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Reduced CTL Response and Increased Viral Burden in Substance P Receptor-Deficient Mice Infected with Murine -Herpesvirus 68¹

Sherine F. Elsawa^*, William Taylor^*, Cynthia C. Petty^*, Ian Marriott^*, Joel V. Weinstock and Kenneth L. Bost^2,*

^* Department of Biology, University of North Carolina, Charlotte, NC 28223; and Division of Gastroenterology-Hepatology, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242

One component of the protective host response against mucosal pathogens includes the local production and increased expression of certain neuropeptides and their receptors. The present study further demonstrates this fact by investigating the contribution that substance P receptor expression makes toward immunity against a -herpesvirus infection. Following intragastric inoculation with murine -herpesvirus 68 (HV-68), expression of substance P and its receptor was increased in mucosal and peripheral lymphoid organs in wild-type strains of mice. These results suggested that this receptor/ligand pair might be an important component of the host response against this viral infection. Such a hypothesis was supported by the demonstration that mice, genetically deficient in substance P receptor expression, showed an increased viral burden when compared with syngeneic C57BL/6 mice. Furthermore, substance P receptor-deficient mice showed a reduced CTL response against HV-68, suggesting a mechanism to explain this increased viral burden. Such limitations in the Ag-specific CTL response in substance P receptor-deficient mice could result from lowered expression of IL-12 during viral infection. Consistent with this hypothesis, increases in mRNA encoding IL-12 and secretion of this cytokine into sera of infected, wild-type animals were markedly reduced in substance P receptor-deficient mice. These studies demonstrate that genetic elimination of substance P receptors in mice results in an increased -herpesvirus burden and an altered host response.

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