November 1, 1998Journal of VirologyOpen Access

A Protein Critical for a Theiler’s Virus-Induced Immune System-Mediated Demyelinating Disease Has a Cell Type-Specific Antiapoptotic Effect and a Key Role in Virus Persistence

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Population

BHK-21 cells, P388D1 mouse macrophage cells, and weanling 3-week-old SJL/J mice (n=28)

Comparison

Infection with wild-type DA strain of Theiler's… vs Infection with DAL*-1 mutant virus, GDVII virus…

Design

Preclinical

Follow-up

6 weeks

Authors

Discussion

L* anti-apoptosis in macrophages supports TMEV persistence; leaves open relevance to human CNS viral disease.

Population

BHK-21 cells, P388D1 mouse macrophage cells, and weanling 3-week-old SJL/J mice (n=28)

Intervention

Infection with wild-type DA strain of Theiler's murine encephalomyelitis virus (TMEV) which synthesizes the L* protein

Comparator

Infection with DAL*-1 mutant virus (which fails to synthesize L*), GDVII virus, or mock infection

Outcome

Apoptosis in macrophage cells and virus persistence in the central nervous system

The L* protein of TMEV exerts an antiapoptotic effect in macrophages, which is essential for viral persistence in the central nervous system.

Ghadge et al. (1998) studied this question.

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