Multiple sclerosis drug blocks HIV infection and infection in human immune cells

An immunomodulator called finingolimod, which has been approved for the treatment of multiple sclerosis, was found to be human immunodeficiency virus (HIV) and human immune cell infection, according to a study published in the Open Access Journal on August 13. Block PLOS pathogen Dr. Rachel Lessopp and Associate Professor Albert Bosque of George Washington University. Future research in animals and humans is needed, but these preliminary findings suggest that this compound may be a promising new therapeutic for the treatment and prevention of HIV.

Currently, approximately 40 million people live with HIV worldwide. The ability of the virus to establish a latency period by integrating its genome into the host cell’s genome allows treatment of infections to last a lifetime and potentially reactivate the virus in the future. By establishing latency, HIV avoids host defense mechanisms and drug eradication. HIV is currently controlled by antiretroviral drugs, it does not specifically target latent infections, may have side effects, and has limited use in preventing transmission of the virus between individuals. .. For this reason, discovering new strategies to target HIV infection and latency is crucial.

Bosque et al. investigated another tactic to combat HIV infection by targeting the sphingosine-1-phosphate (S1P) receptor, a component of the immune system involved in the progression of infection. To that end, they focused on FTY720 (fingolimod), a well-tolerated drug approved by the US Food and Drug Administration that blocks the action of the S1P receptor. They found that FTY720 blocks HIV infection of human immune cells called CD4 + T cells by interfering with multiple steps in the HIV life cycle. For example, FTY720 reduces the density of CD4, a protein on the surface of T cells, which blocks viral binding and fusion. The drug blocked HIV infection between cells and consequently reduced detectable latent virus. The authors have previously reported the role of S1P signaling in the establishment of HIV infection, and the potential regulation of this pathway to alter the infection pathway and prevent the establishment of a potential reservoir of CD4 + T cells. Not. Therefore, targeting the S1P pathway with FTY720 could be a new strategy to block HIV replication and reduce potential reservoirs.

“These results indicate that fingolimod deserves further investigation as an exciting new treatment for HIV,” the authors say.

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Peer Review; Experimental Studies; Cells

Funding: The studies reported in this publication are NIAID (https://www.niece.here.government/) This study of NIH under grants R01-AI124722, R21/R33-AI116212 to AB is supported by the NIH Funding Program (AI117970) The following NIH joint funds and participating institutions and centers: NIAID, NCI, NICJD, NHLBI, NIDA, NINH, NIA, FIC, NIGGIS, NDDK, and OAR (https://dccfar.gwu.edu /). The content is solely the responsibility of the authors and does not necessarily represent the official NIH position. The funder was not involved in study design, data collection and analysis, publication decisions, or manuscript preparation.

Competing interests: The author has declared that there are no competing interests.

Sources: Resop RS, Fromentin R, Newman D, Rigsby H, Dubrovsky L, Bukrinsky M, etc. (2020) Fingolimod interferes with multiple stages of the HIV-1 life cycle. PLoS Pathog 16 (8): e1008679. https://Doi.org/Ten.1371 /journal.ppat.1008679

Author’s affiliation:

Microbiology, immunology and tropical medicine,

George Washington University, Washington DC, USA

Canada, Montreal, University of Montreal, CHUM Research Center, Department of Microbiology, Infections and Immunology

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