학술논문
RV144 vaccine imprinting constrained HIV-1 evolution following breakthrough infection
Document Type
Report
Author
Lewitus, Eric; Sanders-Buell, Eric; Bose, Meera; O'Sullivan, Anne Marie; Poltavee, Kultida; Li, Yifan; Bai, Hongjun; Mdluli, Thembi; Donofrio, Gina; Slike, Bonnie; Zhao, Hong; Wong, Kim; Chen, Lennie; Miller, Shana; Lee, Jenica; Ahani, Bahar; Lepore, Steven; Muhammad, Sevan; Grande, Rebecca; Tran, Ursula; Dussupt, Vincent; Mendez-Rivera, Letzibeth; Nitayaphan, Sorachai; Kaewkungwal, Jaranit; Pitisuttithum, Punnee; Rerks-Ngarm, Supachai; O'Connell, Robert J.; Janes, Holly; Gilbert, Peter B.; Gramzinski, Robert; Vasan, Sandhya; Robb, Merlin L.; Michael, Nelson L.; Krebs, Shelly J.; Herbeck, Joshua T.; Edlefsen, Paul T.; Mullins, James I.; Kim, Jerome H.; Tovanabutra, Sodsai; Rolland, Morgane
Source
Virus Evolution. November, 2021, Vol. 7 Issue 2, p1h, p13 p.
Subject
Language
English
Abstract
The scale of the HIV-1 epidemic underscores the need for a vaccine. The multitude of circulating HIV-1 strains together with HIV-1's high evolvability hints that HIV-1 could adapt to a future vaccine. Here, we wanted to investigate the effect of vaccination on the evolution of the virus post-breakthrough infection. We analyzed 2,635 HIV-1 env sequences sampled up to a year post-diagnosis from 110 vaccine and placebo participants who became infected in the RV144 vaccine efficacy trial. We showed that the Env signature sites that were previously identified to distinguish vaccine and placebo participants were maintained over time. In addition, fewer sites were under diversifying selection in the vaccine group than in the placebo group. These results indicate that HIV-1 would possibly adapt to a vaccine upon its roll-out. Key words: HIV-1; vaccine; within-host evolution; sieve analysis
1. Introduction HIV-1 infection is typically established by a single variant (Keele et al., 2008), which diversifies rapidly through repeated, fragmentary selective sweeps driven by the host immune response (Alizon [...]
1. Introduction HIV-1 infection is typically established by a single variant (Keele et al., 2008), which diversifies rapidly through repeated, fragmentary selective sweeps driven by the host immune response (Alizon [...]