Abstract
The coevolution of viruses and their hosts led to the repeated emergence of cellular alert signals and viral strategies to counteract them. The herpesvirus family of viruses displays the most sophisticated repertoire of immune escape mechanisms enabling infected cells to evade immune recognition and thereby maintain infection. The herpesvirus family consists of nine viruses that are capable of infecting humans: herpes simplex virus 1 and 2 (HSV-1, HSV-2), varicella zoster virus (VZV), Epstein–Barr virus (EBV), human cytomegalovirus (HCMV), roseoloviruses (HHV-6A, HHV-6B, and HHV-7), and Kaposi’s-sarcoma-associated herpesvirus (KSHV). Most of these viruses are highly prevalent and infect a vast majority of the human population worldwide. Notably, research over the past 15 years has revealed that cellular ligands for the activating receptor natural-killer group 2, member D (NKG2D)—which is primarily expressed on natural killer (NK) cells—are common targets suppressed during viral infection, i.e., their surface expression is reduced in virtually all lytic herpesvirus infections by diverse mechanisms. Here, we review the viral mechanisms by which all herpesviruses known to date to downmodulate the expression of the NKG2D ligands. Also, in light of recent findings, we speculate about the importance of the emergence of eight different NKG2D ligands in humans and further allelic diversification during host and virus coevolution.
Highlights
Faculty of Medicine, The Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem, Israel
The herpesvirus family consists of nine viruses that are capable of infecting humans: herpes simplex virus 1 and 2 (HSV-1, HSV-2), varicella zoster virus (VZV), Epstein–Barr virus (EBV), human cytomegalovirus (HCMV), roseoloviruses (HHV-6A, HHV-6B, and HHV-7), and Kaposi’ssarcoma-associated herpesvirus (KSHV)
Research over the past 15 years has revealed that cellular ligands for the activating receptor natural-killer group 2, member D (NKG2D)—which is primarily expressed on natural killer (NK) cells— are common targets suppressed during viral infection, i.e., their surface expression is reduced in virtually all lytic herpesvirus infections by diverse mechanisms
Summary
Nine different herpesviruses capable of infecting humans have been identified: HSV-1, HSV-2, varicella zoster virus (VZV), Epstein–Barr virus (EBV), human cytomegalovirus (HCMV), HHV-6A, HHV-6B, HHV-7, and Kaposi’s-sarcoma-associated herpesvirus (KSHV) [2]. Despite their different life cycle and growth properties, cellular tropisms and they cause different diseases, all herpesviruses share common features. Research over the past few years revealed that all herpesviruses use common strategies during primary infection, reactivation, and sometimes even during latency, in order to evade the immune surveillance during the different phases of herpesvirus life cycle. Since both MICA (except the allele MICA*008) and MICB are transmembrane proteins and were not affected by the miR-H8 overexpression, MICA
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