Study Shows Cannabis is Effective Against HIV: Mount Sinai School of Medicine (New York)

via Marijuana.com:

“A study at the Mount Sinai School of Medicine in Manhattan has determined that chemicals found in cannabis can “directly inhibit a type of HIV found in late-stage AIDs.” The findings, first reported in PLoS ONE, seem to indicate that marijuana not only relieves symptoms of the HIV virus, but can also prevent the virus from spreading.

HIV infects active immune cells that carry the viral receptor CD4, which makes these cells unable to fight off the infection. In order to spread, the virus requires that “resting” immune cells be activated. In advanced AIDS, HIV mutates so it can infect these resting cells, gaining entry into the cell by using a signaling receptor called CXCR4. By treating the cells with a cannabinoid agonist that triggers CB2, Dr. Costantino and the Mount Sinai team found that CB2 blocked the signaling process, and suppressed infection in resting immune cells.

http://www.marijuana.com/news/2012/03/scientists-discover-how-cannabis-can-help-relieve-contain-aids/

Cannabinoid Receptor 2-Mediated Attenuation of CXCR4-Tropic HIV Infection in Primary CD4+ T Cells

Agents that activate cannabinoid receptor pathways have been tested as treatments for cachexia, nausea or neuropathic pain in HIV-1/AIDS patients. The cannabinoid receptors (CB1R and CB2R) and the HIV-1 co-receptors, CCR5 and CXCR4, all signal via Gαi-coupled pathways. We hypothesized that drugs targeting cannabinoid receptors modulate chemokine co-receptor function and regulate HIV-1 infectivity. We found that agonism of CB2R, but not CB1R, reduced infection in primary CD4+ T cells following cell-free and cell-to-cell transmission of CXCR4-tropic virus. As this change in viral permissiveness was most pronounced in unstimulated T cells, we investigated the effect of CB2R agonism on to CXCR4-induced signaling following binding of chemokine or virus to the co-receptor. We found that CB2R agonism decreased CXCR4-activation mediated G-protein activity and MAPK phosphorylation. Furthermore, CB2R agonism altered the cytoskeletal architecture of resting CD4+ T cells by decreasing F-actin levels. Our findings suggest that CB2R activation in CD4+ T cells can inhibit actin reorganization and impair productive infection following cell-free or cell-associated viral acquisition of CXCR4-tropic HIV-1 in resting cells. Therefore, the clinical use of CB2R agonists in the treatment of AIDS symptoms may also exert beneficial adjunctive antiviral effects against CXCR4-tropic viruses in late stages of HIV-1 infection.

Cristina Maria Costantino1,2, Achla Gupta2, Alice W. Yewdall1, Benjamin M. Dale1, Lakshmi A. Devi2*, Benjamin K. Chen1*

1 Department of Infectious Diseases, Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, New York, New York, United States of America, 2 Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York, United States of America

Abstract Top

Agents that activate cannabinoid receptor pathways have been tested as treatments for cachexia, nausea or neuropathic pain in HIV-1/AIDS patients. The cannabinoid receptors (CB1R and CB2R) and the HIV-1 co-receptors, CCR5 and CXCR4, all signal via Gαi-coupled pathways. We hypothesized that drugs targeting cannabinoid receptors modulate chemokine co-receptor function and regulate HIV-1 infectivity. We found that agonism of CB2R, but not CB1R, reduced infection in primary CD4+ T cells following cell-free and cell-to-cell transmission of CXCR4-tropic virus. As this change in viral permissiveness was most pronounced in unstimulated T cells, we investigated the effect of CB2R agonism on to CXCR4-induced signaling following binding of chemokine or virus to the co-receptor. We found that CB2R agonism decreased CXCR4-activation mediated G-protein activity and MAPK phosphorylation. Furthermore, CB2R agonism altered the cytoskeletal architecture of resting CD4+ T cells by decreasing F-actin levels. Our findings suggest that CB2R activation in CD4+ T cells can inhibit actin reorganization and impair productive infection following cell-free or cell-associated viral acquisition of CXCR4-tropic HIV-1 in resting cells. Therefore, the clinical use of CB2R agonists in the treatment of AIDS symptoms may also exert beneficial adjunctive antiviral effects against CXCR4-tropic viruses in late stages of HIV-1 infection.

Citation: Costantino CM, Gupta A, Yewdall AW, Dale BM, Devi LA, et al. (2012) Cannabinoid Receptor 2-Mediated Attenuation of CXCR4-Tropic HIV Infection in Primary CD4+ T Cells. PLoS ONE 7(3): e33961. doi:10.1371/journal.pone.0033961

Editor: Yuntao Wu, George Mason University, United States of America

Received: October 12, 2011; Accepted: February 20, 2012; Published: March 20, 2012

Copyright: © 2012 Costantino et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033961

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One Response to “Study Shows Cannabis is Effective Against HIV: Mount Sinai School of Medicine (New York)”

  1. Amazing. It is time that we start funding more research for medical marijuana. For more information on marijuana as a mind enhancer, see http://www.sebastianmarincolo.wordpress.com

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