TY - JOUR
T1 - Murine gammaherpesvirus 68 bcl-2 homologue contributes to latency establishment in vivo
AU - Lima, Brigitte D. de
AU - May, Janet S.
AU - Marques, Sofia
AU - Simas, J. Pedro
AU - Stevenson, Philip G.
PY - 2005/1/1
Y1 - 2005/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=11444254723&partnerID=8YFLogxK
U2 - 10.1099/vir.0.80480-0
DO - 10.1099/vir.0.80480-0
M3 - Article
C2 - 15604429
AN - SCOPUS:11444254723
SN - 0022-1317
VL - 86
SP - 31
EP - 40
JO - Journal of General Virology
JF - Journal of General Virology
IS - 1
ER -