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Herpesviruses replication is a “multi-step process”

February 1, 2019 0 Comment

Herpesviruses replication is a “multi-step process”. After the onset of infection, DNA is uncoated and transported to the nucleus of the host cell. Then transcription of “immediate-early genes” occurs, which encode for the regulatory proteins. Expression of “immediate-early gene” products is followed by the expression of proteins encoded by early and then late genes.(60)
Assembly of the viral core and capsid takes place within the nucleus. Followed by envelopment at the nuclear membrane and transport out of the nucleus through the endoplasmic reticulum and the “Golgi apparatus”. “Glycosylation” of the viral membrane occurs in the “Golgi apparatus”.(61)
Then transportation of mature virions to the outer membrane of the host cell inside vesicles. Release of “progeny virus” is accompanied by cell death. Replication for all herpesviruses is considered ineffective, with a high ratio of non-infectious to infectious viral particles.(62)
Herpesviruses have the ability to establish latent infection. Each virus within the family has the ability to establish latency in specific host cells, and the latent viral genome may be either “extra-chromosomal” or incorporated into host cell DNA.(63)
“Herpes simplex virus 1 and 2” and “varicella-zoster virus” all establish latency in the dorsal root ganglia. “Epstein-Barr virus” can sustain latency within B lymphocytes and salivary glands. “Cytomegalovirus”, “human herpesvirus 6 and 7”, “Kaposi’s sarcoma herpesvirus” and “B virus” have unknown sites of latency.(64)
Reactivation of latent virus may occur and enter a replicative cycle anytime. This is a well-recognized biologic phenomenon, but not clearly understood from a biochemical or genetic standpoint.(65)
Reactivation of latent herpes simplex virus have been reported to be associated with different stimuli including stress, menstruation, and exposure to ultraviolet light.(66)
Exactly how these factors interact at the level of the ganglia remains to be defined. Reactivation of herpesviruses may be clinically asymptomatic, or it may produce life-threatening disease.(67)

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