Volume 3 Supplement 1

2006 International Meeting of The Institute of Human Virology

Open Access

Vitamin A deficiency and proinflammatory cytokine, mu opioid receptor, and HIV expression in the HIV-1 Tg rat

  • Walter RoyalIII1,
  • Huiyun Wang1,
  • Odell Jones2,
  • Hieu Tran2 and
  • Joseph L Bryant2
Retrovirology20063(Suppl 1):P53

https://doi.org/10.1186/1742-4690-3-S1-P53

Published: 21 December 2006

Background

Drug users with HIV-1 infection are at increased risk for the development of HIV-related complications that may be exacerbated by vitamin A deficiency.

Materials and methods

T cells in whole blood samples from transgenic (Tg) and non-Tg rats on either a vitamin A deficient (VA-) or normal (VA+) diet were examined for interferon (IFN)-y, tumor necrosis factor (TNF)-y, mu opioid receptor (MOR), and HIV-1 expression before and after stimulation with phytohemagglutinin (PHA) by PCR and flow cytometry and in enzyme immunoassays.

Results

PHA-stimulated T cells from VA-/Tg rats produced higher percentages of IFN-y + T cells, secreted the highest levels of TNF-y, and showed the greatest expression of MOR. In addition, gp120 and nef gene expression was higher for T cells from VA-/Tg rats than from VA+/Tg rats.

Conclusion

These data, obtained in the HIV-1 Tg rat, suggest that vitamin A deficiency in drug users may promote HIV disease progression through effects on proinflammatory cytokine, HIV protein, and MOR expression.

Authors’ Affiliations

(1)
Department of Neurology, University of Maryland School of Medicine
(2)
Institute of Human Virology, University of Maryland Biotechnology Institute, University of Maryland

Copyright

© Royal et al; licensee BioMed Central Ltd. 2006

This article is published under license to BioMed Central Ltd.

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