Herpes - Symptoms, Diagnosis, Treatments, Cure & Causes

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Herpes simplex virus-From Wikipedia, the free encyclopedia

?Herpes simplex virus

Microscopy image of a herpes simplex virus.

Virus classification

Group: Group I (dsDNA)

Family: Herpesviridae

Subfamily: Alphaherpesvirinae

Genus: Simplexvirus

Species: Herpes simplex virus 1 (HSV-1)

Species: Herpes simplex virus 2 (HSV-2)

This article is about the virus. For information about the disease, see Herpes simplex. For information on the United States Navy Ship, see HSV-2 Swift.

Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are two strains of the Herpes virus family, Herpesviridae, which cause infections in humans. HSV-1 and 2 are also referred to as Human Herpes Virus 1 and 2 (HHV-1 and HHV-2).

After an initial, or primary, infection, HSV establishes latency, during which the virus is present in the cell bodies of nerves which innervate the area of original outbreak. During reactivation, virus is produced in the cell and transported outwardly via the nerve cell's axon to the skin.[1] The ability of Herpes virus to establish latency leads to the chronic nature of Herpes infection; after the initial infection subsides, Herpes symptoms may periodically recur in the form of outbreaks of herpetic sores near the site of original infection.

Herpes infections are marked by painful, watery blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals. The blisters resemble those seen in Chickenpox — an infection caused by a third member of the alpha-Herpesviridae subfamily, Varicella Zoster Virus (VZV), also known as Human Herpes Virus 3 (HHV-3). Lesions heal with a crudescent scab, the hallmark of herpetic disease. Herpes is contagious if the carrier is producing and releasing ("shedding") virus. This is particularly likely during an outbreak, although individuals may shed virus between outbreaks. Although no cure is yet available, treatments exist which reduce the likelihood of viral shedding. An HSV infection on the lips is commonly known as a "cold sore" or "fever blister" and should not to be confused with a canker sore; canker sores are not caused by the HSV virus.

Contents

1 Life cycle

1.1 Transmission

1.2 Cellular entry

1.3 Replication

2 Treatment

2.1 Nucleoside Analogs

2.2 Fusion Inhibitors

2.3 Helicase-Primase Inhibitors

2.4 Dietary Supplements

2.5 Other

3 Vaccine Research

4 References

5 External Links

Life cycle

Transmission

HSV is generally transmitted by direct contact of lips or genitals when the sores are present, or just before they appear (known as shedding). In addition, herpes may be transmitted during childbirth, which can be fatal to the infant. The immature immune system of the child is unable to defend against the virus and even if treated, infection can result in brain damage. Transmission occurs while passing through the birth canal and the risk of infection is minimal if there are no symptoms or exposed blisters during delivery. The first outbreak after exposure to HSV is commonly more severe than future outbreaks, as the body has not had a chance to produce antibodies; this first outbreak also carries the risk of developing meningitis.

Cellular entry

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell.

The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.[2]

In the case of Herpes virus, initial interactions occur when glycoprotein C, on the surface of the viral envelope, binds to a cell surface particle, heparan sulfate. Glycoprotein D binds specifically to the herpesvirus entry mediator receptor (HVEM), thus providing a strong, fixed attachment to the host cell. These interactions bring the membrane surfaces into mutual proximity and allow for other surface glycoproteins to interact.

Once bound to the HVEM, glycoprotein D changes its conformation and interacts with glycoproteins H and L, which form a complex. The interaction of these membrane proteins results in the hemifusion state. Afterward, glycoprotein B interaction with the glycoprotein H and L complex creates an entry pore.[2] Glycoprotein B interacts with host cell surface glycosaminoglycans.

Replication

After the viral envelope contents of capsid with tegument proteins has entered the cell via the entry pore, the viral particles migrate to the nucleus, where the genome is replicated using enzymes from the host cell. Upon entering the cell, an α-TIF protein also joins the viral particle and aids in immediate early Transcription. The virion host shutoff protein (VHF-UL41) is very important to viral replication. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene expression of viral proteins. While the viral genome immediately travels to the nucleus, the VHF protein remains in the cytoplasm.

The packaging of the viral particles, which include the genome, core and the capsid, occur in the nucleus. In the nucleus, cleavage of genome concatemers occurs and these are placed into pre-formed capsids. The viral envelope is acquired from the nuclear envelope, more specifically the inner lamellae of the membrane.[3]

Treatment

Nucleoside Analogs

Treatment is available in the form of antiviral medications such as nucleoside analog, which reduce the duration of symptoms and accelerate healing.

Nucleoside analogs are molecules which possess a similarity to natural nucleosides — the building-blocks of DNA and RNA. Because the replicating virus incorporates these analogs into viral DNA, the genetic material produced contains defects and mutations. As a result, the subsequent generation of virus produced is damaged and reduced in number.

Oral Prodrug

Drug Analog of Nucleoside Nucleoside Family

Famciclovir[4]

(bioavailability: 75% oral)

(trade names: Famvir) Penciclovir

(1.5% oral, IV, locally topical)

(Denavir, Fenistil) guanosine purine

Valaciclovir

(55% oral)

(Valtrex) Aciclovir

(10-20% oral)

(Zovirax, Zovir)

Valganciclovir

(60% oral)

(Valcyte) Ganciclovir

(5% oral, IV, locally intraocular)

(Cytovene, Cymevene)

Brivudine[5](BVDU) thymidine pyrimidine

Treatment should begin at the first symptoms of an outbreak for best results as far as duration and healing; should treatment begin before the lesions appear, it is possible that the outbreak can be averted. Another option is the use of daily suppressive therapy, in which antivirals are taken every day over the course of years. Suppressive therapy reduces frequency of symptoms and recurrence of outbreaks. In addition, suppressive therapy reduces subclinical shedding, lowering the risk of transmission through sexual contact or kissing.

Of these, Ganciclovir is known to have cytotoxic effects on infected cells, while Aciclovir is not known to have this effect.[6]

Fusion Inhibitors

Fusion inhibitors prevent "fusion" of the viral envelope with the cell membrane. This prevents viral entry to the cell.

Docosanol

Helicase-Primase Inhibitors

One of three key protein structures involved in HSV DNA replication is the Helicase-Primase structure. New research compounds which bind to this megamolecule show remarkable effectiveness against HSV. In particular, BAY 57-1293 has been used to treat infant HSV-2 encephalitis, and has also shown positive results in animals models of HSV infection.[7]

Dietary Supplements

The amino acid lysine has demonstrated the ability to reduce the duration of infection through inhibiting the replication of the HSV. When foods high in lysine (such as cheese) are consumed in preference to foods high in arginine, HSV replication may be inhibited; conversely, consuming foods high in arginine (such as nuts or peanuts) may interfere with the therapeutic use of lysine.[8][9] However, according to the American Social Health Association: "While some studies have suggested that lysine supplements can reduce the frequency of recurrences or healing time, other trials have been unable to replicate those results. Therefore, there is not sufficient information to discern how effective it may be, in addition to what the effective dosages or frequency of L-lysine may be."[10]

Other

Undecylenic acid (Castor oil derivative) is also proven to have anti-bacterial and anti-viral properties that are effective on viral skin infections such as the herpes simplex virus (HSV).

Butylated Hydroxytoluene (BHT), commonly available as a food preservative, has been shown in in-vitro laboratory studies to inactivate the herpes virus.[11] In-vivo studies in animals confirmed the anti-viral activity of BHT against genital herpes.[12] However BHT has not been clinically tested and approved to treat herpes infections in humans.

Vaccine Research

Herpevac, a vaccine for HSV-2 (the herpesvirus variant that causes genital herpes) is currently (as of February 2007) undergoing clinical testing in women in the United States and Canada[13][14]. Previous studies have determined that this vaccine is approximately 70% effective in women, but does not prevent the disease in men. [15]

References

^ Herpes simplex. DermNet NZ — New Zealand Dermatological Society (16 Sep 2006). Retrieved on 2006 October 15.

^ a b Subramanian RP, Geraghty RJ (20 Feb 2007). "Herpes simplex virus type 1 mediates fusion through a hemifusion intermediate by sequential activity of glycoproteins D, H, L, and B". Proceedings of the National Academy of Sciences, USA 104 (8). PMID 17299053.

^ Microbiologybytes

^ American Social Health Association article on Famciclovir

^ CIUCCI A., LAFRATE E. M., MANZINI S., GIACHETTI A.. "Mechanism of antiviral action of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) : direct evidence with 14-C-BVDU in herpes simplex virus-infected cells".

^ RUBSAM L. Z.,DAVIDSON B. L.,SHEWACH D. S. (1998). "Superior cytotoxicity with ganciclovir compared with acyclovir and 1-β-D-arabinofuranosylthymine in herpes simplex virus-thymidine kinase-expressing cells : A novel paradigm for cell killing". Cancer Research.

^ Crumpacker, C.S. & Schaffer, P.A. (2002). New anti-HSV therapeutics target the helicase−primase complex. Nature Medicine 8, 327 - 328. doi:10.1038/nm0402-327 on-line

^ Alternative medicine for HSV, retrieved December 6th, 2006

^ Referenced page on Cold Sores, retrieved December 6th, 2006

^ Treatment for genital herpes at the American Social Health Association

^ Snipes W, Person S, Keith A, Cupp J. "Butylated hydroxytoluene inactivates lipid-containing viruses" Science. 1975;188(4183):64-6

^ Richards JT, Katz ME, Kern ER. "Topical butylated hydroxytoluene treatment of genital herpes simplex virus infections of guinea pigs" Antiviral Res 1985;5(5):281-90

^ First herpes vaccine under study. , retrieved March 5th, 2007

^ Herpevac Trial for Women (NIH Site), retrieved March 5th, 2007

^ Major Herpes Vaccine Trial Launched in Women, retrieved March 5, 2007

Microbiologybytes: Herpes Simplex (HSV-1/2, HHV 1/2). Retrieved on 2007 February 24.

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