Kinetics of immune responses in deer mice experimentally infected with Sin Nombre virus.

Abstract:

:Deer 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 observed in viral infections. Several chemokine and cytokine genes were elevated, and markers of a T cell response occurred but then declined days later. Splenic transforming growth factor beta (TGF-β) expression was elevated early in infection, declined, and then was elevated again late in infection. Together, these data suggest that a subtle immune response that fails to clear the virus occurs in deer mice.

journal_name

J Virol

journal_title

Journal of virology

authors

Schountz T,Acuña-Retamar M,Feinstein S,Prescott J,Torres-Perez F,Podell B,Peters S,Ye C,Black WC 4th,Hjelle B

doi

10.1128/JVI.06875-11

subject

Has Abstract

pub_date

2012-09-01 00:00:00

pages

10015-27

issue

18

eissn

0022-538X

issn

1098-5514

pii

JVI.06875-11

journal_volume

86

pub_type

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