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The Journal of Immunology, Vol 155, Issue 5 2533-2544, Copyright © 1995 by American Association of Immunologists

ARTICLES

Progression of a vesicular stomatitis virus infection in primary lymphocytes is restricted at multiple levels during B cell activation

MR Schmidt, KA Gravel and RT Woodland
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655, USA.

Small resting B cells do not support a productive vesicular stomatitis virus (VSV) infection, but are induced by B cell activators to become fully permissive for VSV replication. Nonpermissive B cell populations restrict VSV expression at multiple points: transcript levels, translation, and maturation. Unstimulated resting G0 B cells can be infected by VSV and support the synthesis of all VSV mRNAs. Steady- state levels of viral transcripts are selectively enhanced by T cell- derived cytokines to an extent comparable with that seen for cytokine- regulated cellular mRNAs. However, viral proteins are not detected in immunoprecipitates from unstimulated or cytokine-stimulated B cells despite the fact that viral mRNAs are associated with polysomes and can be translated in vitro. This translational block is released by stimulation of infected B cells with mitogenic anti-lg or LPS, or non- mitogenic PMA. VSV virion maturation is also regulated by activation signals, because neither anti-lg nor PMA-stimulated B cells produce high levels of infectious VSV particles. Because anti-lg stimulation supports viral genome replication, maturational arrest is apparently at virus assembly or release. PMA and ionomycin induces changes beyond those seen with anti-lg, because these B cells produce PFUs at levels comparable with those seen with LPS-activated B cells and VSV- permissive cell lines. Activation-dependent regulation of virus expression provides a new paradigm for assessing activator-induced events in B cell differentiation not revealed by previous assessments of proliferation of Ab synthesis.


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