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ACIVIR-200 DT Tablets 1*10Tablet


ACIVIR DT is indicated for the treatment of Herpes simplex virus infections of the skin and mucous membrane, including initial and recurrent genital herpes, suppression of recurrent Herpes simplex infections in immune-competent patients; prophylaxis of Herpes simplex infection in immunocompromised patients; VZV infections (chickenpox) and Herpes zoster (shingles) infections; and management of severely immunocompromised patients, namely those with HIV disease (CD4+ counts <200/mm3, including patients with AIDS or severe ARC), or after bone marrow transplantation.

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Aciclovir is a synthetic purine nucleoside analogue with in vitro and in vivo inhibitory activity against human herpes viruses, including herpes simplex virus (HSV) types 1 and 2, varicella zoster virus (VZV), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). In cell culture, aciclovir has the greatest antiviral activity against HSV-1, followed (in decreasing order of potency) by HSV-2, VZV, EBV and CMV.

The inhibitory activity of aciclovir for HSV 1 and HSV 2, VZV, EBV and CMV is highly selective. The enzyme thymidine kinase (TK) of normal, non-infected cells does not use aciclovir effectively as a substrate, hence toxicity to mammalian host cells is low; however, TK encoded by HSV, VZV and EBV converts aciclovir to aciclovir monophosphate, a nucleoside analogue, which is further converted to the diphosphate and finally to the triphosphate by cellular enzymes. Aciclovir triphosphate interferes with the viral DNA polymerase and inhibits viral DNA replication, with resultant chain termination following its incorporation into the viral DNA.

Prolonged or repeated courses of aciclovir in severely immune compromised individuals may result in the selection of virus strains with reduced sensitivity, which may not respond to continued aciclovir treatment.

Most of the clinical isolates with reduced sensitivity have been relatively deficient in viral TK; however, strains with altered viral TK or viral DNA polymerase have also been reported. In vitro exposure of HSV isolates to aciclovir can also lead to the emergence of less sensitive strains. The relationship between the in vitro-determined sensitivity of HSV isolates and clinical response to aciclovir therapy is not clear.

All patients should be cautioned to ensure they avoid the potential of virus transmission, particularly when active lesions are present.


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