AI Article Synopsis
- Ebola virus (EBOV) and Marburg virus (MARV) are dangerous pathogens that cause serious outbreaks of hemorrhagic fever, posing a global health risk and necessitating new treatments.
- The EBOV VP40 protein is crucial for virus assembly and release, and it can be targeted for destruction by the body's autophagy process, which is supported by proteins BAG3 and HSPA/HSP70.
- Research shows that the EBOV glycoprotein activates MTORC1, a key regulator of autophagy, and inhibiting this pathway with rapamycin can promote autophagy, block viral release, and open doors for new antiviral strategies.
Article Abstract
Ebola virus (EBOV) and Marburg virus (MARV) are zoonotic, virulent pathogens that cause sporadic and global outbreaks of severe hemorrhagic fever. Reemergence of these filoviruses remains a global public health threat, highlighting the need for novel countermeasures to control and treat future disease outbreaks. The EBOV VP40 matrix protein drives virion assembly and egress. We recently reported that BAG3 and HSPA/HSP70, two central components of chaperone-assisted selective autophagy (CASA), target VP40 for autophagic sequestration and degradation, thereby inhibiting virus egress and spread. In addition, we found that expression of the EBOV glycoprotein (GP) activates MTORC1, the gateway regulator of autophagy. Notably, pharmacological suppression of MTORC1 signaling by rapamycin activates autophagy and blocks filovirus egress. These findings highlight the MTORC1-CASA axis as a regulator of filovirus egress and suggest new opportunities for antiviral development and intervention.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10472846 | PMC |
| http://dx.doi.org/10.1080/15548627.2023.2178781 | DOI Listing |
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