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

Brigitte D. de Lima, Janet S. May, Sofia Marques, J. Pedro Simas, Philip G. Stevenson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

44 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)31-40
Number of pages10
JournalJournal of General Virology
Issue number1
Publication statusPublished - 1 Jan 2005
Externally publishedYes


Dive into the research topics of 'Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo'. Together they form a unique fingerprint.

Cite this