Abstract
In a recently published study [Vassão RC, Mello IGC, Pereira CA (1994) Arch Virol 137: 277-288] we have shown that the genetically selected high antibody responder mice (HIII) are susceptible and the low antibody responder counterparts (LIII) are resistant to death induced by experimental infection with mouse hepatitis virus 3 (MHV3). This report shows that the MHV3 titers in the peritoneal exudate (PE) of HIII mice, 3 days after infection, were more than 2 log greater than in the resistant LIII mice, the interferon gamma (IFN gamma) titers in the PE of both mouse populations being not significantly different. The treatment with monoclonal antibodies (mAb) against CD4+ or CD8+ T cells induced susceptibility among LIII mice. The depletion of CD4+ T-cell subset in LIII mice was evidenced by, and led to a significant reduction in, the IFN gamma synthesis in their PEs with a 100 fold increase in MHV3 titers. When lymph node cells (LNC) were harvested from MHV3-infected mice and stimulated "in vitro" with MHV3 inactivated by ultraviolet radiation (uv-MHV3), only LNC from LIII mice were capable of proliferating and synthesizing significant amounts of interleukin 2 (IL-2). The LNC proliferation and IL-2 synthesis were inhibited by treatment with mAbs against CD4 or CD8 molecules. The MHV3 infection induced in both lines of mice a profound depression of the mitogenic response of LNC to phytohemaglutinin (PHA). A correlation between the specific T-cell response and the resistance to MHV3 infection is discussed.
Published Version
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