Author: A. Lucchiari, Maria; Modolell, Manuel; Eichmann, Klaus; A. Pereira, Carlos
Title: In vivo depletion of interferon-gamma leads to susceptibility of A/J mice to mouse hepatitis virus 3 infection Cord-id: rxzgfk1k Document date: 2011_11_2
ID: rxzgfk1k
Snippet: The possible role of interferon-gamma (IFN-γ) in the resistance of A/J mice to MHV3 infection was investigated. Monoclonal antibodies specific for IFN-γ, CD4 and CD8 molecules were administered in vivo to deplete selectively the IFN-y synthesized or the appropriate subset of T cells. The animals were then infected with MHV3 and the course of infection was followed by studying different parameters, such as, the mortality, the virus growth in the tissues and the IFN-γ synthesis in sera and peri
Document: The possible role of interferon-gamma (IFN-γ) in the resistance of A/J mice to MHV3 infection was investigated. Monoclonal antibodies specific for IFN-γ, CD4 and CD8 molecules were administered in vivo to deplete selectively the IFN-y synthesized or the appropriate subset of T cells. The animals were then infected with MHV3 and the course of infection was followed by studying different parameters, such as, the mortality, the virus growth in the tissues and the IFN-γ synthesis in sera and peritoneal exudates. After MHV3 infection, a full resistance of control A/J mice was observed, in contrast to the high mortality rate observed among the depleted animals, where higher virus titers were found in different tissues. The IFN-γ synthesis in sera and peritoneal exudates of depleted mice, after MHV3 infection, drastically decreased when compared to that detected in control mice. The data presented are consistent with the hypothesis that IFN-γ plays an essential role in the resistance of A/J mice to MHV3 infection.
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