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Chronic cannabinoid administration lowers viral replication in lymph nodes of SIV infected Rhesus macaques
Author(s) -
Walker Edith M,
Amedee Angela,
Birke Leslie,
Stouwe Curtis Vande,
LaCour Nedra,
Winsauer Peter,
Molina Patricia
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.752.6
Subject(s) - simian immunodeficiency virus , viral load , lymph , viral replication , immunology , lymph node , inflammation , immune system , cytokine , lymphatic system , virus , cannabinoid receptor , virology , lentivirus , biology , medicine , receptor , viral disease , pathology , agonist
The primary psychoactive component of marijuana, Δ 9 ‐tetrahydrocannabinol (Δ 9 ‐THC), is used to mitigate AIDS‐associated wasting. Cannabinoid receptors are expressed on cells of the immune system suggesting that chronic Δ 9 ‐THC administration may impact on human immunodeficiency virus progression. Ongoing studies indicate that Δ 9 ‐THC ‐treated, simian immunodeficiency virus (SIV)‐infected rhesus macaques have increased survival and lower plasma viral loads. We hypothesized that chronic Δ 9 ‐THC treatment decreases viral replication by anti‐inflammatory effects at lymphoid tissues. Plasma and lymph nodes obtained at necropsy of SIVmac251‐infected macaques, treated twice daily i.m. with Δ 9 ‐THC (0.32 mg/kg) or vehicle (500μl) were used to quantitate viral load and cytokine levels. Chronic Δ 9 ‐THC treatment resulted in lower plasma viral load (5.28 vs 6.11 log copies of gagRNA/ml plasma), lymph node proviral DNA (1.57 vs 1.99 log copies/10,000 cells) and viral gagRNA (1.14 vs 2.08 log copies/total RNA), irrespective of disease stage. Lymph node content of IL‐1b, IL‐6, IL‐8, and MCP‐1 positively correlated with levels of plasma viral load across all animals (p<0.05). No effect of Δ 9 ‐THC was found on cytokine expression. These results suggest that chronic Δ 9 ‐THC treatment enhances control of viral replication but does not appear to be mediated by decreased inflammation. Supported NIDA‐020419‐01A1.

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