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Interplay between HIV-1 infection and host microRNAs.

Sun G, Li H, Wu X, Covarrubias M, Scherer L, Meinking K, Luk B, Chomchan P, Alluin J, Gombart AF, Rossi JJ - Nucleic Acids Res. (2011)

Bottom Line: While microRNA-223 levels were significantly enriched in HIV-1-infected CD4(+)CD8(-) PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced.Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3'-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region.Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223.

View Article: PubMed Central - PubMed

Affiliation: Graduate School of Biological Science, Department of Molecular and Cellular Biology, Beckman Research Institute of City of Hope, 1500 E. Duarte Road, Duarte, CA 91010, USA.

ABSTRACT
Using microRNA array analyses of in vitro HIV-1-infected CD4(+) cells, we find that several host microRNAs are significantly up- or downregulated around the time HIV-1 infection peaks in vitro. While microRNA-223 levels were significantly enriched in HIV-1-infected CD4(+)CD8(-) PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced. Based on the potential for microRNA binding sites in a conserved sequence of the Nef-3'-LTR, several host microRNAs potentially could affect HIV-1 gene expression. Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3'-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region. Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223.

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A map of the interactions between HIV-1, miR-223 and the miR-29 family.
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gkr961-F6: A map of the interactions between HIV-1, miR-223 and the miR-29 family.

Mentions: In summary, we provide a detailed picture of the possible functions of miRNAs whose levels are perturbed in the acute phase of HIV-1 infection. Combining the results from miR-223 and miR-29a/b target modulation, we propose a possible regulatory network that is established following HIV-1 infection, which primarily involves these two host miRNAs (Figure 6). Further testing of this model will be required to establish the validity of this circuit of regulation of host factors that can affect HIV replication and pathogenesis.Figure 6.


Interplay between HIV-1 infection and host microRNAs.

Sun G, Li H, Wu X, Covarrubias M, Scherer L, Meinking K, Luk B, Chomchan P, Alluin J, Gombart AF, Rossi JJ - Nucleic Acids Res. (2011)

A map of the interactions between HIV-1, miR-223 and the miR-29 family.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3300021&req=5

gkr961-F6: A map of the interactions between HIV-1, miR-223 and the miR-29 family.
Mentions: In summary, we provide a detailed picture of the possible functions of miRNAs whose levels are perturbed in the acute phase of HIV-1 infection. Combining the results from miR-223 and miR-29a/b target modulation, we propose a possible regulatory network that is established following HIV-1 infection, which primarily involves these two host miRNAs (Figure 6). Further testing of this model will be required to establish the validity of this circuit of regulation of host factors that can affect HIV replication and pathogenesis.Figure 6.

Bottom Line: While microRNA-223 levels were significantly enriched in HIV-1-infected CD4(+)CD8(-) PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced.Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3'-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region.Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223.

View Article: PubMed Central - PubMed

Affiliation: Graduate School of Biological Science, Department of Molecular and Cellular Biology, Beckman Research Institute of City of Hope, 1500 E. Duarte Road, Duarte, CA 91010, USA.

ABSTRACT
Using microRNA array analyses of in vitro HIV-1-infected CD4(+) cells, we find that several host microRNAs are significantly up- or downregulated around the time HIV-1 infection peaks in vitro. While microRNA-223 levels were significantly enriched in HIV-1-infected CD4(+)CD8(-) PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced. Based on the potential for microRNA binding sites in a conserved sequence of the Nef-3'-LTR, several host microRNAs potentially could affect HIV-1 gene expression. Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3'-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region. Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223.

Show MeSH
Related in: MedlinePlus