| Literature DB >> 31471273 |
Marie-Angélique De Scheerder1, Bram Vrancken2, Simon Dellicour3, Timothy Schlub4, Eunok Lee5, Wei Shao6, Sofie Rutsaert7, Chris Verhofstede8, Tessa Kerre9, Thomas Malfait10, Dimitri Hemelsoet11, Marc Coppens12, Annemieke Dhondt13, Danny De Looze14, Frank Vermassen15, Philippe Lemey2, Sarah Palmer5, Linos Vandekerckhove16.
Abstract
Viral rebound upon stopping combined antiretroviral therapy poses a major barrier toward an HIV cure. Cellular and anatomical sources responsible for reinitiating viral replication remain a subject of ardent debate, despite extensive research efforts. To unravel the source of rebounding viruses, we conducted a large-scale HIV-STAR (HIV-1 sequencing before analytical treatment interruption to identify the anatomically relevant HIV reservoir) clinical trial. We collected samples from 11 participants and compared the genetic composition of (pro)viruses collected under treatment from different cellular and anatomical compartments with that of plasma viruses sampled during analytical treatment interruption. We found a remarkably heterogeneous source of viral rebound. In addition, irrespective of the compartment or cell subset, genetically identical viral expansions played a significant role in viral rebound. Our study suggests that although there does not seem to be a primary source for rebound HIV, cellular proliferation is an important driver of HIV persistence and should therefore be considered in future curative strategies.Entities:
Keywords: HIV persistence; HIV rebound; HIV-1 reservoir; analytical treatment interruption; cellular and anatomical compartments; cellular proliferation; cure research; in-depth sampling; single-genome sequencing
Mesh:
Substances:
Year: 2019 PMID: 31471273 DOI: 10.1016/j.chom.2019.08.003
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023