Abstract
Alphaherpesviruses cause various diseases and establish life-long latent infections in humans and animals. These viruses encode multiple viral proteins and miRNAs to evade the host immune response, including both innate and adaptive immunity. Alphaherpesviruses evolved highly advanced immune evasion strategies to be able to replicate efficiently in vivo and produce latent infections with recurrent outbreaks. This review describes the immune evasion strategies of alphaherpesviruses, especially against cytotoxic host immune responses. Considering these strategies, it is important to evaluate whether the immune evasion mechanisms in cell cultures are applicable to viral propagation and pathogenicity in vivo. This review focuses on cytotoxic T lymphocytes (CTLs), natural killer cells (NK cells), and natural killer T cells (NKT cells), which are representative immune cells that directly damage virus-infected cells. Since these immune cells recognize the ligands expressed on their target cells via specific activating and/or inhibitory receptors, alphaherpesviruses make several ligands that may be targets for immune evasion. In addition, alphaherpesviruses suppress the infiltration of CTLs by downregulating the expression of chemokines at infection sites in vivo. Elucidation of the alphaherpesvirus immune evasion mechanisms is essential for the development of new antiviral therapies and vaccines.
Highlights
Herpesviridae is a large family of DNA viruses that cause various diseases in humans and animals
ICP47 directly interacts with the transporter associated with antigen processing (TAP) complex and blocks viral peptide binding to the TAP complex, thereby inhibiting viral antigen presentation by major histocompatibility complex (MHC) class I molecules to cytotoxic T lymphocytes (CTLs) in cell cultures (Figure 1A) [18,19]
UL49.5 in varicelloviruses (i.e., bovine herpes virus 1 (BHV-1), EHV-1/4 and pseudorabies virus (PRV)) inhibits the function of TAP by several different mechanisms, resulting in downregulation of MHC class I molecules at the cell surface (Figure 1B) [33,35,36,37,38], as follows
Summary
Herpesviridae is a large family of DNA viruses that cause various diseases in humans and animals. Viruses 2020, 12, 1354 equine herpesvirus 1 and 4 (EHV-1 and EHV-4), and bovine herpes virus 1 (BHV-1) belong to the alphaherpesvirus subfamily. Since herpesvirus infections are life-long, the virus must evade its host’s immune responses during latent infection to prevent it from being eliminated by its host [1]. Even in a recurrent infection, the virus needs to evade its host’s immune responses for efficient viral propagation and pathogenicity. NK cells express various activating and inhibitory receptors that control their functions, such as cytotoxicity Cellular stress, such as viral infection, can induce the expression of ligands that are recognized by NK cell activating receptors. NK cells express multiple types of inhibitory receptors that recognize ligands like MHC class I molecules. In this review we focus on the mechanisms used by alphaherpesvirus viral proteins and miRNAs to evade the cell-mediated immune response, those that evade the cell-mediated killing of infected cells
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
