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Orthoherpesviridae, previously named and more widely known as Herpesviridae, is a large family of that cause infections and certain diseases in animals, including humans. (2025). 9780838585290, McGraw Hill. ISBN 9780838585290 The members of this family are commonly known as herpesviruses. The family name is derived from the Greek word ( 'to creep'), referring to spreading cutaneous lesions, usually involving blisters, seen in flares of herpes simplex 1, herpes simplex 2 and herpes zoster (shingles). In 1971, the International Committee on the Taxonomy of Viruses (ICTV) established Herpesvirus as a genus with 23 viruses among four groups. Since then, the number of identified herpesviruses has grown to more than 100. Herpesviruses can cause both Virus latency and Lytic cycle infections.
Nine herpesvirus types are known to primarily infect humans, at least five of which are extremely widespread among most human populations, and which cause common diseases: herpes simplex 1 and 2 (HSV-1 and HSV-2, also known as HHV-1 and HHV-2; both of which can cause orolabial herpes and genital herpes), varicella zoster (VZV or HHV-3; the cause of chickenpox and herpes zoster), Epstein–Barr (EBV or HHV-4; implicated in several diseases, including mononucleosis and some cancers), and human cytomegalovirus (HCMV or HHV-5). More than 90% of adults have been infected with at least one of these, and a Virus latency of the virus remains in almost all humans who have been infected. In the United States, as many as 15% of adults between 35 and 72 years of age have been infected. National Center for Infectious Diseases Other human herpesviruses are human herpesvirus 6A and 6B (HHV-6A and HHV-6B) and human herpesvirus 7 (HHV-7), which are the etiological agents for Roseola, and HHV-8 (also known as KSHV) which is responsible for causing Kaposi's sarcoma. (2007). 9780470023860, John Wiley & Sons. ISBN 9780470023860 HHV here stands for "Human Herpesvirus".
In total, more than 130 herpesviruses are known, some of them from mammals, birds, fish, reptiles, amphibians, and molluscs. Among the animal herpesviruses are pseudorabies virus causing Aujeszky's disease in pigs, and bovine herpesvirus 1 causing bovine infectious rhinotracheitis and pustular vulvovaginitis.
A number of other herpesviruses were previously recognized as species but were abolished, so their exact taxonomic placement is uncertain. These viruses include: Chelonid alphaherpesvirus 6, Cercopithecine gammaherpesvirus 14, Equid gammaherpesvirus 7, Iguanid herpesvirus 2, Phocid gammaherpesvirus 2, and Saguinine gammaherpesvirus 1.
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Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.
During symptomatic infection, infected cells transcribe lytic cycle viral genes. In some host cells, a small number of viral genes termed HHV LAT (LAT) accumulate, instead. 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.
Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. When the virus enters a cell, the cellular immune response is to protect the cell. The cell does so by wrapping the viral DNA around histones and condensing it into chromatin, causing the virus to become dormant, or latent. If cells are unsuccessful and the chromatin is loosely bundled, the viral DNA is still accessible. The viral particles can turn on their genes and replicate using cellular machinery to reactivate, starting a lytic infection.
Reactivation of latent viruses has been implicated in a number of diseases (e.g. Herpes Zoster, pityriasis rosea). Following activation, transcription of viral genes transitions from LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. 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 and immunological findings such as reduced levels of natural killer cells.
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.
| Oral-fecal, aerosol |
| Contact |
| Urine, saliva |
| Aerosol |
| Sex, saliva |
| Sex, saliva |
| Respiratory contact |
| Sex, saliva |
| Aerosol |
| Aerosol |
| Sex, saliva |
| Saliva |
| Contact |
All the currently known bird and reptile species are alphaherpesviruses. Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to coevolve this is suggestive that the alphaherpesviruses may have been the earliest branch.
The time of origin of the genus Iltovirus has been estimated to be 200 mya while those of the mardivirus and simplex genera have been estimated to be between 150 and 100 mya.
It was found that cmvIL-10 functions through phosphorylation of the Stat3 protein. It was originally thought that this phosphorylation was a result of the JAK-STAT pathway. However, despite evidence that JAK does indeed phosphorylate Stat3, its inhibition has no significant influence on cytokine synthesis inhibition. Another protein, PI3K, was also found to phosphorylate Stat3. PI3K inhibition, unlike JAK inhibition, did have a significant impact on cytokine synthesis. The difference between PI3K and JAK in Stat3 phosphorylation is that PI3K phosphorylates Stat3 on the S727 residue whereas JAK phosphorylates Stat3 on the Y705 residue. This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis. In fact, when a PI3K inhibitor is added to cells, the cytokine synthesis levels are significantly restored. The fact that cytokine levels are not completely restored indicates there is another pathway activated by cmvIL-10 that is inhibiting cytokine system synthesis. The proposed mechanism is that cmvIL-10 activates PI3K which in turn activates AKT (Akt). PKB may then activate mTOR, which may target Stat3 for phosphorylation on the S727 residue.
| + Zoonotic herpesviruses |
| Very unusual, with only approximately 25 human cases reported. Untreated infection is often deadly; sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment. Symptom awareness and early treatment are important for laboratory workers facing exposure. Herpes-B Fact Sheet |
| Zoonotic infection more common in laboratory workers handling infected mice. ELISA tests show factor-of-four (x4) false positive results, due to antibody cross-reaction with other herpesviruses. |
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