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122 Interplay Between HIV Replication and MicroRNAs

Chable-Bessia, C; Meziane, O; D, Cerutti; Emiliani, S; Schwartz, O; Lambotte, O; Lévy, Y; Autran, B; Reynes, J; Bennasser, Y; Benkirane, M

JAIDS Journal of Acquired Immune Deficiency Syndromes: April 2011 - Volume 56 - Issue - p 49
doi: 10.1097/01.qai.0000397310.79094.e8
Abstracts
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Institute of Human Genetic, CNRS, Laboratory of Molecular Virology, Montpellier, France

The outcome of HIV-1 infection results from complex interactions between viral compounds and host cell factors. In most of cases, HIV-1 successfully hijacks cellular pathways and bypasses restriction factors for optimal replication leading to continuous rounds of infection, replication and cell death. Continuous viral replication causes the loss of CD4+T cells and progression to immunodeficiency in infected individuals. However, situations where successful control of virus replication was achieved have been reported. First, HAART treatment revealed the existence of a pool of resting memory CD4+ T cells harbouring integrated but silent HIV-1 provirus. Although this situation occurs in a small number of cells, it suggests that intracellular defence mechanisms can be effective against HIV. Second, HIV-infected individuals who are able to control their plasma viremia to undetectable levels for many years in absence of any treatment have been identified and referred to as Elite HIV controllers. Again, this is a rare situation observed in 0.5% of infected patients. Still, it demonstrates that it is possible to effectively control HIV replication and disease progression. We will discuss how HIV-1 uses microRNA pathway and cellular miRNAs to overcome restriction factors activity and there implication in viral latency.

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