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Review
. 2024 Jun 19:15:1392814.
doi: 10.3389/fmicb.2024.1392814. eCollection 2024.

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Yimin Wang #  1   2 , Caoyuan Ma #  1   2   3 , Shan Wang #  1   2 , Hongxia Wu  3 , Xuanqi Chen  1   2 , Jinyou Ma  1   2 , Lei Wang  1   2 , Hua-Ji Qiu  3 , Yuan Sun  1   2   3
Affiliations
Review

Advances in the immunoescape mechanisms exploited by alphaherpesviruses

Yimin Wang et al. Front Microbiol. .

Abstract

Alphaherpesviruses, categorized as viruses with linear DNA composed of two complementary strands, can potentially to induce diseases in both humans and animals as pathogens. Mature viral particles comprise of a core, capsid, tegument, and envelope. While herpesvirus infection can elicit robust immune and inflammatory reactions in the host, its persistence stems from its prolonged interaction with the host, fostering a diverse array of immunoescape mechanisms. In recent years, significant advancements have been achieved in comprehending the immunoescape tactics employed by alphaherpesviruses, including pseudorabies virus (PRV), herpes simplex virus (HSV), varicella-zoster virus (VZV), feline herpesvirus (FeHV), equine herpesvirus (EHV), and caprine herpesvirus type I (CpHV-1). Researchers have unveiled the intricate adaptive mechanisms existing between viruses and their natural hosts. This review endeavors to illuminate the research advancements concerning the immunoescape mechanisms of alphaherpesviruses by delineating the pertinent proteins and genes involved in virus immunity. It aims to furnish valuable insights for further research on related mechanisms and vaccine development, ultimately contributing to virus control and containment efforts.

Keywords: alphaherpesviruses; immune regulatory proteins; immunoescape; latency; signaling pathways.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
The process of PRV infection of neurons. 1. Virus surface proteins attach to the cell membrane. 2. The virus passes through the cytoplasm and reaches the nucleus 3. IE180 is activated by VP16 protein and expressed in the cytoplasm. 4. IE180 returns to the nucleus and activate RNA polymerase II. 5. Viral proteins are produced within the cytoplasm. 6. These proteins can promote viral DNA replication. 7. Viral DNA synthesis is considered a late stage in the PRV replication cycle. 8. Capsid protein is synthesized in the cytoplasm. 9. The protein is sent back to the nucleus and preliminarily packaged. 10. The fully assembled virus leaves the nucleus. 11. The virus enters the trans-Golgi apparatus by binding to the envelope and envelope proteins. 12. The mature virus is conveyed to the cellular surface.
Figure 2
Figure 2
The spread of PRV within the nervous system. The figures for this study can be found in the biorender (BioRender.com).
See this image and copyright information in PMC

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