Abstract
Several viruses are recognized as the direct or indirect causative agents of human tumors and other severe human diseases. Vascular endothelial growth factor (VEGF) is identified as a principal proangiogenic factor that enhances the production of new blood vessels from existing vascular network. Therefore, oncogenic viruses such as Kaposi’s sarcoma herpesvirus (KSHV) and Epstein-Barr virus (EBV) and non-oncogenic viruses such as herpes simplex virus (HSV-1) and dengue virus, which lack their own angiogenic factors, rely on the recruitment of cellular genes for angiogenesis in tumor progression or disease pathogenesis. This review summarizes how human viruses exploit the cellular signaling machinery to upregulate the expression of VEGF and benefit from its physiological functions for their own pathogenesis. Understanding the interplay between viruses and VEGF upregulation will pave the way to design targeted and effective therapeutic approaches for viral oncogenesis and severe diseases.
Highlights
Angiogenesis is an important physiologic process which involves formation of new blood vessels from already existing vasculature
Several stimulators are involved in the angiogenesis process including vascular endothelial growth factor (VEGF), which plays a crucial role in activating endothelial cells through binding to receptors on the cell surface called vascular endothelial growth factor receptor (VEGFR) [1]
VEGFR3 is the receptor for VEGF-D and VEGF-C and expected to play a role in lymphatic endothelium development [6]
Summary
Angiogenesis is an important physiologic process which involves formation of new blood vessels from already existing vasculature. It plays a vital role during development and wound healing and during disease pathology such as tumor growth and progression. Several stimulators are involved in the angiogenesis process including vascular endothelial growth factor (VEGF), which plays a crucial role in activating endothelial cells through binding to receptors on the cell surface called vascular endothelial growth factor receptor (VEGFR) [1]. There are four VEGF isoforms in mammals (VEGF-A,B,C,D) and the placental growth factor (PlGF) encoded by different but related genes [2]. Tahreisarveaviileawbled. isVcEuGssFess tahnedinthveoilrveremceepnttoorsf VhEavGeFsbeaennd timhepilricraetceedptionrsthine viral diseaptsheaetsihraonrpedhcyetsphitoeolropsgoyisnsoivbf ilmreaaltnhdyeirsoaefapsteheusetsaiecnddaipstephalesicepsa.otisToshinbissle.rTetvahibeerlwaep1deuiastnciucdsaFspeisgpultihcreaetii1nonsvuso.lmvTemambaelernitz1eoafcnoVdmEFGmiFgosunraenhd1uman virusseusmanmdartihzeeicrodmimveornsehummeacnhvainruissmes aonfdutphreeirgduilvaetrisoenmoefcVhaEnGisFmeoxfpurpersesgiuolna.tion of VEGF expression
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