Innate Immune Evasion of Alphaherpesvirus Tegument Proteins

Abstract

Alphaherpesviruses are a large family of highly successful human and animal DNA viruses that can establish lifelong latent infection in neurons. All alphaherpesviruses have a protein-rich layer called the tegument that, connects the DNA-containing capsid to the envelope. Tegument proteins have a variety of functions, playing roles in viral entry, secondary envelopment, viral capsid nuclear transportation during infection, and immune evasion. Recently, many studies have made substantial breakthroughs in characterizing the innate immune evasion of tegument proteins. A wide range of antiviral tegument protein factors that control incoming infectious pathogens are induced by the type I interferon (IFN) signaling pathway and other innate immune responses. In this review, we discuss the immune evasion of tegument proteins with a focus on herpes simplex virus type I.

The Role of VP16 in the Life Cycle of Alphaherpesviruses

“…Then, nucleocapsids can bind in an orderly manner to tegument proteins (mainly inner tegument proteins) and be transported through microtubules to trans-Golgi-derived vesicles that combine viral glycoproteins with outer tegument proteins, budding into vesicles via secondary envelopment to form complete virions. Eventually, the vesicles carry fully assembled virions to the plasma membrane for egress via the exocytosis pathway (Guo et al, 2010;Crump, 2018;Yang et al, 2019).…”

Alphaherpesvirus Major Tegument Protein VP22: Its Precise Function in the Viral Life Cycle

“…Many herpesvirus viral proteins can evade the innate immune response of the host ( Christensen et al, 2016 ; Liu et al, 2018 ; Yang et al, 2019 ; You et al, 2019 ). In addition to playing an important role in innate immune evasion, VP22 can also play a role in specific immune evasion ( Liu et al, 2016 ).…”

“…Twenty-six tegument proteins have been found in HSV-1 ( Loret et al, 2008 ; Kelly et al, 2009 ; Kukhanova et al, 2014 ). Tegument proteins play different roles during the viral life cycle, serving as structural components of the virion and functioning in transcriptional regulation, kinase activity, viral assembly, and immune evasion ( Owen et al, 2015 ; Wang Y. et al, 2018 ; Tobler et al, 2019 ; Yang et al, 2019 ); for example, the Us3 protein can regulate the expression of viral genes, affect the immune function of the host, affect the spread of the virus between host cells, resist host cell apoptosis, and disrupt the host cell cytoskeleton ( Van den Broeke et al, 2009 ; Chang et al, 2013 ; Grauwet et al, 2016 ).…”

Two nuclear localization signals regulate intracellular localization of the Duck enteritis virus UL13 protein

“…The target segment (UL13 left arm-FRT-Kan-FRT-UL14 right arm) was PCR-amplified using the ΔUL13&UL14 F F/R primers (Table 2). Then, the infectious clone DEV CHv-ΔUL13&UL14-G was generated by employing a recombinating system based on the genetic manipulation of the DEV CHv-G infectious clone [34][35][36][37]. Briefly, the pKD46 plasmid, which encodes the recombination genes exo, beta, and gam under the tight control of a ParaB promoter, was first introduced into E. coli DH10B containing the DEV CHv-G plasmid by electrophoretic transfer.…”