VEGF Upregulation in Viral Infections and Its Possible Therapeutic Implications

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.

Keywords

• angiogenesis
• vascular endothelial growth factor (VEGF)
• vascular endothelial growth factor receptor (VEGFR)
• Epstein-Barr virus (EBV)
• Kaposi’s sarcoma herpesvirus (KSHV)
• Hepatitis C Viruses (HCV)
• Hepatitis B Viruses (HBV)
• Herpes Simplex Virus (HSV)
• Hantavirus
• Dengue fever virus
• therapeutics