Abstract

Human cytomegalovirus (HCMV), a ubiquitous beta-herpesvirus, is able to establish lifelong latency after initial infection. Periodical reactivation occurs after immunosuppression, remaining a major cause of death in immunocompromised patients. HCMV has to reach a structural and functional balance with the host at its earliest entry. Virion-carried mediators are considered to play pivotal roles in viral adaptation into a new cellular environment upon entry. Additionally, one clear difference between primary infection and reactivation is the idea that virion-packaged factors are already formed such that those molecules can be used swiftly by the virus. In contrast, virion-carried mediators have to be transcribed and translated; thus, they are not readily available during reactivation. Hence, understanding virion-carried molecules helps to elucidate HCMV reactivation. In this article, the impact of virion-packaged molecules on viral structure, biological behavior, and viral life cycle will be reviewed.

Highlights

  • Human cytomegalovirus (HCMV), officially referred to as human herpesvirus 5 (HHV5), is one of nearly 100 known herpesviruses and is subclassified as a beta-herpesvirus

  • Seronegativity does not show a complete correlation with negativity for HCMV DNA in CD34+ hematopoietic progenitor cells (HPCs) (Khaiboullina et al, 2004)

  • The virus becomes latent in HPCs upon initial infection, the strategies used by HCMV to dampen immune response toward virion-delivered foreign molecules such as glycoproteins on envelope and tegument proteins remain to be understood

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Summary

Introduction

Human cytomegalovirus (HCMV), officially referred to as human herpesvirus 5 (HHV5), is one of nearly 100 known herpesviruses and is subclassified as a beta-herpesvirus. ­ Highly immunogenic and pp150 antigen can be detected by ELISA ­ Interact with capsomeres and triplex on capsid and directs translocation of nucleocapsid for further envelopment ­ Be involved in nuclear targeting, organization of assembly compartment, tegumentation and virion egress during late infection ­ Restricts viral IE gene expression

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