Abstract
In the process of infecting the host, alphaherpesviruses have derived a series of adaptation and survival strategies, such as latent infection, autophagy and immune evasion, to survive in the host environment. Infected cell protein 22 (ICP22) or its homologue immediate early protein 63 (IE63) is a posttranslationally modified multifunctional viral regulatory protein encoded by all alphaherpesviruses. In addition to playing an important role in the efficient use of host cell RNA polymerase II, it also plays an important role in the defense process of the virus overcoming the host immune system. These two effects of ICP22/IE63 are important survival strategies for alphaherpesviruses. In this review, we summarize the complex mechanism by which the ICP22 protein regulates the transcription of alphaherpesviruses and their host genes and the mechanism by which ICP22/IE63 participates in immune escape. Reviewing these mechanisms will also help us understand the pathogenesis of alphaherpesvirus infections and provide new strategies to combat these viral infections.
Highlights
Herpesviruses are a type of linear double-stranded DNA virus with the same morphology and capsule
We summarize the complex mechanism by which the Infected cell protein 22 (ICP22) protein regulates the transcription of alphaherpesviruses and their host genes and the mechanism by which ICP22/immediate early protein 63 (IE63) participates in immune escape
After HSV-1 ICP22 is phosphorylated by the viral UL13 protein kinase, it participates in changing the phosphorylation status of polymerase II (Pol II), thereby promoting the transcriptional expression of late genes [16]; the transcriptional inhibition region of varicella zoster virus (VZV) IE63 is located in the carboxy terminal region (210–278 aa), where CDK1mediated phosphorylation of VZV IE63 Ser-224 and Thr-222 is essential to inhibit the basic activity of viral gene promoters, indicating that phosphorylation of IE63 is necessary for its suppressive properties [17,18,19]
Summary
Herpesviruses are a type of linear double-stranded DNA virus with the same morphology and capsule. It has been found that it plays an important role in evading the host immune response. The important role played by ICP22/IE63 in transcriptional regulation and defense against host immunity has promoted the survival of aHV. We describe the recent role of the ICP22/IE63 protein in viral and host gene transcription and its role in evading the host immune response. These effects are important strategies for the survival of a-HV in vivo. Any drug that interferes with these steps may decrease viral survival, which will help develop new antiviral drugs and vaccines
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