Early T cell response in the central nervous system  in canine distemper virus infection

Canine distemper is a systemic infection, frequently lethal in dogs. The canine distemper virus(CDV) causes a persistent infection within the central nervous system resulting in aprogressive, multifocal demyelinating disease. In dogs, CDV infection may lead togastrointestinal and/or respiratory signs, frequently with central nervous system involvement.Myoclonus has been a common and characteristic sign observed in dogs with distemperencephalomyelitis. However, the nervous form of distemper may occur in the absence ofmyoclonus and systemic involvement. This review will point the clinical course and theneurological signs of nervous distemper, as well the clinical syndromes of CDV infection,neuropathology of acute and chronic demyelination, and diagnostic aids of CDVencephalomyelitis.

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Protective autoimmunity as a T-cell response to central nervous system trauma: prospects for therapeutic vaccines

Progress in Neurobiology ◽

10.1016/s0301-0082(01)00009-0 ◽

2001 ◽

Vol 65 (5) ◽

pp. 489-496 ◽

Cited By ~ 38

Author(s):

Michal Schwartz

Keyword(s):

Central Nervous System ◽

Nervous System ◽

T Cell ◽

Cell Response ◽

T Cell Response ◽

Therapeutic Vaccines ◽

Protective Autoimmunity ◽

Central Nervous System Trauma

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Studies on canine distemper virus persistence in the central nervous system

Acta Neuropathologica ◽

10.1007/bf00307649 ◽

1995 ◽

Vol 89 (5) ◽

pp. 438-445 ◽

Cited By ~ 40

Author(s):

Cornelia F. M�ller ◽

Rosmarie S. Fatzer ◽

Karin Beck ◽

Marc Vandevelde ◽

Andreas Zurbriggen

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Canine Distemper Virus ◽

Canine Distemper ◽

Virus Persistence ◽

The Central Nervous System

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Priming of CD8+ T Cells during Central Nervous System Infection with a Murine Coronavirus Is Strain Dependent

Journal of Virology ◽

10.1128/jvi.00106-08 ◽

2008 ◽

Vol 82 (13) ◽

pp. 6150-6160 ◽

Cited By ~ 11

Author(s):

Katherine C. MacNamara ◽

Susan J. Bender ◽

Ming Ming Chua ◽

Richard Watson ◽

Susan R. Weiss

Keyword(s):

Central Nervous System ◽

T Cells ◽

Nervous System ◽

T Cell ◽

Cell Response ◽

T Cell Response ◽

Cns Infection ◽

Cervical Lymph Nodes ◽

T Cell Priming ◽

The Brain

ABSTRACT Virus-specific CD8+ T cells are critical for protection against neurotropic coronaviruses; however, central nervous system (CNS) infection with the recombinant JHM (RJHM) strain of mouse hepatitis virus (MHV) elicits a weak CD8+ T-cell response in the brain and causes lethal encephalomyelitis. An adoptive transfer model was used to elucidate the kinetics of CD8+ T-cell priming during CNS infection with RJHM as well as with two MHV strains that induce a robust CD8+ T-cell response (RA59 and SJHM/RA59, a recombinant A59 virus expressing the JHM spike). While RA59 and SJHM/RA59 infections resulted in CD8+ T-cell priming within the first 2 days postinfection, RJHM infection did not lead to proliferation of naïve CD8+ T cells. While all three viruses replicated efficiently in the brain, only RA59 and SJHM/RA59 replicated to appreciable levels in the cervical lymph nodes (CLN), the site of T-cell priming during acute CNS infection. RJHM was unable to suppress the CD8+ T-cell response elicited by RA59 in mice simultaneously infected with both strains, suggesting that RJHM does not cause generalized immunosuppression. RJHM was also unable to elicit a secondary CD8+ T-cell response in the brain following peripheral immunization against a viral epitope. Notably, the weak CD8+ T-cell response elicited by RJHM was unique to CNS infection, since peripheral inoculation induced a robust CD8+ T-cell response in the spleen. These findings suggest that the failure of RJHM to prime a robust CD8+ T-cell response during CNS infection is likely due to its failure to replicate in the CLN.

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