English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Studies carried out till date to elucidate the pathways involved in HIV-1-induced T-cell depletion has revealed that apoptosis underlie the etiology, however, a clear molecular understanding of HIV-1-induced apoptosis has remained elusive. Although evidences pointing towards the importance of mitochondrial energy generating system in apoptosis exist but it's exact role remains to be clearly understood. Here, we describe for the first time specific downregulation of a complex I subunit NDUFA6 with simultaneous impairment of mitochondrial complex I activity in HIV infection. We also show that NDUFA6 gene silencing induces apoptosis and its overexpression reduces apoptosis in HIV-infected cells. Finally, sensitivity to complex I inhibitor Rotenone is reduced in HIV-1-infected T cells indicating an important role for it in the death process. Our data provide a novel molecular basis as to how the virus might interfere with host cell energy generating system during apoptotic cell death.

Mitochondrial complex I activity is impaired during HIV-1-induced T-cell apoptosis