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The Journal of Immunology, 2002, 168: 1204-1211.
Copyright © 2002 by The American Association of Immunologists

Mechanisms of Central Nervous System Viral Persistence: the Critical Role of Antibody and B Cells1

Chandran Ramakrishna*, Stephen A. Stohlman*, Roscoe D. Atkinson{dagger}, Mark J. Shlomchik{ddagger} and Cornelia C. Bergmann2,*,{dagger}

Departments of * Neurology and {dagger} Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033; and {ddagger} Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, CT 06510

Contributions of humoral and cellular immunity in controlling neurotropic mouse hepatitis virus persistence within the CNS were determined in B cell-deficient JHD and syngeneic H-2d B cell+ Ab-deficient mice. Virus clearance followed similar kinetics in all mice, confirming initial control of virus replication by cellular immunity. Nevertheless, virus reemerged within the CNS of all Ab-deficient mice. In contrast to diminished T cell responses in H-2b B cell-deficient µMT mice, the absence of B cells or Ab in the H-2d mice did not compromise expansion, recruitment into the CNS, or function of virus-specific CD4+ and CD8+ T cells. The lack of B cells and lymphoid architecture thus appears to manifest itself on T cell responses in a genetically biased manner. Increasing viral load did not enhance frequencies or effector function of virus-specific T cells within the CNS, indicating down-regulation of T cell responses. Although an Ab-independent antiviral function of B cells was not evident during acute infection, the presence of B cells altered CNS cellular tropism during viral recrudescence. Reemerging virus localized almost exclusively to oligodendroglia in B cell+ Ab-deficient mice, whereas it also replicated in astrocytes in B cell-deficient mice. Altered tropism coincided with distinct regulation of CNS virus-specific CD4+ T cells. These data conclusively demonstrate that the Ab component of humoral immunity is critical in preventing virus reactivation within CNS glial cells. B cells themselves may also play a subtle role in modulating pathogenesis by influencing tropism.




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