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Herpes Medications


There are several types of herpes viruses that cause diseases in humans:

  • Herpes simplex virus (HSV-1) - causes fever blisters (cold sores), gingivostomatitis, herpes keratitis
  • Herpes simplex virus 2 (HSV-2) - causes genital lesions, neonatal infections
  • Varicella-Zoster virus (VZV) - chickenpox, shingles
  • Epstein-Barr Virus (EBV) - infectious mononucleosis
  • Cytomegalovirus (CMV) - usually asymptomatic infection

They belong to the subfamily Alphaherpesvirinae in the family Herpesviridae and are ubiquitous and extremely well adapted pathogens. The hallmark of herpesvirus infections is the establishment of a lifelong latency with subsequent reactivation and outbreaks. The name "herpes" comes from the Greek '"Herpein" which means to creep, describing the latent or recurrent nature of viruses.

Herpes simplex virus

Herpes simplex virus (HSV) is a DNA virus that may enter the body through abraded skin or intact mucous membranes. Epithelial cells are the initial targets. Once infected, these cells die, releasing clear fluid intradermally to form vesicles and merging with other cells to create multinucleated giant cells.

HSV exists as two separate types, labeled 1 and 2. Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are closely related but differ in where they typically establish latency in the body - the "site of preference."

HSV-1 usually establishes latency in the trigeminal ganglion, a group of nerve cells near the ear. From there, it tends to reactivate on the lower lip or face. HSV-1 is usually acquired in childhood.

HSV-2 usually establishes latency in the sacral ganglion at the base of the spine. From there, it reactivates more commonly in the genital area. Sexual intercourse is the most frequent way of transmission of the infection. HSV-2 may also occur in other locations, but is usually found below the waist.

However, lesion location does not necessarily indicate the viral type. HSV-1 and HSV-2 can infect both the upper and lower parts of the body, and the proportion of genital HSV-1 is now on the increase.

If a person has contracted the HSV-1 virus, he can contract the HSV-2 also. However, prior HSV-1 provides moderate protection against getting HSV-2, and reduces its severity2, 3. A prior genital HSV-1 infection may give more protection against genital HSV-2 than a prior oral infection with HSV-1. Having a primary HSV-2 infection seems to provide some immunity to an HSV-12. That’s because the virus causes the body to produce antibodies that provide some crossover protection against the other type.

More information on Acyclovir for cold sore treatment

Varicella-Zoster virus

Varicella-zoster virus (VZV) closely resembles the herpes simplex virus. It causes chickenpox and herpes zoster. After primary infection, VZV remains dormant in neurosensory ganglia for life. Upon reactivation, the virus migrates down the sensory nerve to the skin, causing the characteristic painful vesicular rash.

More information on Valacyclovir for herpes zoster treatment

Herpes Medications

Antiviral agents used to treat herpes virus infections are nucleoside analogs. They include acyclovir (the original and prototypical member of this class), valacyclovir, penciclovir, and famciclovir.

Nucleoside analogs work by interfering with viral replication, stopping the virus from multiplying, and providing a greater opportunity for the immune response. They are initially phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit viral DNA polymerase with 30-50 times the potency of human alpha-DNA polymerase.

Antiviral agents can be used to treat an outbreak, hasten lesion healing, reduce the frequency of outbreaks, suppress viral shedding, and to prevent the transmission of herpes virus to sexual partner. However, all currently available antiviral medications do not cure herpes infections as they don't eradicate dormant virus.

Acyclovir (Zovirax), a purine nucleoside analog, revolutionized the treatment of herpes simplex infections. Its main disadvantages are low bioavailability and five-times-daily regimen.

Valacyclovir (Valtrex) is the l-valine ester prodrug of acyclovir. It is well absorbed and rapidly converted to its active form. The increased bioavailability allows a more convenient dosing. Oral valacyclovir can reach blood levels similar to those obtained with intravenous acyclovir.

Famciclovir (Famvir) is a prodrug of penciclovir with improved oral bioavailability. Penciclovir is phosphorylated by viral enzyme thymidine kinase to its active form. Famciclovir provides convenient twice-daily dosing, long intracellular half-life1, and good bioavailability.

Penciclovir (Denavir) is used topically for the treatment recurrent herpes labialis.

Note: Resistant cases of HSV infections are treated with foscarnet or cidofovir4. Viral strains resistant to acyclovir are almost always cross-resistant to other nucleoside analogs such as famciclovir 5.

See also:

References

  • 1. Earnshaw DL, Bacon TH, Darlison SJ, Edmonds K, Perkins RM, Vere Hodge RA Mode of antiviral action of penciclovir in MRC-5 cells infected with herpes simplex virus type 1 (HSV-1), HSV-2, and varicella-zoster virus. Antimicrob Agents Chemother 1992;36: 2747–2757
  • 2. Nahmias AJ, Lee FK, Beckman-Nahmias S. Sero-epidemiological and -sociological patterns of herpes simplex virus in the world. Scand J Infect Dis Suppl. 1990;69:19-36.
  • 3. Sturn B, Schneweis KE. Protective effect of an oral infection with herpes simplex virus type 1 against subsequent genital herpes simplex virus type 2. Med Microbiol Immunol. 1978 Jul 4;165(2):119-27.
  • 4. Chilukuri S, Rosen T. Management of acyclovir-resistant herpes simplex virus. Dermatol Clin. 2003 Apr;21(2):311-20. PubMed
  • 5. Morfin F, Thouvenot D. Herpes simplex virus resistance to antiviral drugs. J Clin Virol. 2003 Jan;26(1):29-37.

Written by HealthyStock.net, October 2009.
Last updated: October, 2015


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