Journal
AUTOPHAGY
Volume 4, Issue 5, Pages 704-706Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.6105
Keywords
autophagy; HIV-1; neuroAIDS; HIV-associated dementia; HIV pathogenesis; beclin 1; AIDS; HIV-related cognitive impairment
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Funding
- NIAID NIH HHS [P30 AI036214, UM1 AI068632, AI-68632, AI-39004, U01 AI068632, AI-36214, R01 AI039004, U01 AI068632-03] Funding Source: Medline
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Human immunodeficiency virus type 1 (HIV-1) establishes a persistent infection characterized by progressive depletion of CD4(+) lymphocytes and immunosuppression. Although extensive research has examined the importance of apoptosis as a cause of cell death associated with HIV-1 infection, the role of autophagy has been largely ignored. Our laboratory has examined the autophagic process in HIV-1-infected cells. Following infection of human peripheral blood CD4(+) T-cells or U937 cells with HIV-1 for 48 hours, the autophagy proteins Beclin 1 and LC3-II were found to be markedly decreased. Beclin 1 mRNA expression and autophagosomes were also reduced in HIV-1 infected cells. Thus, our data indicate that HIV-1 infection inhibits autophagy in infected cells in contrast to the previously described induction of autophagy by gp120 in uninfected bystander cells. It is likely that HIV-1 has evolved this mechanism as part of an elaborate attempt to evade the immune system while promoting its own replication. We believe that autophagy is an overlooked mechanism in HIV-1 pathogenesis and plays a particularly important role in the early cognitive impairment and dementia often associated with advanced AIDS. A model is presented that describes the potential role of autophagy in NeuroAIDS.
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