Expression of CD20 after viral reactivation renders HIV-reservoir cells susceptible to Rituximab

Carla Serra-Peinado, Judith Grau-Expósito, Laura Luque-Ballesteros, Antonio Astorga-Gamaza, Jordi Navarro, Jenny Gallego-Rodriguez, Mario Martin, Adrià Curran, Joaquin Burgos, Esteban Ribera, Berta Raventós, Rein Willekens, Ariadna Torrella, Bibiana Planas, Rosa Badía, Felipe Garcia, Josep Castellví, Meritxell Genescà, Vicenç Falcó and Maria J. Buzon ()
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Carla Serra-Peinado: Universitat Autònoma de Barcelona
Judith Grau-Expósito: Universitat Autònoma de Barcelona
Laura Luque-Ballesteros: Universitat Autònoma de Barcelona
Antonio Astorga-Gamaza: Universitat Autònoma de Barcelona
Jordi Navarro: Universitat Autònoma de Barcelona
Jenny Gallego-Rodriguez: Universitat Autònoma de Barcelona
Mario Martin: Universitat Autònoma de Barcelona
Adrià Curran: Universitat Autònoma de Barcelona
Joaquin Burgos: Universitat Autònoma de Barcelona
Esteban Ribera: Universitat Autònoma de Barcelona
Berta Raventós: Universitat Autònoma de Barcelona
Rein Willekens: Universitat Autònoma de Barcelona
Ariadna Torrella: Universitat Autònoma de Barcelona
Bibiana Planas: Universitat Autònoma de Barcelona
Rosa Badía: Universitat Autònoma de Barcelona
Felipe Garcia: Universitat de Barcelona
Josep Castellví: Universitat Autònoma de Barcelona
Meritxell Genescà: Universitat Autònoma de Barcelona
Vicenç Falcó: Universitat Autònoma de Barcelona
Maria J. Buzon: Universitat Autònoma de Barcelona

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract The identification of exclusive markers to target HIV-reservoir cells will represent a significant advance in the search for therapies to cure HIV. Here, we identify the B lymphocyte antigen CD20 as a marker for HIV-infected cells in vitro and in vivo. The CD20 molecule is dimly expressed in a subpopulation of CD4-positive (CD4+) T lymphocytes from blood, with high levels of cell activation and heterogeneous memory phenotypes. In lymph node samples from infected patients, CD20 is present in productively HIV-infected cells, and ex vivo viral infection selectively upregulates the expression of CD20 during early infection. In samples from patients on antiretroviral therapy (ART) this subpopulation is significantly enriched in HIV transcripts, and the anti-CD20 monoclonal antibody Rituximab induces cell killing, which reduces the pool of HIV-expressing cells when combined with latency reversal agents. We provide a tool for targeting this active HIV-reservoir after viral reactivation in patients while on ART.

Date: 2019
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DOI: 10.1038/s41467-019-11556-4

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