Expression of CD20 after viral reactivation renders HIV-reservoir cells susceptible to Rituximab.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31420544.
- Also identified by DOI 10.1038/s41467-019-11556-4 and PMC identifier 6697690.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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<sup>+</sup>) 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.
Medical subject headings
- Antigens, CD20
- CD4-Positive T-Lymphocytes
- HIV Infections
- Immunologic Factors
- Rituximab
- Virus Activation
- Virus Latency