Call us
301-363-4651 (Available 9 a.m. to 5 p.m. CST from Monday to Friday)
Herpes is caused by two different but similar viruses: herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). HSV-1 and HSV-2 are two members of the human Herpesviridae family, produce viral infections in the majority of humans [1]. HSV-1 more commonly causes infections around the mouth while HSV-2 more commonly causes genital infections [2]. Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. They are transmitted by direct contact with body fluids or lesions of an infected individual.
Read on to learn more about Herpes simplex virus (HSV), including structure, the important proteins, infection Symptoms, transmission, Diagnosis and Treatment.
The structure of the herpes virus consists of a relatively large double-stranded linear DNA genome wrapped in an icosahedral protein cage. The genomes of HSV-1 and HSV-2 are contain two unique regions called the long unique region (UL) and the short unique region (US). Of the 74 known ORFs, UL contains 56 viral genes, whereas US contains only 12 [3]. Five proteins from (UL) form viral capsids-UL6, UL18, UL35, UL38 and the major capsid protein UL19 [4].
Entry of HSV into a host cell involves several glycoproteins on the surface of the enveloped virus binding to their transmembrane receptors on the cell surface. Initial interactions occur when glycoprotein C (gC) and glycoprotein B (gB) bind to a cell surface particle called heparan sulfate. Next, the major receptor binding protein, glycoprotein D (gD), binds specifically to at least one of three known entry receptors [5]. These cell receptors include herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate.
| Target | Uniprot No. | Protein Name | Description |
|---|---|---|---|
| gB | P10211 | Envelope glycoprotein B (HHV-1) | Envelope glycoprotein that forms spikes at the surface of virion envelope. Involved in fusion of viral and cellular membranes leading to virus entry into the host cell. |
| P08666 | Envelope glycoprotein B (HHV-2) | ||
| gC | P10228 | Envelope glycoprotein C (HHV-1) | Major attachment protein that mediates binding of the virus to cell surface heparan sulfate or chondroitin sulfate. Plays also a role in host immune evasion by inhibiting the host complement cascade activation. |
| P03173 | Envelope glycoprotein C (HHV-2) | ||
| gD | P57083 | Envelope glycoprotein D (HHV-1) | Envelope glycoprotein that binds to the potential host cell entry receptors TNFRSF14/HVEM, NECTIN1 and 3-O-sulfated heparan sulfate. |
| P03172 | Envelope glycoprotein D (HHV-2) | ||
| gG | P06484 | Envelope glycoprotein G (HHV-1) | Chemokine-binding protein that inhibits neutrophils' chemotaxis. |
| P81780 | Envelope glycoprotein G (HHV-2) | ||
| gL | Q96912 | Envelope glycoprotein L (HHV-1) | The heterodimer glycoprotein H-glycoprotein L is required for the fusion of viral and plasma membranes leading to virus entry into the host cell. |
| P06764 | Envelope glycoprotein I (HHV-2) | ||
| TK | P03176 | Thymidine kinase (HHV-1) | Catalyzes the transfer of the gamma-phospho group of ATP to thymidine to generate dTMP in the salvage pathway of pyrimidine synthesis. |
| P89446 | Thymidine kinase (HHV-2) | ||
| UL48 | P04486 | Tegument protein VP16 (HHV-1) | Transcriptional activator of immediate-early (IE) gene products (alpha genes). |
| P68335 | Tegument protein VP16 (HHV-2) | ||
| UL49 | P10233 | Tegument protein VP22 (HHV-1) | Participates in both the accumulation of viral mRNAs and viral protein translation at late time of infection. Plays a role in microtubule reorganization that occurs after viral infection by stabilizing microtubule network |
| P89468 | Tegument protein VP22 (HHV-2) | ||
| US11 | P04487 | Accessory factor US11 (HHV-1) | Plays a role in the inhibition of host immune response. Participates in the inhibition of host autophagy by interacting with and inhibiting host PKR/EIF2AK2. |
| P89479 | Probable RNA-binding protein (HHV-2) | ||
| US12 | P03170 | ICP47 protein (HHV-1) | Plays a role in the inhibition of host immune response. |
| P14345 | ICP47 protein (HHV-2) |
Herpes simplex is an infection that is caused by a herpes simplex virus (HSV). HSV type 1 most commonly causes cold sores, it can also cause genital herpes. HSV type 2 is the usual cause of genital herpes, but it also can infect the mouth. Infections are categorized based on the part of the body infected.
Oral herpes causes cold sores around the mouth or face. It may result in small blisters in groups often called cold sores or fever blisters or may just cause a sore throat.
Genital herpes is a sexually transmitted disease (STD). It affects the genitals, buttocks or anal area, may have minimal symptoms or form blisters that break open and result in small ulcers.
Other disorders caused by herpes simplex include: herpetic whitlow when it involves the fingers, herpes of the eye, herpes infection of the brain, and neonatal herpes when it affects a newborn, among others [6].
Herpes cycles between periods of active disease followed by periods without symptoms. The first episode is often more severe and may be associated with fever, muscle pains, swollen lymph nodes and headaches.
HSV-1 and HSV-2 are transmitted by contact with an infected person who has reactivations of the virus. Spread from skin-to-skin contact with infected areas, often during vaginal sex, oral sex, anal sex, and kissing.
HSV-1 is often acquired orally during childhood. It may also be sexually transmitted, including contact with saliva, such as kissing and mouth-to-genital contact (oral sex).
HSV-2 is primarily a sexually transmitted infection, subclinical shedding may account for most of the transmission. HSV-2 is periodically shed in the human genital tract, most often asymptomatically. Most sexual transmissions occur during periods of asymptomatic shedding [7].
Both HSV-1 and HSV-2 may also be transmitted vertically during childbirth. However, the risk of infection transmission is minimal if the mother has no symptoms or exposed blisters during delivery. The risk is considerable when the mother is infected with the virus for the first time during late pregnancy [8].
This type of virus is generally diagnosed with a physical exam. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.
Laboratory testing is often used to confirm a diagnosis of genital herpes, include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction to test for presence of viral DNA. Blood tests for antibodies to HSV-1 and HSV-2 can also help diagnose these infections.
There is currently no cure for the virus. The focus of treatment is to eliminate sores and limit disease outbreaks. Treatment usually involves generic antiviral drugs that interfere with the replication of the virus, reduce the physical severity of the disease associated with the disease outbreak, and reduce the chance of transmission to others.
References
[1] Chayavichitsilp P, Buckwalter JV, Krakowski AC, et al. Herpes simplex [J]. Pediatr Rev. 2009 Apr; 30(4):119-29.
[2] Balasubramaniam R, Kuperstein AS, Stoopler ET. Update on oral herpes virus infections [J]. PDent Clin North Am. 2014 Apr; 58(2):265-80
[3] McGeoch DJ, Rixon FJ, Davison AJ. Topics in herpesvirus genomics and evolution [J]. PVirus Res. 2006 Apr; 117(1):90-104.
[4] Mettenleiter TC1, Klupp BG, Granzow H. Herpesvirus assembly: a tale of two membranes [J]. PCurr Opin Microbiol. 2006 Aug; 9(4):423-9.
[5] Akhtar J, Shukla D. Viral entry mechanisms: cellular and viral mediators of herpes simplex virus entry [J]. PFEBS J. 2009 Dec; 276(24):7228-36.
[6] Stephenson-Famy A, Gardella C. Herpes simplex virus infection during pregnancy [J]. PObstet Gynecol Clin North Am. 2014 Dec; 41(4):601-14.
[7] Schiffer JT1, Mayer BT, Fong Y, Swan DA, Wald A. Herpes simplex virus-2 transmission probability estimates based on quantity of viral shedding [J]. PJ R Soc Interface. 2014 Mar 26; 11(95)
[8] Kimberlin DW. Herpes simplex virus infections of the newborn [J]. PSemin Perinatol. 2007 Feb; 31(1):19-25.
Proteins
Antibodies
ELISA Kits
