Borna disease virus infection in Lewis rats induces a biphasic immune response in the central nervous system, transitioning from an acute Th1-like cellular response to a chronic Th2-like humoral response.
May inform phase-specific immunomodulation in neurovirology models; leaves open translation to human CNS infections.
Borna disease virus infection of Lewis rats results in an immune-mediated disease associated with transient meningoencephalitis and persistent viral infection. In the acute phase of disease, perivascular immune cell infiltrates consisted of CD4 + and CD8 + T cells, macrophages and NK cells with peak expression of mRNAs encoding the cytokines IL1alpha, IL2, IL6, TNFalpha, and IFNgamma. In the chronic phase of disease, numbers of NK cells, B cells and activated microglia increased in the brain parenchyma with peak expression of IL4 mRNA. These data were consistent with a switch from a Th1-like, cellular immune response to a Th2-like, humoral immune response.
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Hatalski et al. (1998) studied this question.
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