Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-9931
Ayash-Rashkovsky, M; Chenine, A L; Steele, L N; Lee, S J; Song, R; Ong, H; Rasmussen, R A; Hofmann-Lehmann, R; Else, J G; Augostini, P; McClure, H M; Secor, W E; Ruprecht, R M (2007). Coinfection with Schistosoma mansoni reactivates viremia in rhesus macaques with chronic simian-human immunodeficiency virus clade C infection. Infection and Immunity, 75(4):1751-1756.
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We tested the hypothesis that helminth parasite coinfection would intensify viremia and accelerate disease progression in monkeys chronically infected with an R5 simian-human immunodeficiency virus (SHIV) encoding a human immunodeficiency virus type 1 (HIV-1) clade C envelope. Fifteen rhesus monkeys with stable SHIV-1157ip infection were enrolled into a prospective, randomized trial. These seropositive animals had undetectable viral RNA and no signs of immunodeficiency. Seven animals served as virus-only controls; eight animals were exposed to Schistosoma mansoni cercariae. From week 5 after parasite exposure onward, coinfected animals shed eggs in their feces, developed eosinophilia, and had significantly higher mRNA expression of the T-helper type 2 cytokine interleukin-4 (P = 0.001) than animals without schistosomiasis. Compared to virus-only controls, viral replication was significantly increased in coinfected monkeys (P = 0.012), and the percentage of their CD4(+) CD29(+) memory cells decreased over time (P = 0.05). Thus, S. mansoni coinfection significantly increased viral replication and induced T-cell subset alterations in monkeys with chronic SHIV clade C infection.
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|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||05 Vetsuisse Faculty > Veterinary Clinic > Department of Farm Animals > Clinical Laboratory|
|DDC:||570 Life sciences; biology
|Deposited On:||20 Mar 2009 15:51|
|Last Modified:||28 Nov 2013 02:12|
|Publisher:||American Society for Microbiology|
|Additional Information:||Copyright: American Society for Microbiology|
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