Contribution of T cells to mortality in neurovirulent Sindbis virus encephalomyelitis

• Published in: Journal of neuroimmunology 2002-06, Vol.127 (1), p.106-114
• Main Authors: Rowell, Jennifer F., Griffin, Diane E.
• Format: Article
• Language: English
• Subjects: Alphavirus Infections - immunology; Alphavirus Infections - mortality; Alphavirus Infections - pathology; Animals; Axons - pathology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - virology; CD8-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - virology; Cell Line; Cricetinae; Encephalitis, Viral - immunology; Encephalitis, Viral - mortality; Encephalitis, Viral - pathology; Female; Gene Expression - immunology; Infectious immunity-virus; Interferon-gamma - genetics; Kidney - cytology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Nerve Degeneration - immunology; Nerve Degeneration - mortality; Nerve Degeneration - pathology; RNA, Viral - immunology; Sindbis Virus; T lymphocytes; Transgenic/knockout
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/S0165-5728(02)00108-X

Intranasal inoculation of C57BL/6 mice with a neurovirulent strain of Sindbis virus (SV) results in fatal encephalomyelitis. Mice with selective immune deficiencies were studied to determine the role of the immune response in fatal outcome. Mortality was decreased in mice deficient in αβ, but not γδ, T cells demonstrating a contribution of αβ T cells. Mice lacking either CD4 + or CD8 + T cells also had reduced mortality and mice lacking interferon (IFN)-γ were completely protected. Clearance of infectious virus was identical in mice without T cells or IFN-γ, but clearance of viral RNA was delayed compared to normal mice. Mice unable to produce antibody, perforin, Fas, TNF-α receptor1, IL-6 or IL-12 were not protected. These data suggest that T cells contribute to fatal acute viral encephalomyelitis through the production of IFN-γ.