โ Scribed by Dani P Bolognesi
No coin nor oath required. For personal study only.
32 base pair deletion DC dendritic cell HAART highly active antiretroviral therapy NSI nonsyncytium-inducing
The three topics featured in this issue's 'HIV' section are central to HIV infection, pathogenesis and treatment. Each reflects the various interactions taking place between HIV and the components of the immune system, the major place of residence for the virus.
More than a decade long search for a factor needed, in addition to CD4, for HIV entry into cells has triumphantly culminated in the identification of the chemokine family of co-receptors. Almost instantaneously, new horizons have become available for a better understanding of HIV interactions with its target cells and fresh avenues have opened up for vaccine and treatment strategies. Much of this is covered by the comprehensive review of Moore, Trkola and Dragic (pp 551-562) but a few issues and new developments are highlighted in this overview. One relates to the infectability of individuals who are homozygous for a 32 base pair deletion (A32) in CCR5, the receptor used by macrophage tropic nonsyncytium inducing (NSI) HIV isolates. This mutation appears to be null with respect to the overall immune competence of the carrier but there is undoubtedly a benefit towards protection against infection by HIV-1. Nonetheless, several cases are now documented in which HIV-1 infections have occurred in this setting.
Although the number of such infections is small, some appear to be with the cytopathic syncytium-inducing (SI) viruses that are able to utilize another co-receptor, CXCR4 (CL Cellum et al.
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