SHIV-1157i and Passaged Progeny Viruses Encoding R5 HIV-1 Clade C Env Cause AIDS in Rhesus Monkeys

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SHIV-1157i and Passaged Progeny Viruses Encoding R5 HIV-1 Clade C Env Cause AIDS in Rhesus Monkeys

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Title: SHIV-1157i and Passaged Progeny Viruses Encoding R5 HIV-1 Clade C Env Cause AIDS in Rhesus Monkeys
Author: Song, Ruijiang; Ong, Helena; Sharma, Prachi; Chenine, Agnès L; Kramer, Victor G; Xu, Weidong; Else, James G; Novembre, Francis J; Strobert, Elizabeth; O'Neil, Shawn P; Humbert, Michael; Rasmussen, Robert Anthony; Siddappa, Nagadenahalli B.; Ruprecht, Ruth Margrit

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Citation: Humbert, Michael, Robert A. Rasmussen, Ruijiang Song, Helena Ong, Prachi Sharma, Agnès L. Chenine, Victor G. Kramer, et al. 2008. SHIV-1157i and passaged progeny viruses encoding R5 HIV-1 clade C env cause AIDS in rhesus monkeys. Retrovirology 5: 94.
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Abstract: Background: Infection of nonhuman primates with simian immunodeficiency virus (SIV) or chimeric simian-human immunodeficiency virus (SHIV) strains is widely used to study lentiviral pathogenesis, antiviral immunity and the efficacy of AIDS vaccine candidates. SHIV challenges allow assessment of anti-HIV-1 envelope responses in primates. As such, SHIVs should mimic natural HIV-1 infection in humans and, to address the pandemic, encode HIV-1 Env components representing major viral subtypes worldwide. Results: We have developed a panel of clade C R5-tropic SHIVs based upon env of a Zambian pediatric isolate of HIV-1 clade C, the world's most prevalent HIV-1 subtype. The parental infectious proviral clone, SHIV-1157i, was rapidly passaged through five rhesus monkeys. After AIDS developed in the first animal at week 123 post-inoculation, infected blood was infused into a sixth monkey. Virus reisolated at this late stage was still exclusively R5 tropic and mucosally transmissible. Here we describe the long-term follow-up of this initial cohort of six monkeys. Two have remained non-progressors, whereas the other four gradually progressed to AIDS within 123–270 weeks post-exposure. Two progressors succumbed to opportunistic infections, including a case of SV40 encephalitis. Conclusion: These data document the disease progression induced by the first mucosally transmissible, pathogenic R5 non-clade B SHIV and suggest that SHIV-1157i-derived viruses, including the late-stage, highly replication-competent SHIV-1157ipd3N4 previously described (Song et al., 2006), display biological characteristics that mirror those of HIV-1 clade C and support their expanded use for AIDS vaccine studies in nonhuman primates.
Published Version: doi:10.1186/1742-4690-5-94
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