Abstract

Publisher Summary This chapter presents data on the molecular and biological aspects of human immunodeficiency virus-1 (HIV‐1) vertical transmission and molecular mechanisms of HIV‐1 pathogenesis in infants. Progress has been made in understanding the molecular mechanisms of HIV‐1 vertical transmission and pathogenesis in infected infants. Several maternal factors including advanced clinical stages, low CD4+ lymphocyte counts, and high viral load, immune response, and disease progression have been implicated in an increased risk of vertical transmission. While use of antiretroviral therapy (ART) during pregnancy has been shown to reduce the risk of mother‐to‐infant transmission, selective transmission of ART‐resistant mutants has also been documented. HIV‐1‐infected neonates and infants develop symptomatic acquired immune deficiency syndrome (AIDS) more rapidly than infected adults, including their own infected mothers do. By using HIV‐1‐ infected mother–infant pairs as a transmitter-recipient model the minor genotype s of HIV‐1 with R5 phenotypes found in infected mothers were transmitted to their infants and initially maintained in the infants with the same properties.

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