Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections

Abstract

The oncogenic and persistent Epstein Barr virus (EBV) is carried by more than 95% of the human adult population. While asymptomatic in most of these, EBV can cause a wide variety of malignancies of lymphoid or epithelial cell origin. Some of these are also associated with co-infections that either increase EBV-induced tumorigenesis or weaken its immune control. The respective pathogens include Kaposi-sarcoma-associated herpesvirus (KSHV), Plasmodium falciparum and human immunodeficiency virus (HIV). In this review, I will discuss the respective tumor entities and possible mechanisms by which co-infections increase the EBV-associated cancer burden. A better understanding of the underlying mechanisms could allow us to identify crucial features of EBV-associated malignancies and defects in their immune control. These could then be explored to develop therapies against the respective cancers by targeting EBV and/or the respective co-infections with pathogen-specific therapies or vaccinations.

Keywords

• Epstein Barr virus (EBV)
• Kaposi-sarcoma-associated herpesvirus (KSHV)
• malaria
• <i>Plasmodium falciparum</i>
• human immunodeficiency virus (HIV)
• human cytomegalovirus (HCMV)