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{ITEM-100%-1-2}TEM micrograph of a herpes simplex virus. Bornaviridae Filoviridae Nyamiviridae Paramyxoviridae Rhabdoviridae. It oscars online also be sexually transmitted, including contact with saliva, such as kissing and mouth-to-genital contact oral sex. The late proteins form the capsid and the receptors on the surface of the virus. Another protein, PI3Kwas also found to phosphorylate Stat3. Ateline herpesvirus 1 Bovine herpesvirus 2 Cercopithecine herpesvirus 2 Human herpesvirus 1 Human herpesvirus 2 Leporid herpesvirus 4 Macacine herpesvirus 1 Macropodid herpesvirus 1 Macropodid herpesvirus 2 Papiine herpesvirus 2 Saimiriine herpesvirus 1. From Lotto gewinnen wahrscheinlichkeit, the free encyclopedia. When HSV particles are exposed to doses of a DNA damaging agent that would be lethal in single infections, mega joker are then allowed to undergo multiple infection i. Baron S; et al. The family name is derived from the Scharner word herpein "to creep"referring to spreading cutaneous lesions, usually involving blisters, seen in flares of herpes simplex 1, herpes simplex 2 and herpes zoster shingles [4]. Both viruses may also be transmitted vertically during childbirth. The MHC cannot reach the cell surface and therefore cannot activate the T cell response.{/ITEM}

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By maintaining the host cells, LAT expression preserves a reservoir of the virus, which allows subsequent, usually symptomatic, periodic recurrences or "outbreaks" characteristic of nonlatency.

Whether or not recurrences are symptomatic, viral shedding occurs to infect a new host. A protein found in neurons may bind to herpes virus DNA and regulate latency.

When bound to the viral DNA elements, histone deacetylation occurs atop the ICP4 gene sequence to prevent initiation of transcription from this gene, thereby preventing transcription of other viral genes involved in the lytic cycle.

The herpes simplex 1 genomes can be classified into six clades. This suggests that the virus may have originated in East Africa.

Herpes simplex 2 genomes can be divided into two groups: However, most of the mutations occur in the thymidine kinase gene rather than the DNA polymerase gene.

Another analysis has estimated the mutation rate in the herpes simplex 1 genome to be 1. The herpes viruses establish lifelong infections thus cannot be eradicated from the body.

Treatment usually involves general-purpose antiviral drugs that interfere with viral replication, reduce the physical severity of outbreak-associated lesions, and lower the chance of transmission to others.

Studies of vulnerable patient populations have indicated that daily use of antivirals such as aciclovir [47] and valaciclovir can reduce reactivation rates.

A retrospective study from Taiwan on 33, patients found that being infected with herpes simplex virus increased the risk of dementia 2. However, HSV-infected patients who were receiving anti-herpetic medications acyclovir, famciclovir, ganciclovir, idoxuridine, penciclovir, tromantadine, valaciclovir, or valganciclovir showed no elevated risk of dementia compared to patients uninfected with HSV.

Multiplicity reactivation MR is the process by which viral genomes containing inactivating damage interact within an infected cell to form a viable viral genome.

MR was originally discovered with the bacterial virus bacteriophage T4, but was subsequently also found with pathogenic viruses including influenza virus, HIV-1, adenovirus simian virus 40, vaccinia virus, reovirus, poliovirus and herpes simplex virus.

When HSV particles are exposed to doses of a DNA damaging agent that would be lethal in single infections, but are then allowed to undergo multiple infection i.

HSV-1, upon infecting host cells, induces inflammation and oxidative stress. Modified Herpes simplex virus is considered as a potential therapy for cancer and has been extensively clinically tested to assess its oncolytic cancer killing ability.

Herpes simplex virus is also used as a transneuronal tracer defining connections among neurons by virtue of traversing synapses. However, it prevents atherosclerosis which histologically mirrors atherosclerosis in humans in target animals vaccinated.

From Wikipedia, the free encyclopedia. This article is about the virus. For information about the disease caused by the virus, see Herpes simplex.

This article is about the human viruses. For for the genus of animalian simplex viruses, see Simplexvirus. Sherris Medical Microbiology 4th ed.

Retrieved September 22, Genital herpes is common in the United States. More than one out of every six people aged 14 to 49 years have genital herpes.

Infectious Diseases in Obstetrics and Gynecology. J R Soc Interface. Annual Review of Medicine. New England Journal of Medicine. Cellular and viral mediators of herpes simplex virus entry".

Mol Biol Evol doi: PLoS One 6 7: Retrieved 30 October Infection, Genetics and Evolution. Role of Herpesvirus in Artherogenesis. Viral cutaneous conditions, including viral exanthema B00—B09 , — Herpes simplex Herpetic whitlow Herpes gladiatorum Herpes simplex keratitis Herpetic sycosis Neonatal herpes simplex Herpes genitalis Herpes labialis Eczema herpeticum Herpetiform esophagitis.

Chickenpox Herpes zoster Herpes zoster oticus Ophthalmic zoster Disseminated herpes zoster Zoster-associated pain Modified varicella-like syndrome.

Parvovirus B19 Erythema infectiosum Reticulocytopenia Papular purpuric gloves and socks syndrome. Merkel cell polyomavirus Merkel cell carcinoma.

Rubella virus Rubella Congenital rubella syndrome "German measles" Alphavirus infection Chikungunya fever. Dinodnavirus Pithovirus Pandoravirus nonenveloped: Adenoviridae Papillomaviridae Papovaviridae obsolete Polyomaviridae genera: Arteriviridae Coronaviridae Mesoniviridae Roniviridae.

Comoviridae obsolete Dicistroviridae Iflaviridae Marnaviridae Picornaviridae Secoviridae Sequiviridae obsolete genera: Alphaflexiviridae Betaflexiviridae Gammaflexiviridae Tymoviridae.

Bornaviridae Filoviridae Nyamiviridae Paramyxoviridae Rhabdoviridae. Arenaviridae Ophioviridae Orthomyxoviridae genera: Retrieved from " https: Simplexviruses Sexually transmitted diseases and infections.

Views Read Edit View history. In other projects Wikimedia Commons. This page was last edited on 1 February , at By using this site, you agree to the Terms of Use and Privacy Policy.

TEM micrograph of a herpes simplex virus. Ribonucleotide reductase large subunit. Tegument protein; virion host shutoff [29]. Latent , recurring infections are typical of this group of viruses, though the family name does not refer to latency.

At least five species of the Herpesviridae — HSV-1 and HSV-2 both of which can cause orolabial herpes and genital herpes , varicella zoster virus the cause of chickenpox and shingles , Epstein—Barr virus implicated in several diseases, including mononucleosis and some cancers , and cytomegalovirus — are extremely widespread among humans.

Nine herpesvirus types are known to infect humans: Herpesviruses all share a common structure— relatively large, double-stranded, linear DNA genomes encoding genes encased within an icosahedral protein cage called the capsid , which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a lipid bilayer membrane called the envelope.

This whole particle is known as a virion. 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 viral genes.

In some host cells, a small number of viral genes termed latency-associated transcript 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.

Reactivation of latent viruses has been implicated in a number of diseases e. 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 lymph nodes and immunological findings such as reduced levels of natural killer cells.

The herpesvirus was first isolated from the blue wildebeest in by veterinary scientist Walter Plowright. This genus consisted of 23 viruses and 4 groups of viruses.

Because of possible confusion with viruses derived from reptiles this name was changed in the third report in to Herpesviridae. In this report the family Herpesviridae was divided into 3 subfamilies Alphaherpesvirinae , Betaherpesvirinae and Gammaherpesvirinae and 5 unnamed genera: In the family Herpesviridae was elevated to the order Herpesvirales.

This elevation was necessitated by the discovery that the herpes viruses of fish and molluscs were only distantly related to those of birds and mammals.

Two new families were created — the family Alloherpesviridae which incorporates bony fish and frog viruses and the family Malacoherpesviridae which contains those of molluscs.

This order currently has 3 families, 3 subfamilies plus 1 unassigned, 17 genera, 90 species and plus 48 as yet unassigned viruses. The system of naming herpes viruses was originated in and has been elaborated considerably since.

The recommended naming system specified that each herpes virus should be named after the taxon family or subfamily to which its primary natural host belongs.

The subfamily name is used for viruses from members of the family Bovidae or from primates the virus name ending in —ine, e.

Human herpes viruses have been treated as an exception human rather than hominid. Following the host-derived term, the word herpes virus is added, followed by an Arabic numeral 1,2,3, These last two additions bear no implied meaning about taxonomic or biological properties of the virus.

Some exceptions to this system exist. Epstein—Barr virus are so widely used that it is impractical to attempt to insist on their replacement.

This has led to a dual nomenclature in the literature for some herpes viruses. All herpes viruses described since this system was adopted have been named in accordance with it.

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

Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion.

Herpesviruses have many different ways of evading the immune system. One such way is by encoding a protein mimicking human interleukin 10 hIL and another is by downregulation of the major histocompatibility complex II MHC II in infected cells.

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

There is, however, much similarity in the functions of hIL and cmvIL These two events allow for immune evasion by suppressing the cell-mediated immune response and natural killer cell response, respectively.

This indicates that cmvIL may lack the stimulatory effects that hIL has on these cells. It was found that cmvIL functions through phosphorylation of the Stat3 protein.

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. 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 that is inhibiting cytokine system synthesis.

This is observed in almost every human herpesvirus. As discussed above, one way is by a viral chemokine homolog such as IL The MHC cannot reach the cell surface and therefore cannot activate the T cell response.

The MHCs can also be targeted for destruction in the proteasome or lysosome. This prevents the natural killer cell response.

Below are the distinct viruses in this family known to cause disease in humans. In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans.

These are zoonotic infections:. In animal virology , the best known herpesviruses belong to the subfamily Alphaherpesvirinae.

PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unraveling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1 , the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis , is analyzed to elucidate molecular mechanisms of latency.

The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.

Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. From Wikipedia, the free encyclopedia.

Herpesviridae Virus classification unranked: Gammaherpesvirinae Lymphocryptovirus Macavirus Percavirus Rhadinovirus Herpesviridae is a large family of DNA viruses that cause infections and certain diseases in animals, including humans.

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