Herpes simplex virus

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Herpes Simplex Virus

Herpes simplex virus type 1 (HSV-1) affects 90% of the world's population, in order to understand how they can infect so many people we will look at the structure, life cycle, disease, and kinds of treatment for this virus3. In addition we will overview the epidemiology of the virus.

Herpes simplex virus type 1 is a linear dsDNA virus classified in Baltimore class I. Since it is a dsDNA virus their genome is about 200 kilobase pairs. The general structure of HSV-1 consists of an envelope, glycoproteins, icosahedral capsid, and linear dsDNA in the center. The envelope is covered with viral glycoproteins, gC and gD, that bind to heparin-sulfate receptors on the cell surface to initiate infection4. Within the envelope is the tegument which links the envelope to the capsid. The tegument also contains proteins and mRNAs that are ready to disrupt cellular processes. Within the center of the HSV-1 structure is the icosahedral capsid that protects the linear dsDNA inside4.

HSV-1 life's cycle begins with the attachment of gC receptors to epithelial cell surface heparin-sulfate receptors, which in turn anchors and pulls HSV-1 towards the cell surface3. Then gD receptors binds with cell surface HveA receptors which induces fusion of the envelope into the plasma membrane, therefore releasing tegument proteins and the icosahedral capsid. Tegument proteins immediately shuts down the host's cellular processes as well as activates viral transcription. The capsid travels to the nucleus and begins association with the nuclear pore. Linear dsDNA along with some tegument proteins are release inside the nucleus, which initiates immediate early gene transcription4. Linear dsDNA is circularized by host's cellular DNA repair enzymes.

Utilizing host's cellular transcriptional mechanism; viral promoter sites are initialized by alpha-TIF protein binding to cellular Oct-1 that is already bound to TAATGARAT sequence. Then the pre-initiation complex is form at the TATA box. Then uses cellular DNA-dependent RNA polymerase mediated transcription at the viral promoter site. During transcription mRNAs are capped and poly-adenylation by host enzymes. Then mRNAs are transported to the cytoplasm for translation into early proteins and migrate back to the nucleus, which mediates viral DNA replication4.

Herpes simplex virus type 1 encodes its own DNA dependent DNA polymerase and proteins that are needed for DNA replication. These proteins include ssDNA binding proteins, origin binding protein, and helicase/primase complex4. The first step of DNA replication is the binding of origin binding protein +ATP to the replication origin in order to denature DNA to open up a replication hole. Then helicase/primase complex synthesize new HSV-1 genomes and are cleaved forming a rolling circle intermediate. As rolling circle DNA replication continues to grow a specific sequence will mediate cleaving which creates and transport the new HSV-1 genomes for packaging in the capsid4.

Late gene transcription occurs when early proteins switch to enhancing late gene transcription and inhibits early gene transcription. Structural proteins, glycoproteins, and icosahedral capsids are synthesized and transported to the nucleus4. Assembly of icosahedral capsids and viral proteins occurs in the nucleus around scaffolding proteins4. Encapsidation occurs and the HSV-1 dsDNA genomes are cleaved and packaged into the capsid. The capsids obtain their envelope from the nuclear membrane, Golgi, vesicles, and then egress by budding off from the plasma membrane4.

Herpes simplex virus type 1 goes into latency phase, usually after acute infection, when they infect non-replicating sensory neurons of trigeminal ganglia4. In which HSV-1 moves up the axon and enters the nucleus, where the viral genomes is integrated in host's histones. Histones contain cellular DNA and viral circular dsDNA that replicates in conjunction with the host's DNA replication. In addition immediate early genes are absent during latent infection, which means no viral genes are expressed. Instead Latency associated transcript (LAT) mRNA are transcribed and expressed abundantly maintaining the latent state by inhibiting apoptosis and immediate early gene transcription4. Reactivation usually occurs from psychological stress that triggers immediate early gene transcription in histones, which blocks LAT mRNA transcription leading to activation of the lytic cycle.

Herpes simplex virus type 1 infection is a recurring life long disease because of the virus ability to invade the sensory neurons to establish latency and evading the immune system. When HSV-1 infection is active it is highly contagious, which is transmitted through skin-to-skin contact with sores and saliva. HSV-1 evades the immune system by interfering with MHC class I presentation of antigen on the cell surface. To achieve this HSV-1 secretes ICP-47 proteins early in the infection, which inhibits TAP2. TAP is a transporter that is responsible to capture viral proteins and present antigen on the cell surface for CD8+ T cell recognition via golgi apparatus. Thus CD8+ T cells won't be able to mediate an immune response2.

HSV-1 diseases are based on anatomic location, age, and immune status of the host. HSV-1 infection can cause gingivostomatitis, pharyngitis, cold sores, whitlow, and encephalitis. Gingivostomatits is the infection of children aged 6 months to 5 years. Symptoms includes fever, anorexia and sores in cheeks that lasts 5-7 days, however viral shedding in the saliva can last 3 weeks or more. Pharyngitis is the inflammation of the pharynx in adults3. Symptoms include ulcerative lesions in pharynx, fever, headache, malaise, and sore throat. Cold sores are the most common that affects any age group and usually found around the mouth area. Symptoms include burning, pain and tingling at the site, which soon develop into intraepidermal vesicles that puss up. Cold sores last about 5 days and recur about two or more times each year. Whitlow is when HSV-1 infects the fingers and has similar symptoms to cold sores3. Encephalitis is usually the reactivation of HSV-1 and infects the brain, causing inflammation. Encephalitis is a rare disease with symptoms of confusion, disorientation, drowsiness, fever, headache and light-sensitivity. There are treatments for HSV-1 diseases if diagnose early, however HSV-1 can reactivate in the future.

There are no known treatments to eradicate herpes simplex virus type 1 from the body; however there are antiviral drugs that help reduce viral shedding. Most HSV-1 infections go away by themselves in a couple of weeks without treatment3. Treatments for gingivostomatitis, pharyngitis, cold sores, and whitlow are the use of antiviral drugs such as peniclovir, acyclovir, valacyclorvir, or gancyclovir. To prevent reactivation of HSV-1 it is recommended to practice good oral and body hygiene as well as avoiding contact with infected persons3. Encephalitis can be treated with antiviral drugs and supportive care. Supportive care treatment is keeping the infected person hydrated with fluids and making sure they get enough nutrition. Prognosis of encephalitis without treatment will lead the infected person to a rapid death.

Herpes simplex virus type 1 is ubiquitous with 80% of the population are asymptomatic. The virus affects everyone in the world regardless of race, age, and sex. However immune compromise individuals are more susceptible to reactivation of HSV-1 infection. HSV-1 with HIV-1 infection has a higher rate of reactivation compared to the population with only HSV-1, which is found prevalent in sub-Saharan Africa1.

Herpes simplex virus type 1 is a linear dsDNA with unique proteins that aide the virus in evading the immune system and helps the virus maintain its latent state. HSV-1 is found in 90% of the world population. In addition HSV-1 has a unique process of DNA replication called rolling circle replication and assembly of new viruses happens in the nucleus. Most HSV-1 infections goes away with time if no treatment is used and only encephalitis is one of the rare disease that can be fatal. Interestingly HSV-1 with HIV-1 infection cause more frequent reactivation of HSV-1 infection.

References

  1. Baeton, Jared. "HSV Herpes Simplex Virus and HIV-1". 3/30/2010 .
  2. Friedman, HM. "Immune evasion by herpes simplex virus type 1, strategies for virus survival". Trans Am Clin Climatol Assoc. 2003: 103-112.
  3. TMLDirect

  4. Salvaggio, Michelle. "Herpes Simplex Virus". 3/30/2010 .
  5. Wagner, Edward. "Herpes simplex virus Research". 3/30/2010 .

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