Vaccinia virus host entry factors

Vaccinia virus (VACV) entry into host cells is a complex, multi-step process involving a variety of cell surface molecules that facilitate viral attachment and internalization. The primary mediators include glycosaminoglycans (GAGs) such as heparan sulfate and chondroitin sulfate, which act as initial docking sites, and various protein receptors like integrin beta-1, Axl receptor tyrosine kinase, and CD98 that trigger endocytic pathways or macropinocytosis (Schmidt et al., 2012; Chiu et al., 2007). In the context of oncology, these molecules are frequently overexpressed on cancer cell surfaces, making them critical targets for oncolytic vaccinia virus therapies designed to selectively infect and lyse malignant cells. Drugs like Pexastimogene devacirepvec (Pexa-Vec) utilize these entry mechanisms to deliver therapeutic payloads and induce systemic anti-tumor immunity (Kirn & Thorne, 2009). Despite their utility in targeting, the widespread expression of these factors on normal cells necessitates careful engineering of viral vectors to ensure safety and tumor specificity.

Other names

Vaccinia virus receptorsHost cell surface proteins and glycans for VACVVACV attachment factorsOncolytic vaccinia virus entry mediators

Facilitation of viral attachment to the host cell membrane followed by induction of endocytosis or macropinocytosis for viral genome release and subsequent oncolysis.