ABSTRACT Oncoviruses utilise various molecular strategies to modulate host cells and induce microenvironments that favour viral persistence, immune evasion, and disease progression. Endothelial‐to‐mesenchymal transition (EndMT) has recently emerged as a critical, yet underrecognized, pathway hijacked by oncoviral pathogens to modulate endothelial plasticity within the cardiovascular system. Accumulating evidence indicates that Oncogenic and non‐oncogenic viruses, including Kaposi's sarcoma–associated herpesvirus (KSHV/HHV‐8), severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), human immunodeficiency virus (HIV), and other endothelial‐tropic viruses, directly manipulate host signalling networks, such as TGF‐β, Wnt/β‐catenin, Notch, and NF‐κB, to induce partial or complete EndMT. This virus‐driven EndMT contributes to vascular remodelling, chronic inflammation, aberrant angiogenesis, and the development of oncoviral‐associated cardiovascular pathology and vascular tumours. The present review integrates current virological and mechanistic insights into EndMT as a hijacked host process, highlighting its role at the virus–host interface and discussing emerging antiviral and pathway‐targeted strategies aimed at limiting oncovirus‐mediated endothelial dysfunction.
Li et al. (Sat,) studied this question.