原创力文档schistosoma mansoni enhances host susceptibility to mucosal but not intravenous challenge by r5 clade c shiv曼氏裂体吸虫增强宿主对粘膜而不是静脉分支c的r5 shiv挑战.pdfVIP
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schistosoma mansoni enhances host susceptibility to mucosal but not intravenous challenge by r5 clade c shiv曼氏裂体吸虫增强宿主对粘膜而不是静脉分支c的r5 shiv挑战
Schistosoma mansoni Enhances Host Susceptibility to
Mucosal but Not Intravenous Challenge by R5 Clade C
SHIV
1,2 1 1
Nagadenahalli B. Siddappa , Girish Hemashettar , Vivekanandan Shanmuganathan , Amma A.
3 3 3 4 3
Semenya , Elizabeth D. Sweeney , Katherine S. Paul , Sandra J. Lee , W. Evan Secor ,
Ruth M. Ruprecht1,2*
1 Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America, 2 Harvard Medical School, Boston, Massachusetts, United States of America, 3 Centers for
Disease Control and Prevention, Atlanta, Georgia, United States of America, 4 Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute,
Boston, Massachusetts, United States of America
Abstract
Background: The high prevalence of HIV-1/AIDS in areas endemic for schistosomiasis and other helminthic infections has
led to the hypothesis that parasites increase host susceptibility to immunodeficiency virus infection. We previously showed
that rhesus macaques (RM) with active schistosomiasis were significantly more likely to become systemically infected after
intrarectal (i.r.) exposure to an R5-tropic clade C simian-human immunodeficiency virus (SHIV-C) than were parasite-free
controls. However, we could not address whether this was due to systemic or mucosal effects. If systemic immunoactivation
resulted in increased susceptibility to SHIV-C acquisition, a similarly large difference in host susceptibility would be seen
after intravenous (i.v.) SHIV-C challenge. Conversely, if increased host susceptibility was due to parasite-induced
immunoactivation at the mucosal level, i
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