Affiliation:
1. Division
of Virology, Department of Pathology, University of Cambridge,
Cambridge CB2 1QP, United Kingdom
Abstract
ABSTRACT
The
gammaherpesviruses characteristically drive the proliferation of
latently infected lymphocytes. The murine gammaherpesvirus 68 (MHV-68)
MK3 protein contributes to this process in vivo by evading
CD8
+
-T-cell recognition during latency, as well as
during lytic infection. We analyzed some of the molecular mechanisms
that control MK3 expression. No dedicated MK3 mRNA was detected.
Instead, the MK3 open reading frame (ORF) was transcribed as part of a
bicistronic mRNA, downstream of a previously unidentified ORF, 13M. The
13M/MK3 promoter appeared to extend approximately 1 kb 5′ of
the transcription start site and included elements both dependent on
and independent of the ORF50 lytic transactivator. MK3 was translated
from the bicistronic transcript by virtue of an internal ribosome entry
site (IRES) element. RNA structure mapping identified two stem-loops
between 13M and MK3 that were sufficient for IRES activity in a
bicistronic reporter plasmid and a third stem-loop just within the MK3
coding sequence, with a subtler, perhaps regulatory role. Overall,
translation of the MHV-68 MK3 bore a striking resemblance to that of
the Kaposi's sarcoma-associated herpesvirus vFLIP, suggesting that
IRES elements are a common theme of latent gammaherpesvirus immune
evasion in proliferating
cells.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
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