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
Summary
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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