The immune response fails to control HIV early in initial virus spread
Lillian B. Cohn1,2 and Steven G. Deeks2
1Chan Zuckerberg Biohub, San Francisco, California, USA.
2Department of Medicine, UCSF, San Francisco, California, USA.
Address correspondence to: Steven G. Deeks, Ward 84, Building 80, 995 Potero Avenue, San Francisco, California 94110, USA. Phone: 415.476.4082 ext. 404; Email: steven.deeks@ucsf.edu.
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1Chan Zuckerberg Biohub, San Francisco, California, USA.
2Department of Medicine, UCSF, San Francisco, California, USA.
Address correspondence to: Steven G. Deeks, Ward 84, Building 80, 995 Potero Avenue, San Francisco, California 94110, USA. Phone: 415.476.4082 ext. 404; Email: steven.deeks@ucsf.edu.
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First published April 27, 2020 - More info
J Clin Invest. 2020;130(6):2803–2805. https://doi.org/10.1172/JCI136886.
© 2020 American Society for Clinical Investigation
Discontinued antiretroviral therapy (ART) results in uncontrolled HIV replication in most cases. How the virus population that persists during ART escapes immune control remains unknown. In this issue of the JCI, Mitchell and authors investigated plasmacytoid dendritic cells (pDCs) from the blood of individuals living with HIV. After ART was discontinued and as the virus began to spread, an apparently functional pDC response emerged. Notably, these pDCs were initially capable of producing high levels of type I IFN, but rapidly lost this capacity, even before the virus became readily detectable in blood. This study suggests that dysfunctional pDCs are a key initial mechanism associated with poor HIV control. These innate immune responses might be targeted in the emerging efforts to cure HIV disease.
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Copyright © 2020 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)