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- W2107160572 abstract "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." @default.
- W2107160572 created "2016-06-24" @default.
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- W2107160572 date "2005-01-01" @default.
- W2107160572 modified "2023-09-27" @default.
- W2107160572 title "Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo" @default.
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- W2107160572 doi "https://doi.org/10.1099/vir.0.80480-0" @default.
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