See text Orthoherpesviridae, previously named and more widely known as Herpesviridae, is a large family of DNA viruses that cause infections and certain diseases in animals, including humans.

The family has the following subfamilies and genera:[6] A number of other herpesviruses were previously recognized as species but were abolished, so their exact taxonomic placement is uncertain.

The structural components of a typical HSV virion are the Lipid bilayer envelope, Tegument, DNA, Glycoprotein spikes and Nucleocapsid.

The four-component Herpes simplex virion encompasses the double-stranded DNA genome into an icosahedral nucleocapsid.

These are gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL and gM.

They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation.

In some host cells, a small number of viral genes termed latency-associated transcript (LAT) accumulate, instead.

While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.

[citation needed] Chromatin dynamics regulate the transcription competency of entire herpes virus genomes.

The cell does so by wrapping the viral DNA around histones and condensing it into chromatin, causing the virus to become dormant, or latent.

The viral particles can turn on their genes and replicate using cellular machinery to reactivate, starting a lytic infection.

Clinically, lytic activation is often accompanied by emergence of nonspecific symptoms, such as low-grade fever, headache, sore throat, malaise, and rash, as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.

[citation needed] In animal models, local trauma and system stress have been found to induce reactivation of latent herpesvirus infection.

Cellular stressors like transient interruption of protein synthesis and hypoxia are also sufficient to induce viral reactivation.

Speciations within sublineages took place in the last 80 million years probably with a major component of cospeciation with host lineages.

Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting pro-inflammatory cytokine synthesis.

The cmvIL-10 protein has 27% identity with hIL-10 and only one conserved residue out of the nine amino acids that make up the functional site for cytokine synthesis inhibition on hIL-10.

This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis.

Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER).