IL-15 regulates susceptibility of CD4+T cells to HIV infection

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Abstract
Significance: HIV creates a persistent reservoir, which is largely resistant to current antiretroviral treatment aimed at inhibiting HIV replication. CD4+T memory lymphocytes, key components of this reservoir, are generally refractory to infection, but stimulation with γc-chain cytokines, such as IL-15, renders these cells more susceptible to HIV. We found that, by inducing cell cycle entry of CD4+T cells, JAK1 is a key mediator responsible for counteracting the antiviral activity of SAM domain and HD domain-containing protein 1 (SAMHD1). Pharmacological inhibition of these kinases resulted in restoration of SAMHD1 in CD4+T cells. Protecting these cells during the critical IL-15 surge observed during primary infection has the potential to limit reservoir establishment.
Funding Information
  • HHS | NIH | National Institute of Allergy and Infectious Diseases (AI125173-01)
  • HHS | NIH | National Institute of Allergy and Infectious Diseases (AI120998)
  • HHS | NIH | National Institute of Allergy and Infectious Diseases (U19 AI1186101)
  • HHS | NIH | National Institute of Allergy and Infectious Diseases (AI07345)
  • HHS | NIH | National Institute of General Medical Sciences (GM113886)
  • HHS | NIH | National Institute of General Medical Sciences (GM113886-03S1)
  • Department of Health | National Health and Medical Research Council (APP1086178)
  • HHS | NIH | National Institute of Allergy and Infectious Diseases (R01 AI136916)

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