Aciclovir herpes simplex virus

Vidarabine (adenine arabinoside, ara-A) is phos-phorylated in the cell to the triphosphate derivative which blocks DNA synthesis by inhibiting DNA polymerase. It is indicated for infections with herpes simplex virus and varicella-zoster however its use has to a large extend been surpassed by aciclovir. It is administered topically or intravenously. It is inactivated rapidly by adenosine deaminase which for systemic use necessitates constant infusion of the drug. Vidarabine is the least toxic of the purine analogues. Nausea and vomiting are the most frequent adverse effects and neurotoxicity may occur. 

Aciclovir is phosphorylated preferentially by herpes simplex virus-coded thymidine kinase and following further phosphorylation aciclovir triphosphate interferes with herpes virus DNA polymerase and viral DNA replication. Aciclovir topical cream is indicated in the management of initial genital herpes and in limited non-life threatening mucocutaneous herpes simplex virus infections in immunocompromised patients. 

Foscarnet is an inorganic pyrophosphate analogue which causes selective inhibition of viral DNA polymerase and reverse transcriptase. Topical foscarnet cream has appeared to be a safe and effective treatment for aciclovir-unresponsive mucocutaneous herpes simplex virus infection in AIDS patients. 

Aciclovir is prescribed empirically to cover encephalitis (inflammation of the brain parenchyma) caused by the herpes simplex virus (HSV). Confirmed HSV encephalitis is relatively rare (170 laboratory confirmed cases per annum in... 

Aciclovir-resistant herpes simplex virus has been reported in patients with AIDS foscamet (see p. 262) has been used in these cases. 

Foscamet is used i.v. for retinitis due to CMV in patients with HIV infection when ganciclovir is contraindicated it has also been used to treat aciclovir-resistant herpes simplex virus infection (see p. 258). It causes numerous adverse effects, including renal toxicity, nausea and vomiting, neurological reactions and marrow suppression. 

Aciclovir is active against Herpes simplex virus type 1 (HSV-1), HSV-2, Varicella zoster virus (VZV), Herpesvirus simiae, and to a lesser degree Epstein-Barr virus (EBV). Resistant strains of HSV can arise owing to the emergence of thymidine kinase-deficient mutants. Other forms of resistance patterns are less common (2,3). 

Conant MA, Schacker TW, Murphy RL, Gold J, Crutchfield LT, Crooks RJ, Acebes LO, Aiuti F, Akil B, Anderson J, Melville RL, Ballesteros Martin J, Berry A, Weiner M, Black F, Anderson PL, Bockman W, Borelli S, Bradbeer CS, Braffman M, Brandon W, Clark R, Wisniewski T, Bruun JN, Burdge D, Caputo RM, Chateauvert M, LaLonde R, Chiodo F, et al. International Valaciclovir HSV Study Group. Valaciclovir versus aciclovir for Herpes simplex virus infection in HIV-infected individuals two randomized trials. Int J STD AIDS 2002 13(1) 12-21. 

This drug is reported to stimulate the host immune response to virus infection and has been used for mucocutaneous herpes simplex and genital warts (but aciclovir is superior). It is administered by mouth and metabolised to uric acid, so should be used with caution in patients with h5rperuricaemia or gout. 

Viral infections that occur after transplantation are not limited to the lung. Herpes simplex infections are frequent early after the procedure, manifesting as oral vesicles or ulcerations. Less frequent is genital involvement by herpes simple virus, hepatitis or encephalitis. Herpes zoster and varicella reactivate in most patients, particularly if aciclovir prophylaxis is discontinued. Occasionally, severe cerebral arteritis or pneumonia caused by this virus may occur. CMV infection is frequent after transplantation and has to be regularly monitored by antigenemia and/or PCR for early treatment avoiding CMV disease. Epstein Barr virus (EBV) infection and EBV-associated lymphoproliferative disorders have also to be tested on a regular basis, especially in transplants with in... 

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