Mobilizing metabolism against HIV

See allHide authors and affiliations

Science  30 Apr 2021:
Vol. 372, Issue 6541, pp. 477-478
DOI: 10.1126/science.372.6541.477-d

HIV-1 alters the metabolism of infected immune cells, targeting lipid, tryptophan, and glucose metabolic pathways by mechanisms that remain poorly understood. Guo et al. used transcriptomics and proteomics to discern the details. HIV-1 infection enhanced associations between NLRX1, a mitochondrial antiviral pattern recognition receptor, and FASTKD5, a protein that modulates mitochondrial energy use. This change increased oxidative phosphorylation (OXPHOS) and glycolysis, which in turn promoted viral replication. HIV-1 replication in vitro became compromised when OXPHOS was inhibited by the antidiabetic drug metformin. Thus, supplementation of combination antiretroviral therapy with metformin and other drugs targeting these metabolic pathways could be helpful in the treatment of HIV-1.

Nat. Immunol. 22, 423 (2021).

Stay Connected to Science

Navigate This Article