Influenza A bird virus as well as the H2 Hemagglutinin and N2 Neuraminidase genes.
H3N2 INFLUENZA VIRUS
The Hong Kong Flu of 1968 was a H3N2 Influenza A virus which broke out globally after originating from China in July 1968 and lasting till 1970. This pandemic was the third 20th century Influenza A pandemic and it was 11 years after its predecessor, the 1957 Asian flu. It is believed that the H2N2 virus prompted the formation of the H3N2 through a process of antigenic shift, where the Hemagglutinin Antigen H2 on the outer surface of the virus mutated genetically and produced the H3. The Neuraminidase N2 was the same, hence the people that were exposed previously to the H2N2 retained immunity of the Hong Kong virus. The number of deaths caused by this H3N2 virus in the pandemic were one to four million, similar to the H2N2 death numbers. The illnesses caused by this virus were in various intensities in diverse places; it affected a few numbers of people in Japan but was more deadly and widespread in the US. It was highly contagious, and deaths occurred majorly amongst infants and the elderly. The H3N2 virus that caused the pandemic is still considered to be present today but is a strain of seasonal Influenza.
H5N1 INFLUENZA VIRUS
The H5N1 strain of Influenza A virus first occurred in 1997 causing the avian influenza or bird flu resulted in a severe form of human influenza with some deaths in Hong Kong and 254 globally. The infection moved directly from chickens to 408 humans between 2003 and early 2009, passing from the respiratory secretions of the chickens to the chicken guano. In mid-2003 to 2004, the outbreak caused the death of thousands of chickens in many Asian territories. Many chickens were killed in order to curb the outspread. The H5N1 strain hardly moves from person to person but it is of concern because it results in more serious fatality if it gets human transmitted.
H7N9 INFLUENZA VIRUS
2013 recorded an outbreak of influenza caused by H7N9 virus strain. Before 2013, the strain has affected only birds, mostly about 695 chickens. As of July of the same year, 133 people were reported to have Influenza caused by this H7N9 virus, resulting in the death of 43 people, mostly in Taiwan and China. This type of virus does not spread from one person to another. The genes of this virus originate from birds with H7 from ducks and N9 from wild birds and the remaining genes from bramblings in Europe and Asia. It is relatively not as widespread, but it has a mortality rate of 32%.
In summary, the Influenza viruses are of great concern to humans as they are known for causing outbreaks and largely deadly pandemics that occur from time to time. Hence it is constantly a subject of medical studies and discussions.
REFERENCES
- Alexander DJ (2007). An overview of the epidemiology of avian influenza. Vaccine 2007; 25(30), 5637–5644.
- Caini S, Spreeuwenberg P, Donker G (2018) Climatic factors and long‐term trends of influenza‐like illness rates in The Netherlands, 1970–2016. Environ Res. 2018; 167, 307‐313.
- Dowdle WR (2006). Influenza pandemic periodicity, virus recycling, and the art of risk assessment. Emerg Infect Dis 2006; 12(1), 34–39.
- Krauss S, Walker D, Pryor SP et al (2004). Influenza A viruses of migrating wild aquatic birds in North America. Vector Borne Zoonotic Dis 2004; 4(3),177–189.
- Mirsaeidi M, Motahari H, Taghizadeh Khamesi M (2016). Climate change and respiratory infections. Ann Am Thorac Soc. 2016;13(8),1223‐1230.
- Morens DM, Taubenberger JK, Fauci AS (2009). The persistent legacy of the 1918 influenza virus. New England Journal Medicine 2009; 361(3), 225–229.
- Munster VJ, Fouchier RA (2009). Avian influenza virus: of virus and bird ecology. Vaccine 2009; 27(45), 6340–6344.
- Shaman J, Pitzer VE, Viboud C, Grenfell BT, Lipsitch M (2010). Absolute humidity and the seasonal onset of influenza in the continental United States. PLoS Biology 2010;8(2). doi: e1000316.
- Tamerius JD, Shaman J, Alonso WJ (2013). Environmental predictors of seasonal influenza epidemics across temperate and tropical climates. PLoS Pathog. 2013;9(3). doi: e1003194.
- Taubenberger JK, Morens DM (2009). Pandemic influenza – including a risk assessment of H5N1. Rev Sci Tech 2009; 28(1), 187–202.
- Towers S, Chowell G, Hameed R (2013). Climate change and influenza: the likelihood of early and severe influenza seasons following warmer than average winters. PLoS Curr. 2013;5 (2), 101 -154.