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HIV rebound is predominantly fueled by genetically identical viral expansions from diverse reservoirs

(2019) CELL HOST & MICROBE. 26(3). p.347-358
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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.
Keywords
CD4(+) T-CELLS, MULTIPLE SEQUENCE ALIGNMENT, ANTIRETROVIRAL THERAPY, INTACT HIV-1, PERSISTENCE, PROVIRUSES, IDENTIFICATION, MAINTAINS, LATENT, TISSUE

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MLA
De Scheerder, Marie-Angélique, et al. “HIV Rebound Is Predominantly Fueled by Genetically Identical Viral Expansions from Diverse Reservoirs.” CELL HOST & MICROBE, vol. 26, no. 3, 2019, pp. 347–58, doi:10.1016/j.chom.2019.08.003.
APA
De Scheerder, M.-A., Vrancken, B., Dellicour, S., Schlub, T., Lee, E., Shao, W., … Vandekerckhove, L. (2019). HIV rebound is predominantly fueled by genetically identical viral expansions from diverse reservoirs. CELL HOST & MICROBE, 26(3), 347–358. https://doi.org/10.1016/j.chom.2019.08.003
Chicago author-date
De Scheerder, Marie-Angélique, Bram Vrancken, Simon Dellicour, Timothy Schlub, Eunok Lee, Wei Shao, Sofie Rutsaert, et al. 2019. “HIV Rebound Is Predominantly Fueled by Genetically Identical Viral Expansions from Diverse Reservoirs.” CELL HOST & MICROBE 26 (3): 347–58. https://doi.org/10.1016/j.chom.2019.08.003.
Chicago author-date (all authors)
De Scheerder, Marie-Angélique, Bram Vrancken, Simon Dellicour, Timothy Schlub, Eunok Lee, Wei Shao, Sofie Rutsaert, Chris Verhofstede, Tessa Kerre, Thomas Malfait, Dimitri Hemelsoet, Marc Coppens, Annemieke Dhondt, Danny De Looze, Frank Vermassen, Philippe Lemey, Sarah Palmer, and Linos Vandekerckhove. 2019. “HIV Rebound Is Predominantly Fueled by Genetically Identical Viral Expansions from Diverse Reservoirs.” CELL HOST & MICROBE 26 (3): 347–358. doi:10.1016/j.chom.2019.08.003.
Vancouver
1.
De Scheerder M-A, Vrancken B, Dellicour S, Schlub T, Lee E, Shao W, et al. HIV rebound is predominantly fueled by genetically identical viral expansions from diverse reservoirs. CELL HOST & MICROBE. 2019;26(3):347–58.
IEEE
[1]
M.-A. De Scheerder et al., “HIV rebound is predominantly fueled by genetically identical viral expansions from diverse reservoirs,” CELL HOST & MICROBE, vol. 26, no. 3, pp. 347–358, 2019.
@article{8626300,
  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.},
  author       = {De Scheerder, Marie-Angélique and Vrancken, Bram and Dellicour, Simon and Schlub, Timothy and Lee, Eunok and Shao, Wei and Rutsaert, Sofie and Verhofstede, Chris and Kerre, Tessa and Malfait, Thomas and Hemelsoet, Dimitri and Coppens, Marc and Dhondt, Annemieke and De Looze, Danny and Vermassen, Frank and Lemey, Philippe and Palmer, Sarah and Vandekerckhove, Linos},
  issn         = {1931-3128},
  journal      = {CELL HOST & MICROBE},
  keywords     = {CD4(+) T-CELLS,MULTIPLE SEQUENCE ALIGNMENT,ANTIRETROVIRAL THERAPY,INTACT HIV-1,PERSISTENCE,PROVIRUSES,IDENTIFICATION,MAINTAINS,LATENT,TISSUE},
  language     = {eng},
  number       = {3},
  pages        = {347--358},
  title        = {HIV rebound is predominantly fueled by genetically identical viral expansions from diverse reservoirs},
  url          = {http://dx.doi.org/10.1016/j.chom.2019.08.003},
  volume       = {26},
  year         = {2019},
}

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