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Journal of General Virology (2002), 83, 2709-2716.
© 2002 Society for General Microbiology


Animal: RNA Viruses

Natural killer cell activation after infection with lactate dehydrogenase-elevating virus

Dominique Markine-Goriaynoffa,1, Xavier Hulhovenb,1, César L. Cambiaso1, Philippe Monteynec,1, Thérèse Briet1, Maria-Dolores Gonzalez1, Pierre Coulie2 and Jean-Paul Coutelier1

Unit of Experimental Medicine1 and Unit of Cellular Genetics2, Institute for Cellular Pathology, Université Catholique de Louvain, UCL MEXP 7430, Av. Hippocrate 74, 1200 Bruxelles, Belgium

Author for correspondence: Jean-Paul Coutelier. Fax +32 2 764 7430. e-mail coutelier{at}mexp.ucl.ac.be

Early after infection, lactate dehydrogenase-elevating virus (LDV) alters the immune system by polyclonally activating B lymphocytes, which leads to IgG2a-restricted hypergammaglobulinaemia, and by suppressing the secretion of Th2 cytokines. Considering that these alterations may involve cells of the innate immune system and cytokines such as interferon-gamma (IFN-{gamma}), we analysed the effect of LDV on natural killer (NK) cells. Within a few days of infection, a strong and transient NK cell activation, characterized by enhanced IFN-{gamma} message expression and cytolysis, was observed. LDV triggered a large increase in serum IFN-{gamma} levels. Because NK cells and IFN-{gamma} may participate in the defence against virus infection, we analysed their possible role in the control of LDV titres with a new agglutination assay. Our results indicate that neither the activation of NK cells nor the IFN-{gamma} secretion affect the early and rapid virus replication that follows LDV inoculation.




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