The human herpesviruses all share some common properties. One shared property is virus structure - all herpesviruses are composed of relatively large double stranded circular DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a lipid bilayer membrane called the envelope. This particle is known as the virion. Following binding of viral envelope protein to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, viral DNA undergoes limited replication and transcription of a small number of viral genes termed latent genes. In this fashion the virus can persist in the cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. Following activation, the virus switches on transcription of multiple additional non-latent genes termed lytic genes that lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as fever, headache, malaise, rash, etc.
"Epidemiology of cercopithecine herpesvirus 1 (B virus) infection and shedding in a large breeding cohort of rhesus macaques." J Infect Dis 167(2): 257-63.
"Herpesvirus simiae (B virus) antibody response and virus shedding in experimental primary infection of cynomolgus monkeys." Lab Anim Sci 41(4): 360-4.
"Herpesvirus simiae (B virus): replication of the virus and identification of viral polypeptides in infected cells." Arch Virol 93(3-4): 185-98.
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