Mice Lacking Alpha/Beta and Gamma Interferon Receptors Are Susceptible to Junin Virus Infection
Author(s) -
Olga A. Kolokoltsova,
Nadezda Yun,
Allison Poussard,
Jennifer K. Smith,
Jea N. Smith,
Milagros Salazar,
Aida G. Walker,
ChienTe K. Tseng,
Judith F. Aronson,
Slobodan Paessler
Publication year - 2010
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.01389-10
Subject(s) - junin virus , biology , virology , beta (programming language) , alpha (finance) , virus , arenavirus , interferon gamma , immunology , lymphocytic choriomeningitis , immune system , nursing , patient satisfaction , programming language , computer science , medicine , construct validity , cd8
Junin virus (JUNV) causes a highly lethal human disease, Argentine hemorrhagic fever. Previous work has demonstrated the requirement for human transferrin receptor 1 for virus entry, and the absence of the receptor was proposed to be a major cause for the resistance of laboratory mice to JUNV infection. In this study, we present for the first timein vivo evidence that the disruption of interferon signaling is sufficient to generate a disease-susceptible mouse model for JUNV infection. After peripheral inoculation with virulent JUNV, adult mice lacking alpha/beta and gamma interferon receptors developed disseminated infection and severe disease.
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