Limits...
Interfering RNA and HIV: reciprocal interferences.

Corbeau P - PLoS Pathog. (2008)

Bottom Line: In this review, a quick presentation of what interfering RNA (iRNA) are--small RNA able to exert an inhibition on gene expression at a posttranscriptional level, based on sequence homology between the iRNA and the mRNA--will be given.Then, we will discuss the putative effects of these mutual influences on viral replication as well as on viral latency, immune response, and viral cytopathogenicity.Finally, the potential consequences on the human infection of genetic polymorphisms in microRNA genes and the therapeutic potential of iRNA will be presented.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Immunologie, Hôpital Carémeau, Nîmes and Institut de Génétique Humaine, CNRS UPR1142, Montpellier, France. pierre.corbeau@igh.cnrs.fr

ABSTRACT
In this review, a quick presentation of what interfering RNA (iRNA) are--small RNA able to exert an inhibition on gene expression at a posttranscriptional level, based on sequence homology between the iRNA and the mRNA--will be given. The many faces of the interrelations between iRNA and viruses, particularly HIV, will be reviewed. Four kinds of interactions have been described: i) iRNA of viral origin blocking viral RNA, ii) iRNA of viral origin downregulating cellular mRNA, iii) iRNA of cellular origin (microRNA) targeting viral RNA, and iv) microRNA downregulating cellular mRNA encoding cell proteins used by the virus for its replication. Next, HIV strategies to manipulate these interrelations will be considered: suppression of iRNA biosynthesis by Tat, trapping by the HIV TAR sequence of a cell component, TRBP, necessary for iRNA production and action, and induction by the virus of some microRNA together with suppression of others. Then, we will discuss the putative effects of these mutual influences on viral replication as well as on viral latency, immune response, and viral cytopathogenicity. Finally, the potential consequences on the human infection of genetic polymorphisms in microRNA genes and the therapeutic potential of iRNA will be presented.

Show MeSH

Related in: MedlinePlus

Inhibition of HIV Expression by the Silencing Exerted by miR-17-5p and miR-20 on PCAF (A), and Downregulation of This Inhibition by HIV (B)
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2533403&req=5

ppat-1000162-g003: Inhibition of HIV Expression by the Silencing Exerted by miR-17-5p and miR-20 on PCAF (A), and Downregulation of This Inhibition by HIV (B)

Mentions: Finally, a fourth situation, where host miRNAs limit viral proliferation by acting on cellular mRNA, has been recently proposed for HIV [32]. Triboulet et al. have shown that the cellular miRNAs miR-17-5p and miR-20 silence the mRNA encoding the histone acetylase PCAF. PCAF has been previously presented as a host cofactor for Tat transactivation of HIV LTR, and as being recruited by Tat and remodeling the histone architecture in the vicinity of the LTR, promoting thereby HIV gene expression (Figure 3A). This is to say that human cells seem to permanently downregulate HIV-1 replication by depriving the infected cell of an endogenous enzyme that could be necessary for virus gene expression.


Interfering RNA and HIV: reciprocal interferences.

Corbeau P - PLoS Pathog. (2008)

Inhibition of HIV Expression by the Silencing Exerted by miR-17-5p and miR-20 on PCAF (A), and Downregulation of This Inhibition by HIV (B)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2533403&req=5

ppat-1000162-g003: Inhibition of HIV Expression by the Silencing Exerted by miR-17-5p and miR-20 on PCAF (A), and Downregulation of This Inhibition by HIV (B)
Mentions: Finally, a fourth situation, where host miRNAs limit viral proliferation by acting on cellular mRNA, has been recently proposed for HIV [32]. Triboulet et al. have shown that the cellular miRNAs miR-17-5p and miR-20 silence the mRNA encoding the histone acetylase PCAF. PCAF has been previously presented as a host cofactor for Tat transactivation of HIV LTR, and as being recruited by Tat and remodeling the histone architecture in the vicinity of the LTR, promoting thereby HIV gene expression (Figure 3A). This is to say that human cells seem to permanently downregulate HIV-1 replication by depriving the infected cell of an endogenous enzyme that could be necessary for virus gene expression.

Bottom Line: In this review, a quick presentation of what interfering RNA (iRNA) are--small RNA able to exert an inhibition on gene expression at a posttranscriptional level, based on sequence homology between the iRNA and the mRNA--will be given.Then, we will discuss the putative effects of these mutual influences on viral replication as well as on viral latency, immune response, and viral cytopathogenicity.Finally, the potential consequences on the human infection of genetic polymorphisms in microRNA genes and the therapeutic potential of iRNA will be presented.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Immunologie, Hôpital Carémeau, Nîmes and Institut de Génétique Humaine, CNRS UPR1142, Montpellier, France. pierre.corbeau@igh.cnrs.fr

ABSTRACT
In this review, a quick presentation of what interfering RNA (iRNA) are--small RNA able to exert an inhibition on gene expression at a posttranscriptional level, based on sequence homology between the iRNA and the mRNA--will be given. The many faces of the interrelations between iRNA and viruses, particularly HIV, will be reviewed. Four kinds of interactions have been described: i) iRNA of viral origin blocking viral RNA, ii) iRNA of viral origin downregulating cellular mRNA, iii) iRNA of cellular origin (microRNA) targeting viral RNA, and iv) microRNA downregulating cellular mRNA encoding cell proteins used by the virus for its replication. Next, HIV strategies to manipulate these interrelations will be considered: suppression of iRNA biosynthesis by Tat, trapping by the HIV TAR sequence of a cell component, TRBP, necessary for iRNA production and action, and induction by the virus of some microRNA together with suppression of others. Then, we will discuss the putative effects of these mutual influences on viral replication as well as on viral latency, immune response, and viral cytopathogenicity. Finally, the potential consequences on the human infection of genetic polymorphisms in microRNA genes and the therapeutic potential of iRNA will be presented.

Show MeSH
Related in: MedlinePlus