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-Herpesvirus-68-Induced IL-12 Contributes to the Control of Latent Viral Burden, but Also Contributes to Viral-Mediated Leukocytosis 1
Department of Biology, University of North Carolina, Charlotte, NC 28223
Early IFN-
/
production, followed by the development of a viral-specific CTL response, are critical factors in limiting the level of murine 
-herpesvirus-68 (HV-68) infection. Development of a long-lived CTL response requires T cell help, and these CTLs most likely function to limit the extent of infection following reactivation. The importance of IL-12 in the development and/or activity of Th1 cells and CTLs is well documented, and we investigated the kinetics and magnitude of HV-68-induced IL-12 production. Following intranasal infection, IL-12 and IL-23 mRNA expression was up-regulated in lung and spleen and lung, respectively, followed by increased levels of IL-12p40 in lung homogenates and sera. Exposure of cultured macrophages or dendritic cells to HV-68 induced secretion of IL-12, suggesting that these cells might be responsible for IL-12 production in vivo. HV-68 infection of mice made genetically deficient in IL-12p40 expression (IL-12p40-/-) resulted in a leukocytosis and splenomegaly that was significantly less than that observed in syngeneic C57BL/6 mice. IL-12p40-/- mice showed increased levels of infectious virus in the lung, but only at day 9 postinfection. Increased levels of latent virus in the spleen at day 15 postinfection were also observed in IL-12p40-/- mice when compared with syngeneic C57BL/6 mice. An overall reduction in HV-68-induced IFN- production was observed in IL-12p40-/- mice, suggesting that most of the viral-induced IFN- in C57BL/6 mice was IL-12 dependent. Taken together, these results suggest that HV-68-induced IL-12 contributes to the pathophysiology of viral infection while also functioning to limit viral burden.
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