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2014 ; 54
(1
): 67-79
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gab.com Text
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Alternative capture of noncoding RNAs or protein-coding genes by herpesviruses to
alter host T cell function
#MMPMID24725595
Guo YE
; Riley KJ
; Iwasaki A
; Steitz JA
Mol Cell
2014[Apr]; 54
(1
): 67-79
PMID24725595
show ga
In marmoset T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich
noncoding (nc) RNA, HSUR 1, specifically mediates degradation of host microRNA-27
(miR-27). High-throughput sequencing of RNA after crosslinking
immunoprecipitation (HITS-CLIP) identified mRNAs targeted by miR-27 as enriched
in the T cell receptor (TCR) signaling pathway, including GRB2. Accordingly,
transfection of miR-27 into human T cells attenuates TCR-induced activation of
mitogen-activated protein kinases (MAPKs) and induction of CD69. MiR-27 also
robustly regulates SEMA7A and IFN-?, key modulators and effectors of T cell
function. Knockdown or ectopic expression of HSUR 1 alters levels of these
proteins in virally transformed cells. Two other T-lymphotropic ?-herpesviruses,
AlHV-1 and OvHV-2, do not produce a noncoding RNA to downregulate miR-27 but
instead encode homologs of miR-27 target genes. Thus, oncogenic ?-herpesviruses
have evolved diverse strategies to converge on common targets in host T cells.