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The interferon paradox: can inhibiting an antiviral mechanism advance an HIV cure?
Steven G. Deeks, … , Pamela M. Odorizzi, Rafick-Pierre Sekaly
Steven G. Deeks, … , Pamela M. Odorizzi, Rafick-Pierre Sekaly
Published December 12, 2016
Citation Information: J Clin Invest. 2017;127(1):103-105. https://doi.org/10.1172/JCI91916.
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Commentary

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

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