| Literature DB >> 22156530 |
Darci R Smith1, Brian H Bird, Bridget Lewis, Sara C Johnston, Sarah McCarthy, Ashley Keeney, Miriam Botto, Ginger Donnelly, Joshua Shamblin, César G Albariño, Stuart T Nichol, Lisa E Hensley.
Abstract
Rift Valley fever (RVF) virus (RVFV) can cause severe human disease characterized by either acute-onset hepatitis, delayed-onset encephalitis, retinitis and blindness, or a hemorrhagic syndrome. The existing nonhuman primate (NHP) model for RVF utilizes an intravenous (i.v.) exposure route in rhesus macaques (Macaca mulatta). Severe disease in these animals is infrequent, and large cohorts are needed to observe significant morbidity and mortality. To overcome these drawbacks, we evaluated the infectivity and pathogenicity of RVFV in the common marmoset (Callithrix jacchus) by i.v., subcutaneous (s.c.), and intranasal exposure routes to more closely mimic natural exposure. Marmosets were more susceptible to RVFV than rhesus macaques and experienced higher rates of morbidity, mortality, and viremia and marked aberrations in hematological and chemistry values. An overwhelming infection of hepatocytes was a major consequence of infection of marmosets by the i.v. and s.c. exposure routes. Additionally, these animals displayed signs of hemorrhagic manifestations and neurological impairment. Based on our results, the common marmoset model more closely resembles severe human RVF disease and is therefore an ideal model for the evaluation of potential vaccines and therapeutics.Entities:
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Year: 2011 PMID: 22156530 PMCID: PMC3302397 DOI: 10.1128/JVI.06190-11
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103