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14.04.2014

Herpes simplex virus treatment guidelines, what causes herpes outbreaks on buttocks - Try Out

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The drug acyclovir (Zovirax) does not have activity against viral pathogens until it is converted to the active form acyclovir triphosphate. Although prior research in animal models suggested that thymidine kinase-negative HSV isolates have decreased virulence[12], several reports have shown that acyclovir-resistant HSV can cause significant clinical disease in humans[10,11,12,13].
The most common types of acyclovir-resistant HSV infection involve either absent production of viral thymidine kinase (TK-negative mutants), or partially reduced production of viral thymidine kinase (TK-partial mutants). The herpes thymidine kinase is a 376-amino-acid protein encoded by the UL23 gene and the herpes DNA polymerase is a larger protein (approximately 1,200-amino-acids long) and it is encoded by the UL30 gene[6].
Perioral Lesion with Extension to Face Caused by Acyclovir-Resistant Herpes Simplex Virus">Figure 4). If acyclovir resistance is suspected, testing for HSV should include a viral culture of the sample, since resistance testing will require isolation of virus. Drugs such as ganciclovir (Cytovene) and valganciclovir (Valcyte), that use a similar viral kinase are also ineffective. Because cidofovir does not require activation by a viral kinase, it should theoretically have activity against acyclovir-resistant HSV infections. In this illustration, the notation TK- refers to deficient production of viral thymidine kinase, either through TK-negative mutants or TK-partial mutants.


Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. Acyclovir triphosphate, the active form of acyclovir, is present in 40- to 100-fold higher concentrations in herpes simplex virus (HSV)-infected cells than in uninfected cells.
The DNA polymerase mutants result from a mutation in the HSV pol gene that causes a decreased binding of acyclovir-triphosphate to viral DNA polymerase. Laboratory testing for acyclovir resistance includes a variety of phenotypic assays, such as the plaque-reduction assay, dye-uptake assays, and viral DNA-inhibition assays[5].
Rarely, acyclovir-resistant HSV infections result from altered viral thymidine kinase and these strains of HSV could theoretically respond to famciclovir.
The acyclovir triphosphate competes with 2-deoxyguanosine triphosphate (dGTP) as a substrate for viral DNA polymerase, as well as acting as a chain terminator. As a result of the deficient production of TK, the HSV strains fail to effectively generate acyclovir triphosphate and thus acyclovir does not effectively inhibit viral DNA polymerase. Acyclovir triphosphate has a two-pronged mechanism of action: (1) it competes with 2-deoxyguanosine triphosphate (dGTP) as a substrate for viral DNA polymerase and (2) once it becomes incorporated into the replicating viral DNA, it acts as a chain terminator because it does not have a terminal 3' hydroxyl group. Among HIV-infected individuals with acyclovir-resistant HSV infection, they typically have advanced AIDS, a history of recurrent HSV infection, and significant prior treatment with acyclovir, famciclovir, or valacyclovir (Valtrex)[9,11].


Because foscarnet does not require activation by viral thymidine kinase, it retains activity against HSV strains with absent, partially reduced, or altered production of thymidine kinase. In actual infection, the HSV releases its naked capsid that delivers DNA to the human nucleus; the active drug acyclovir triphosphate exerts its action on the viral DNA located in the nucleus. In contrast, penciclovir, the active component of the prodrug famciclovir (Famvir), does not act as a chain terminator because it has a terminal 3' hydroxyl group that permits viral primer-template extension. Rare reports have documented acyclovir-resistant HSV infection in persons without prior treatment with acyclovir, famciclovir, or valacyclovir[5]. Within a single lesion, heterogeneous virus populations may exist composed of susceptible and resistant strains. Foscarnet (Foscavir) is a pyrophosphate analog that directly inhibits viral DNA polymerase by reversibly blocking the pyrophosphate binding site of the viral polymerase (in addition to inhibiting the cleavage of pyrophosphate from deoxynucleotide triphosphates)[1].
The 2009 opportunistic infections guidelines note topical therapy with trifluridine, cidofovir, and imiquimod has been successful as shown in case reports and these topical agents are listed as alternative therapies to foscarnet[17].



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