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Characterization of alpha-Defensins Plasma Levels in Macaca Fascicularis and Correlations with Virological Parameters during SHIV89.6P(cy11) Experimental Infection.

Baroncelli S, Negri DR, Rovetto C, Belli R, Ciccozzi M, Catone S, Michelini Z, Borghi M, Leone P, Fagrouch Z, Heeney J, Cara A

National AIDS Center , Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, 00161, Rome, Italy., Department of Drug Research and Evaluation , Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, 00161, Rome, Italy., Present address: Department of Drug Research and Evaluation, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.

alpha-Defensins have been shown to inhibit HIV-1 replication in vitro and may contribute to the overall control of viral replication in vivo . In the present work, we quantitatively measured the levels of alpha-defensins in the plasma of healthy and experimentally SHIV-infected Macaca fascicularis (cynomolgus monkeys), an animal model of AIDS pathogenesis and vaccine development. Characterization of physiological plasma alpha-defensins levels was performed in 12 healthy monkeys following longitudinal analysis using an alpha-defensins ELISA kit currently validated for macaque use. Subsequently, alpha-defensins levels were quantitatively measured in 23 cynomolgus monkeys during titration protocols following both the mucosal and systemic routes of infection with the pathogenic SHIV89.6P(cy11). A significant increase in plasma alpha-defensins levels was consistently observed at early time points in all infected animals, regardless of the infection route. Moreover, a positive correlation was observed between viral replication and levels of alpha-defensins during the acute phase of infection. Interestingly, in the animals infected through the mucosal route, alpha-defensins levels remained significantly higher at later time points, up to 19 weeks from the infection, while in cynomolgus infected intravenously, alpha-defensins levels returned to baseline levels by 4 weeks from infection, suggesting that the different route of infection may differently activate the innate immune response.

Published 2 March 2007 in AIDS Res Hum Retroviruses, 23(2): 287-296.
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