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Tumor cell surface receptors mediating oncolytic virus entry are a diverse group of membrane proteins that serve as the primary docking sites for therapeutic viruses to infect malignant cells. These receptors include the Coxsackievirus and Adenovirus Receptor (CAR), Nectin-1 (CD111), CD46 (membrane cofactor protein), and Nectin-4, which are frequently overexpressed in various solid tumors [1][2]. The interaction between the viral capsid or envelope proteins and these specific cell surface receptors determines the viral tropism and the efficiency of viral uptake [3]. Once the virus enters the tumor cell, it hijacks the cellular machinery to replicate, eventually leading to oncolysis and the release of progeny virions to infect adjacent cells [4]. This process also triggers the release of tumor-associated antigens and damage-associated molecular patterns (DAMPs), which stimulate a robust systemic anti-tumor immune response [5]. Therapeutic strategies often involve engineering oncolytic viruses to specifically target these receptors or to bypass them in healthy tissues to minimize off-target toxicity [1][6]. Consequently, the expression levels of these receptors on a patient's tumor are often used as biomarkers to predict the potential efficacy of oncolytic virotherapy [2].
Viral attachment and entry, Oncolysis, Induction of systemic anti-tumor immunity
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