The interferon paradox: can inhibiting an antiviral mechanism advance an HIV cure?

Abstract

While antiretroviral therapy (ART) has improved the quality of life and increased the life span of many HIV-infected individuals, this therapeutic strategy has several limitations, including a lack of efficacy in fully restoring immune function and a requirement for life-long treatment. Two studies in this issue of the JCI use a humanized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infection and that type I IFN-associated gene signatures persist, even during ART. Importantly, blockade of type I IFN improved immune function, reduced the HIV reservoir, and caused a delay in viral rebound after ART interruption. Together, these two studies support further evaluation of IFN blockade as a supplement to ART.

• Authors: Steven G Deeks, Pamela M Odorizzi, Rafick-Pierre Sekaly
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 127 Issue 1 Pg. 103-105 (01 03 2017) ISSN: 1558-8238 [Electronic] United States
• PMID: 27941242 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Retroviral Agents
• Interferon Type I

Topics

• Animals
• Anti-Retroviral Agents (pharmacology)
• Disease Models, Animal
• HIV Infections (drug therapy, immunology)
• HIV-1 (immunology)
• Humans
• Interferon Type I (immunology)
• Mice