Herpes+simplex+virus+Type+1+(HSV-1)

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Taxonomy Classification
Kingdom: N/A Phylum: Vira Class: Group 1 dsDNA Virus Order: Herpesvirales Family: Herpes Viridae Genus: Simplexvirus Species: HSV-1

**Background**
Herpes simplex virus Type 1 is an Alphaherpesvirinae viral disease that is part of the group 1 dsDNA class of viruses. HSV-1 is the leading viral disease, second to only the common cold and influenza. According to the University of Maryland, as many as 90% of Americans have been exposed to the virus. It has the ability to stay dormant for months or even years before being reactivated. HSV-1 is the main cause of herpes infections on the mouth and lips, including cold sores and fever blisters. It is transmitted through kissing or shared drinking materials. Although genital herpes is primarily caused by HSV-2, HSV-1 can also be the culprit. The onset of symptoms may be brought about by a number situations such as sun exposure, fever, menstruation, stress, weakened immune system, or illness.

**Viral Structure**
HSV-1 are considered envelope viruses that bud from the inner membrane which can be modified by the insertion of herpes glycoproteins. The viral membrane is known to be very unstable and if damaged, the virus cannot be infectious. The viral envelope is sensitive to acids, detergents, and organic solvents which all help to degrade the virus lipid envelope. HSV-1 have capsids which are doughnut shaped and measure around 200 nm. The viral DNA material is double stranded.

Figure 1.0 Histology of HSV-1

**Identification Factors**
The identification factors for HSV-1 come in the form of three ways. First are the physical characteristics of a present viral outbreak on a subject. This usually presents as a blister – like structure on the outside of the lip or corner of the mouth. The edges are symmetrical and could contain a clear or serous fluid. The second is the characteristics of the virus under microscopy. They present with very distinct lipid envelopes around the outside of the virus (shown in the picture above). HSV-1 has three unique morphological units. A DNA-containing, icosahedral capsid is surrounded by a layer termed the tegument, which in turn is surrounded by a protein-containing lipid bilayer which is the envelope. Spikes can also be observed from using an immunoelectron microscopy
 * Figure 2: Diagram of HSV-1 Structures**
 * openi.nlm.nih.gov**


 * Figure3: Cryoelectron Microscopy of HSV-1**
 * people.virginia.edu**

**Cellular Entry**
HSV-1 gains access to host cells by way of interacting with several glycoproteins on the surface of the virus and the receptors of the particular host cell. Once bound the host’s receptor, the virus gains entry by creating a pore to gain access.

**HSV-1 Replication**
Once HSV-1 gains access to the host cell, it begins to replicate. This is achieved by a number of viral proteins that act as early and late lytic cycles. **This is why HSV-1 can lay dormant for so long. The early proteins are used for gene regulation and replication of the virus while the late proteins are used for the capsids and receptors for the virus. Once the virus replication is complete, the late proteins provide the packaging of the viral material and acquire the envelope from vesicles within the cytoplasm.

**Diagnosis**
More often than not, HSV-1 can be diagnosed through simple physical examination. There are also other ways to confirm the virus as well. Several lab tests can be done to figure out the structure of the virus through microscopy. A PCR machine can also map out the genomic characteristics to help reveal the true nature of the virus. A culture of the site can also render the identification of the virus. This is done by Direct fluorescent antibody (DFA) test.

**Treatment**
Although there is no specific cure for HSV-1, there are medications to help reduce the overall symptoms or signs associated with a viral outbreak. Most cases are mild and do not render treatment. For prolonged outbreaks that last an extended amount of time, antiviral medications such as acyclovir (Zovirax), famciclovir (Famvir), and valacyclovir (Valtrex) can be given. Antivirals such as Acyclovir work by converting viral thymidine kinase to acyclovir monophosphate which is then converted by host cell kinases to Acyclovir triphosphate. This competitively inhibits and inactivates DNA polymerases to incorporate itself into the viral DNA chain. Resistance to Antivirals is rare.

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References

 * 1) ===1. Hunt, Richard (2010). //Virology: Herpes Viruses// Retrieved from http://pathmicro.med.sc.edu/virol/herpes.htm ===
 * 2) ===2. Jamin, A., Thunuguntla, P., Wicklund, A., Jones, C., & Wiebe, M. S. (2014). //Barrier to Autointegration Factor Becomes Dephosphorylated during HSV-1 Infection and Can Act as a Host Defense by Impairing Viral DNA Replication and Gene Expression. Plos ONE//, 9(6), 1-10. doi:10.1371/journal.pone.0100511 ===
 * 3) ===3. Homa, F., Huffman, J., Toropova, K., Lopez, H., Makhov, A., & Conway, J. (2013). Structure of the Pseudorabies Virus Capsid: Comparison with Herpes Simplex Virus Type 1 and Differential Binding of Essential Minor Proteins. Journal Of Molecular Biology,425(18), 3415-3428. doi:10.1016/j.jmb.2013.06.034 ===
 * 4) ===4. Subhan, S., Jose, R., Duggirala, A., Hari, R. R., Krishna, P., Reddy, S. B., & Sharma, S. (2004). Diagnosis of herpes simplex virus-1 keratitis: Comparison of Giemsa stain, immunofluorescence assay and polymerase chain reaction. Current Eye Research,29(2/3), 209-213. ===
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 * 8) ===8. @http://pathmicro.med.sc.edu/virol/herpes.htm  ===