>Mtmr6|NM_144843|3'UTR
   1 CCTCCTTCCGTGATCCCTGGATGACTGTAGTGTAAGAAATGTATAGTTGTGAGGATGGTCTGTACACATGGGCAGGAGGG
  81 GTTGTTGAGTGACTTTGGGGCTTAGCAGTAAGTGAGAAAGTAGGTAGCTGAGAAAAGGATCATAGCAACTCTTGAGAGGA
 161 GTGAGTCAGCTAAGTGCCATTTGTAACAAGAACATACTCATTTCTGTAGGAAGTGAGTGCTAGTGTGTGTATGTACTGGA
 241 AAGGGGTTACACAGGACTGGTGAGCTGACAGTCTGTTGATTCAGATGTTAATTCCAGCCACGCTCAGTAGCTTTCCTCTA
 321 ACTCTGAGAAAACAGACCTGACAACCTGAACCCTCAGTGACTGATGTGGCATGTGCTTTCAGTTCTGGAGCTGTGTGACT
 401 GTGGATTTTGCAGTCACAAAAATCCAAATATATAGTCAAAAATATAGTGACGTTTTAACATTAAAGTGCCATGAAAAGTA
 481 CTTATGGGACAGCCTTAAAGTAGACTCTCAGTTTATTCTGTGGGTTTTATAGCCGAGGACAGGATGTTTGATCTCTCCTT
 561 TAATCAGCCTTATTTCATATGAAGAACTAACTGCACTCTGATTACTTGGGGGCCGCACACTGCAGTGCTCCACCATGGAA
 641 AGTTGTAGACATACTCTGCTAGTTTGTAATTAGCCAGCTCCACCCGTATTTAAAATCAGTGTTACCGAAGGCTTTGTTCT
 721 CGTTGTCATTTGTTCCAAGCTGCAGCTGACAGTTCATTATTCACAGCTTAGAGGACTCATTTCTTAGGCTAGTATAAGCA
 801 CATTTGGCATTTACTTTCGGCTTACTGCAGTCTATTAATTCTTACTCTGTGGTTGGCTTTAATCCTTTGATAACTGTACA
 881 TTTAAAGTGGCAAAGCTCTAAAGCGTTCTGAGTACTAAATACATTTTTAACTTGACTGTAGCTGCCTATAAACTTTCAGG
 961 TAAAGGAAAAAGGGAAGTGCGGGTAGTGGAGATTTTGCTTGGTTACGAATTCTAAAGCAATCATTTTTGTGTGGAGCATA
1041 TTTCCTTACTCTTAATATAGGAGGGGCAGAGAAGGGAGCACTGGGGGAGCCAGCTAATGTCCAACAGAAGCAGCTTTGAC
1121 GCAGGAAAAGGTTTATTTTGCTTTATAGGCTCATTGTTATTCTGTGCACTGGGGCATACATATCTTTTCTAAAAAATCAC
1201 TTACAACTGTCAGTATTACCAGCTGGCTCTCAAAGTTTAATATCATTGATGGTGTGTGAGGTACAGTTCAGGGGCACTAC
1281 AAAATCTGTGTACATTGTCTTATATACCTCCTGACCACACCTATATCTGTAGTATTTCTTGTGTTAGTTTTGAACATATG
1361 TATCTTTTTTTTTTTTTTGGGAAAAAAAAGGAAAGCTTTATCGTATATGATTTTATCTAGTCCTTATTTTTCCAATTCAC
1441 TTCTGTAAGACCTTATGTAATAAAAACACTGCATTTTAAAAAGTAACAGAAATATACTAAAAATTACAATGTATAATGAA
1521 CAGTGTTTAGACATTGAGAAAGGAAACTTAATCTCTGTGTCCACAACAGGAGGGTTTTGTGCCTTGGTTCCAGTCAAGTT
1601 GTGGTTTTAGACTTCTGTGGCAGACTTCCTAGTCATCTTCTGGGTTCCTTATGCTAATTTTCAACTTCACATGTATATAT
1681 GTGTTTACATGCTCACACAGAAAACATCCTGAGTGACGTACAGGACATACGTTGGCAAAAGTCTGTGTAAATGTCTCATA
1761 AAATTAGATTTATGTTCATTGTGTTTTGGGATGTATAGCATGTAAATTATTTCATGTATTATTTAAAGGCAATTAAATGT
1841 TCATGCTTTAAAAAAAAA

ID	Duplex structure	Position	Score	MFE
1	miRNA 3' uuggguuauaGUUUGUAUAGu 5' || ||||||| Target 5' tgcactggggCATACATATCt 3'	1165 - 1185	147.00	-9.40
2	miRNA 3' uugGGUUAUAGUUUGUAUAgu 5' ::|:| |::||||||| Target 5' gtgTTAGTTTTGAACATATgt 3'	1341 - 1361	142.00	-5.90
3	miRNA 3' uugGGUUAUA-GUUUGUAUAgu 5' | || || ||||:|||| Target 5' tcaCAAAAATCCAAATATATag 3'	414 - 435	130.00	-6.20

- Journal of immunology (Baltimore, Md. : 1950), 2014

HIV replication and the cellular micro-RNA (miRNA) machinery interconnect at several posttranscriptional levels. To understand their regulatory role in the intestine, a major site of HIV/SIV replication, dissemination, and CD4(+) T cell depletion, we profiled miRNA expression in colon following SIV infection (10 acute SIV, 5 uninfected). Nine (four up and five down) miRNAs showed statistically significant differential expression. Most notably, miR-190b expression showed high statistical significance (adjusted p = 0.0032), the greatest fold change, and was markedly elevated in colon and jejunum throughout SIV infection. In addition, miR-190b upregulation was detected before peak viral replication and the nadir of CD4(+) T cell depletion predominantly in lamina propria leukocytes. Interestingly non-SIV-infected macaques with diarrhea and colitis failed to upregulate miR-190b, suggesting that its upregulation was neither inflammation nor immune-activation driven. SIV infection of in vitro-cultured CD4(+) T cells and primary intestinal macrophages conclusively identified miR-190b upregulation to be driven in response to viral replication. Further miR-190b expression levels in colon and jejunum positively correlated with tissue viral loads. In contrast, mRNA expression of myotubularin-related protein 6 (MTMR6), a negative regulator of CD4(+) T cell activation/proliferation, significantly decreased in SIV-infected macrophages. Luciferase reporter assays confirmed MTMR6 as a direct miR-190b target. To our knowledge, this is the first report, which describes dysregulated miRNA expression in the intestine, that identifies a potentially significant role for miR-190b in HIV/SIV pathogenesis. More importantly, miR-190b-mediated MTMR6 downregulation suggests an important mechanism that could keep infected cells in an activated state, thereby promoting viral replication. In the future, the mechanisms driving miR-190b upregulation including other cellular processes it regulates in SIV-infected cells need determination.