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Overview
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Background
Lamivudine, a nucleoside analog, is a potent reverse transcriptase inhibitor, with IC50 value of 0.316 µM against human immunodeficiency virus type 1 (HIV-1) [1].
Reverse transcriptase is a RNA-dependent DNA polymerase, playing a critical role in retroviral replication. Thus, reverse transcriptase has been made a target of antiretroviral chemotherapy [1].
Lamivudine was most potent against simian retrovirus types 1 and 2 (SRV-1, SRV-2), and HIV-1, with IC50 values of 10, 0.316 and 0.316 µM, respectively, but did not inhibit foamy viruses and amphotrophic murine leukaemia virus (MLV-A) [1].
In human coinfected with HIV-1 and hepatitis B virus (HBV), Lamivudine (150 mg, b.i.d., p.o.) displayed dual efficacy through both delayed HIV-1 disease progression and a favorable biochemical and HBV virologic response. Twelve months of Lamivudine therapy led to HBV DNA and hepatitis B e antigen (HBeAg) losses of ∼40% and ∼20%, respectively, and more alanine aminotransferase (ALT) normalization than that in the placebo group [2].[1]. Rosenblum L L, Patton G, Grigg A R, et al. Differential susceptibility of retroviruses to nucleoside analogues. Antiviral Chemistry and Chemotherapy, 2001, 12(2): 91-97.
[2]. Dore G J, Cooper D A, Barrett C, et al. Dual efficacy of lamivudine treatment in human immunodeficiency virus/hepatitis B virus-coinfected persons in a randomized, controlled study (CAESAR). The CAESAR Coordinating Committee. The Journal of Infectious Diseases, 1999, 180(3): 607-613.
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