dc.creatorSchountz, Tony
dc.creatorAcuña Retamar, Mariana
dc.creatorFeinstein, Shira
dc.creatorPrescott, Joseph
dc.creatorTorres Pérez, Fernando
dc.creatorPodell, Brendan
dc.creatorPeters, Staci
dc.creatorYe, Chunyan
dc.creatorBlack, William C.
dc.creatorHjelle, Brian
dc.date.accessioned2019-03-11T13:19:40Z
dc.date.available2019-03-11T13:19:40Z
dc.date.created2019-03-11T13:19:40Z
dc.date.issued2012
dc.identifierJournal of Virology, Volumen 86, Issue 18, 2018, Pages 10015-10027
dc.identifier0022538X
dc.identifier10985514
dc.identifier10.1128/JVI.06875-11
dc.identifierhttps://repositorio.uchile.cl/handle/2250/165701
dc.description.abstractDeer mice are the principal reservoir hosts of Sin Nombre virus, the etiologic agent of most hantavirus cardiopulmonary syndrome cases in North America. Infection of deer mice results in persistence without conspicuous pathology, and most, if not all, infected mice remain infected for life, with periods of viral shedding. The kinetics of viral load, histopathology, virus distribution, and immune gene expression in deer mice were examined. Viral antigen was detected as early as 5 days postinfection and peaked on day 15 in the lungs, hearts, kidneys, and livers. Viral RNA levels varied substantially but peaked on day 15 in the lungs and heart, and antinucleocapsid IgG antibodies appeared in some animals on day 10, but a strong neutralizing antibody response failed to develop during the 20-day experiment. No clinical signs of disease were observed in any of the infected deer mice. Most genes were repressed on day 2, suggesting a typical early downregulation of gene expression often observ
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceJournal of Virology
dc.subjectMicrobiology
dc.subjectImmunology
dc.subjectInsect Science
dc.subjectVirology
dc.titleKinetics of immune responses in deer mice experimentally infected with sin nombre virus
dc.typeArtículo de revista


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