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Int J Clin Exp Pathol. 2008 Jan 1;1(2):169-79.

Yellow fever virus infection in Syrian golden hamsters: relationship between cytokine expression and pathologic changes.

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Department of Pathology and Center for Biodefense and Emerging Infectious Diseases, Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, USA.


Infection of primates by yellow fever virus (YFV) often results in severe multi-organ failure with marked histologic abnormalities. However, the role of host's immune response, particularly innate immunity, in disease process is unclear. In this study, we used a well established hamster model of yellow fever to examine the dynamic changes of cytokine expression and histopathology in the liver, spleen, kidney, and heart during the course of YFV infection. We observed that the levels of inflammatory cytokines (IFN-gamma, IL-2, TNF-alpha) in the liver were significantly reduced in the mid-stage of infection (8 days), but were elevated later (12 days). In contrast, IL-12p40 was elevated throughout the infection. The levels of IFN-gamma, IL-2, and TNF-alpha were increased in the spleen, kidney, and heart throughout the study period. For regulatory cytokines, IL-10 was significantly increased, and TGF-beta was reduced in the liver, spleen and heart in both early and mid-stages of infection, but was elevated in the kidney during the entire course of infection. In view of the pathologic changes, the observed cytokine profiles suggest that YFV has immunosuppressive effects, which contribute to liver damage in the mid-stage of infection, followed by an immunopathogenic mechanism that leads to disease progression during the late-stages of infection. Our findings support the hypothesis that organ injury by YFV is probably due to a combination of multiple factors, including direct viral injury and host innate immune responses.


RT-PCR; Yellow fever virus; cytokines; immunohistochemistry; pathogenesis; pathology

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