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Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo

¹ Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK
² Gulbenkian Institute for Science, 2780-156 Oeiras, Lisbon, Portugal
³ Laboratory of Microbiology, Faculty of Medicine, Lisbon University, Portugal

Correspondence
Philip G. Stevenson
pgs27{at}mole.bio.cam.ac.uk

The gammaherpesviruses are characteristically latent in lymphocytes and exploit lymphocyte proliferation to establish a large, persistent pool of latent genomes. Murine gammaherpesvirus 68 (MHV-68) allows the in vivo analysis of viral genes that contribute to this and other aspects of host colonization. In this study, the MHV-68 bcl-2 homologue, M11, was disrupted either in its BH1 homology domain or upstream of its membrane-localizing C-terminal domain. Each M11 mutant showed normal lytic replication in vitro and in vivo, but had a reduction in peak splenic latency. Lower infectious-centre titres correlated with lower in vivo B-cell activation, lower viral genome loads and reduced viral tRNA expression. This was therefore a true latency deficit, rather than a deficit in ex vivo reactivation. Stable, long-term levels of splenic latency were normal. M11 function therefore contributed specifically to viral latency amplification in infected lymphoid tissue.

Published online ahead of print on 13 October 2004 as DOI 10.1099/vir.0.80480-0.

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