The human herpes viruses all share some common properties. One shared
property is virus structure.
All herpes viruses are composed of relatively large, double-stranded,
circular DNA genomes, encoding 100-200 genes. They are encased within an icosahedral protein cage, called the
capsid. It is wrapped in a lipid, bi-layer 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. This allows 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. These are termed latent genes.
In this fashion, the virus persists 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. These are termed lytic genes. They 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. These include fever, headache,
malaise, and rash.
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