AI Article Synopsis
- Human cytomegalovirus (HCMV) infection is linked to glioblastoma, a severe brain tumor, but the infection mechanism is not fully understood.
- The study reveals that EphA2 is increasingly present in glioblastoma and is associated with poor patient outcomes; its silencing reduces HCMV infection while its overexpression enhances it.
- EphA2 facilitates HCMV infection by binding to the viral gH/gL complex, and targeting EphA2 with inhibitors or antibodies can significantly reduce HCMV infection in glioblastoma cells and organoids, positioning EphA2 as a key player for potential therapeutic strategies.
Article Abstract
Human cytomegalovirus (HCMV) infection is associated with human glioblastoma, the most common and aggressive primary brain tumor, but the underlying infection mechanism has not been fully demonstrated. Here, we show that EphA2 was upregulated in glioblastoma and correlated with the poor prognosis of the patients. EphA2 silencing inhibits, whereas overexpression promotes HCMV infection, establishing EphA2 as a crucial cell factor for HCMV infection of glioblastoma cells. Mechanistically, EphA2 binds to HCMV gH/gL complex to mediate membrane fusion. Importantly, the HCMV infection was inhibited by the treatment of inhibitor or antibody targeting EphA2 in glioblastoma cells. Furthermore, HCMV infection was also impaired in optimal glioblastoma organoids by EphA2 inhibitor. Taken together, we propose EphA2 as a crucial cell factor for HCMV infection in glioblastoma cells and a potential target for intervention.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10191332 | PMC |
| http://dx.doi.org/10.1371/journal.ppat.1011304 | DOI Listing |
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