Please use this identifier to cite or link to this item:
Type
ArticleCopyright
Restricted access
Embargo date
2030-12-31
Collections
- CDTS - Artigos de Periódicos [480]
- IOC - Artigos de Periódicos [12969]
Metadata
Show full item record
HERPES SIMPLEX TYPE 1 ACTIVATES GLYCOLYSIS THROUGH ENGAGEMENT OF THE ENZYME 6-PHOSPHOFRUCTO-1-KINASE (PFK-1)
Author
Affilliation
Abstract
Viruses such as HIV, HCV, Mayaro and HCMV affect cellular metabolic pathways, including glycolysis. Although some studies have suggested that the inhibition of glycolysis affects HSV-1 replication and that HSV-1-infected eyes have increased lactate production, the mechanisms by which HSV-1 induces glycolysis have never been investigated in detail. In this study, we observed an increase in glucose uptake, lactate efflux and ATP content in HSV-1-infected cells. HSV-1 triggered a MOI-dependent increase in the activity of phosphofructokinase-1 (PFK-1), a key rate-limiting enzyme of the glycolytic pathway. After HSV-1 infection, we observed increased PFK-1 expression, which increased PFK-1 total activity, and the phosphorylation of this enzyme at serine residues. HSV-1-induced glycolysis was associated with increased ATP content, and these events were critical for viral replication. In summary, our results suggest that HSV-1 triggers glycolysis through a different mechanism than other herpesviruses, such as HCMV. Thus, this study contributes to a better understanding of HSV-1 pathogenesis and provides insights into novel targets for antiviral therapy.
Share