Origin of rebound virus in chronically SIV-infected Rhesus monkeys following treatment discontinuation

Po-Ting Liu, Brandon F. Keele, Peter Abbink, Noe B. Mercado, Jinyan Liu, Esther A. Bondzie, Abishek Chandrashekar, Erica N. Borducchi, Joseph Hesselgesser, Michael Mish, Gregory Chin, Elena Bekerman, Romas Geleziunas and Dan H. Barouch ()
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Po-Ting Liu: Harvard Medical School
Brandon F. Keele: Frederick National Laboratory for Cancer Research
Peter Abbink: Harvard Medical School
Noe B. Mercado: Harvard Medical School
Jinyan Liu: Harvard Medical School
Esther A. Bondzie: Harvard Medical School
Abishek Chandrashekar: Harvard Medical School
Erica N. Borducchi: Harvard Medical School
Joseph Hesselgesser: Gilead Sciences
Michael Mish: Gilead Sciences
Gregory Chin: Gilead Sciences
Elena Bekerman: Gilead Sciences
Romas Geleziunas: Gilead Sciences
Dan H. Barouch: Harvard Medical School

Nature Communications, 2020, vol. 11, issue 1, 1-9

Abstract: Abstract Viral rebound following antiretroviral therapy (ART) discontinuation in HIV-1-infected individuals is believed to originate from a small pool of CD4+ T cells harboring replication-competent provirus. However, the origin and nature of the rebound virus has remained unclear. Recent studies have suggested that rebound virus does not originate directly from individual latent proviruses but rather from recombination events involving multiple proviruses. Here we evaluate the origin of rebound virus in 16 ART-suppressed, chronically SIV-infected rhesus monkeys following ART discontinuation. We sequence viral RNA and viral DNA in these animals prior to ART initiation, during ART suppression, and following viral rebound, and we compare rebound viral RNA after ART discontinuation with near full-length viral DNA from peripheral blood and lymph node mononuclear cells (PBMC and LNMC) during ART suppression. Sequences of initial rebound viruses closely match viral DNA sequences in PBMC and LNMC during ART suppression. Recombinant viruses are rare in the initial rebound virus populations but arise quickly within 2–4 weeks after viral rebound. These data suggest that intact proviral DNA in PBMC and LNMC during ART suppression is likely the direct origin of viral rebound in chronically SIV-infected rhesus monkeys following ART discontinuation.

Date: 2020
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DOI: 10.1038/s41467-020-19254-2

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