AI Article Synopsis
- Viruses, like the chikungunya virus, hijack host cell machinery to create viral proteins, disrupting the Endoplasmic Reticulum and activating the Unfolded Protein Response (UPR).
- Researchers found that chikungunya virus positively influenced certain UPR branches (IRE1 and ATF6) while suppressing another (PERK).
- By using specific inhibitors for UPR pathways, they observed a significant reduction in viral replication, suggesting a new approach for developing antiviral treatments against chikungunya.
Article Abstract
Abstract: Viruses invade the host cells and maneuver the cellular translation machinery to translate the viral proteins in substantial amounts, which may disturb Endoplasmic Reticulum homeostasis leading to induction of Unfolded Protein Response (UPR), a host response pathway involved in viral pathogenesis. Here, we investigated the effect of UPR pathways on the pathogenesis of chikungunya virus infection. We observed that chikungunya virus mediated the modulation of UPR. A positive modulation was observed in the activation of IRE1 and ATF6 branch while the PERK branch of UPR observed suppressed upon virus infection. We further investigated the effect of the inhibition of UPR pathways on chikungunya virus replication using inhibitors for each branch. Cells treated with 3-ethoxy-5,6-dibromosalicylaldehyde (IRE1 inhibitor) and AEBSF (ATF6 inhibitor) significantly inhibits the viral replication process. This study has provided a novel perspective in designing antivirals against chikungunya virus.
Supplementary Information: The online version contains supplementary material available at 10.1007/s12088-022-01046-5.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9705628 | PMC |
| http://dx.doi.org/10.1007/s12088-022-01046-5 | DOI Listing |
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