PMID- 23439556
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130227
LR  - 20220309
IS  - 1422-0067 (Print)
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 14
IP  - 3
DP  - 2013 Feb 25
TI  - Molecular Analysis of RNA-RNA Interactions between 5' and 3' Untranslated Regions 
      during the Initiation of Translation of a Cardiovirulent and a Live-Attenuated 
      Coxsackievirus B3 Strains.
PG  - 4525-44
LID - 10.3390/ijms14034525 [doi]
AB  - Coxsackievirus B3 (CVB3) is a causative agent of viral myocarditis, meningitis 
      and pancreatitis. CVB3 overcome their host cells by usurping the translation 
      machinery to benefit viral gene expression. This is accomplished through 
      alternative translation initiation in a cap independent manner at the viral 
      internal ribosomal entry site. The 5' untranslated region (5'UTR) of CVB3 genomic 
      RNA is highly structured. It is the site of multiple RNA-protein and RNA-RNA 
      interactions and it plays a critical role during translation initiation. Similar 
      to the 5'UTR, CVB3 3' untranslated region (3'UTR) also contains secondary 
      structural elements consisting of three stem-loops followed by a poly (A) tail 
      sequence. Long-range RNA-RNA interactions between 5' and 3' ends of some viral 
      genomes have been observed. Because of their dual role in translation and 
      replication, the 5' and 3'UTRs represent promising candidates for the study of 
      CVB3 cardiovirulence. Taking into account that efficient initiation of mRNA 
      translation depends on a temporally and spatially orchestrated sequence of 
      protein-protein, protein-RNA and RNA-RNA interactions, and that, at present, 
      little is known about RNA-RNA interactions between CVB3 5' and 3'UTRs, we aimed 
      in the present study, to assess a possible RNA-RNA interaction between 5' and 
      3'UTRs during the initiation of translation of a wild-type and a previously 
      characterized mutant (Sabin3-like) CVB3 strains and to investigate the effect of 
      the Sabin3-like mutation on these potential interactions. For this purpose, 
      "Electrophoretic Mobility Shift" assays were carried out. Data obtained did not 
      show any RNA-RNA direct interactions between the 5'- and 3'- ends. Therefore, we 
      can suggest that the possible mechanism by which 3'UTR enhances CVB3 IRES 
      activity may be by bridging the 5' to the 3' end through RNA-protein interaction 
      and not through RNA-RNA direct contact. However, these findings need to be 
      confirmed by carrying out further experiments.
FAU - Souii, Amira
AU  - Souii A
AD  - Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives 
      (LR99-ES27), Faculte de Pharmacie de Monastir, Avenue Avicenne, Monastir 5000, 
      Tunisia. amira1081@yahoo.fr.
FAU - Gharbi, Jawhar
AU  - Gharbi J
FAU - M'hadheb-Gharbi, Manel Ben
AU  - M'hadheb-Gharbi MB
LA  - eng
PT  - Journal Article
DEP - 20130225
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
PMC - PMC3634434
EDAT- 2013/02/27 06:00
MHDA- 2013/02/27 06:01
PMCR- 2013/03/01
CRDT- 2013/02/27 06:00
PHST- 2013/01/23 00:00 [received]
PHST- 2013/02/16 00:00 [revised]
PHST- 2013/02/20 00:00 [accepted]
PHST- 2013/02/27 06:00 [entrez]
PHST- 2013/02/27 06:00 [pubmed]
PHST- 2013/02/27 06:01 [medline]
PHST- 2013/03/01 00:00 [pmc-release]
AID - ijms14034525 [pii]
AID - ijms-14-04525 [pii]
AID - 10.3390/ijms14034525 [doi]
PST - epublish
SO  - Int J Mol Sci. 2013 Feb 25;14(3):4525-44. doi: 10.3390/ijms14034525.