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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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.[1]


  1. Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo. de Lima, B.D., May, J.S., Marques, S., Simas, J.P., Stevenson, P.G. J. Gen. Virol. (2005) [Pubmed]
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