期刊
CURRENT HIV/AIDS REPORTS
卷 16, 期 3, 页码 224-229出版社
SPRINGER
DOI: 10.1007/s11904-019-00444-7
关键词
IFNAR; ISG; pDC; Inflammation; T cell exhaustion; HIV-1 reservoirs
资金
- NIH [AI127346, AI134631]
- Lineberger Comprehensive Cancer Center at UNC-Chapel Hill
Purpose of ReviewRecent findings on the critical pathogenic role of type 1 interferons (IFN-I) in HIV-1 persistence in humanized mice suggest that inhibiting IFN-I signaling transiently will reverse HIV-induced inflammatory diseases and rescue anti-HIV immunity to control HIV-1 reservoirs.Recent FindingsIn both humanized mice and in monkeys, IFN-I signaling is functionally defined to play an important role in suppressing early HIV-1 and SIV infection. During persistent infection in humanized mice, however, IFN-I signaling is revealed to induce T cell depletion and impairment. Interestingly, in HIV-infected mice with effective combination antiretroviral therapy (cART), blocking IFN-I signaling reverses HIV-induced inflammation, rescues anti-HIV T cells, and reduces HIV-1 reservoirs.SummaryThese findings functionally define the role of IFN-I in HIV-1 reservoir persistence and suggest that blocking IFN-I signaling will provide a novel therapeutic strategy to (i) reverse inflammation-associated diseases in HIV patients under cART, (ii) rescue host anti-HIV immunity, and (iii) reduce or control HIV-1 reservoirs.
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