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04.05.2014

Herpes simplex 3 and 4, herpes simplex laser treatment - PDF Review

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All of the drugs that require initial activation by HSV thymidine kinase (acyclovir, famciclovir, and valacyclovir) generally produce ineffective results against HSV strains that have absent or decreased thymidine kinase production.
In this HSV-infected human cell, the acyclovir molecules enter the cell and are converted to acyclovir monophosphate by the HSV enzyme thymidine kinase (TK). Genital herpes is a disease caused by the herpes simplex virus which is called as HSV in short. Symptoms which are sufficient for symptomatic confirmation of the Herpes Simplex (HSV) appears as a blister or as multiple bllisters on or around affected areas-usually the mouth, genitals or rectum. This test detects the antibodies that are made by the immune system to fight a herpes infection. Sakthi’s Hospital And Research Center are pioneer in the treatment of Sexually Transmitted diseases like Syphilis, gonorrhea, etc. 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). Drugs such as ganciclovir (Cytovene) and valganciclovir (Valcyte), that use a similar viral kinase are also ineffective. 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.
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. 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]. Within a single lesion, heterogeneous virus populations may exist composed of susceptible and resistant strains. 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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