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The prevalence of HSV –II is so high in the whole world that it leaves millions of families vulnerable to genital herpes and other diseases such as HIV. The HSV-II exposes over 400 million families worldwide to the acquisition of genital herpes and HIV diseases (Looker et al. 2). This research looks at the type 2 Herpes Simplex Virus.
HSV-II causes genital herpes. Human beings contract the genital herpes through sexual intercourse and through getting into contact with the genital surfaces or skins of an infected person. The HSV-II causes lifelong infections that have no cure. Genital herpes exhibits mild or no symptoms at all when in the initial stages of infection. At the initial stage, many people usually fail to notice that they have contracted the infection. However, when the symptoms do appear, the symptoms include genital ulcers fever, aching joints and swollen lymph nodes. The genital ulcers represent the blisters at the genital areas or around the anus of the patient.
Herpes viruses fall into three classifications. The three groups for classification of herpes viruses include herpes simplex viruses (types II and I), the alpha herpes virus and the varicella zoster viruses. All viruses contain a caspid structure made of several DNAs surrounded by a 20-faceted layer, known as icosahedral. According to Davison, herpes virus belongs to the order of Herpesvirales, the family of Herpersviridae and a subfamily of Alphaherpesvirinae(52). The herpes Simplex Virus II, as the name suggests is a virus. The medication for HSV-II entails the use of antiviral to reduce the pain it causes to patients. Examples of antiviral drugs for lowering the pain of HSV-II include acyclovir, valacyclovir and famciclovir. Currently, scientists are yet to find the vaccine and or the cure for genital herpes.
Herpes genitals become resistant to the acyclovir drugs. Jiang et al. reported that the treatment of genital herpes, caused by HSV-II virus require short-term therapy and strategies to avoid the drug developing resistance over its treatment drugs (3). According to Jiang et al, the short-term treatment plans is for patients with a strong immune system. Patients with compromised immune systems require a long-term treatment plan and are at a higher risk of developing resistance to the treatment drugs. Therefore, patients with a compromised immune system when exposed to too much acyclovir drugs would develop resistance to the drug.
The HSV-II virus comprises of a large stranded structures surrounded by a caspid cage. The caspid cage comprises of icosahedral proteins. The HSV-II virus comprise of a protein known as genome in its DNA. The HSV-II comprises of two unique sections, the long unique and short unique sections.
The life cycle of HSV-II, encompass different stages from the entry point, genetic inoculation, invasion of the immune system of human beings, the multiplication of the viruses and the latent stage. The HSV –II virus utilizes the glycoprotein on its structures, which the transmembrane receptors of the surface cells pull during the entry of HSV-II virus into the body of human beings. The glycoprotein components of the virus then combine with the cell membrane of the virus creating a hole in the surface skin of human beings where the virus enters the body of human beings. Once the HSV-II virus enters the host body, it then moves to the cell nucleus. After the virus attaches itself to the cell nucleus, it produces its DNA through its caspid portal. HSV-II caspid comprises of twelve forms of portal proteins and long unique regions, which then exits the virus DNA in a single linear arrangements (Wayengera p23). The single linear arrangements of the HSV –II virus then invade the immune system of human beings. The HSV-II virus then blocks the antigen processing system. The blocking of the antigen processing system allows the HSV-II to survive in the body of human beings for some duration.
After the HSV-II virus attacks the immune system of human beings, blocking the antigen processing cycle, the virus then multiples its production of proteins known as immediate -early. The virus uses the produced immediate-early proteins to regulate the genetic multiplication of the virus. Thereafter, the virus produces another protein, known as alpha tiff proteins, which fuse with the immediate –early proteins. The last stage of the life cycle of the HSV-II virus is the latent infection. During the latent stage of infection, the HSV-II virus interferes with the genome of human beings altering the body mechanisms of doing away with worn cells. The HSV-II viruses control human cells causing the various symptoms of genital herpes in human beings.
Works Cited
- Davison, Andrew J. ‘Herpesvirus systematics.’ Veterinary microbiology 143.1 (2010): 52-69. (Google scholar).
- Jiang, Yu-Chen, et al. ‘New strategies against drug resistance to herpes simplex virus.’ International journal of oral science 8.1 (2016): 1-6. (Google Scholar).
- Looker, Katharine J., et al. ‘Global estimates of prevalent and incident herpes simplex virus type 2 infections in 2012.’ PloS one 10.1 (2015). (Google Scholar).
- Wayengera, Misaki. ‘Identity of zinc finger nucleases with specificity to herpes simplex virus type II genomic DNA: novel HSV-2 vaccine/therapy precursors.’ Theoretical Biology and Medical Modelling 8.1 (2011): 23. (Google Scholar).
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