Franklin, AndrewBlanden, Robert2015-12-130161-5890http://hdl.handle.net/1885/90449Somatic hypermutation, which occurs in antigen-activated germinal centre B lymphocytes, diversifies the genes that encode immunoglobulin variable regions and leads to the 'affinity maturation' of the humoral immune response. Hypermutation affects dC/dG and dA/dT pairs with approximately equal frequency in vivo. DNA polymerase-θ contributes to hypermutagenesis at dC/dG pairs and DNA polymerase-η is substantially involved in the generation of hypermutations at dA/dT pairs. The biochemical properties of polymerases-θ and -η indicate that their DNA synthetic activities are potentially susceptible to inhibition by nucleoside analogues, so it is feasible that nucleoside analogues reduce the accumulation of dC/dG- and dA/dT-targeted hypermutations in vivo. Nucleoside analogues could hence impair the humoral adaptive immune response of HIV-infected patients who are prescribed these chemotherapeutic agents.Keywords: abacavir; abacavir plus lamivudine plus zidovudine; complementary DNA; didanosine; DNA polymerase; emtricitabine; lamivudine; lamivudine plus zidovudine; nucleoside derivative; stavudine; tenofovir; zalcitabine; zidovudine; article; DNA synthesis; feasibi Affinity maturation; Human immunodeficiency virus; Nucleoside analogues; Somatic hypermutationPotential inhibition of somatic hypermutation by nucleoside analogues200710.1016/j.molimm.2006.02.0222015-12-12