Characterization of alpha -Defensins Plasma Levels in Macaca fascicularis and Correlations with Virological Parameters during SHIV89.6P sub(Cy11) Experimental Infection
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...
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Veröffentlicht in: | AIDS research and human retroviruses 2007-02, Vol.23 (3), p.287-296 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | 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 sub(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. |
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ISSN: | 0889-2229 |
DOI: | 10.1089/aid.2006.0142 |