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The absence of M1 leads to increased establishment of murine gammaherpesvirus 68 latency in IgD-negative B cells.

J. Virol.2013 Mar;87(6):3597-604. Epub 2013 Jan 09
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摘要


The secreted M1 protein of murine gammaherpesvirus 68 (MHV68) promotes effector Vβ4(+) CD8(+) T cell expansion to impact virus control and immune-mediated pathologies in C57BL/6 mice, but not BALB/c mice. We report a striking increase in the number of genome-positive, IgD(-) B cells during chronic infection of both mouse strains. This suggests a novel role for M1 in influencing long-term maintenance in a major latency reservoir irrespective of the degree of Vβ4(+) CD8(+) T cell expansion.

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