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{{Short description|Family of DNA viruses}}
{{Use dmy dates|date=February 2024}}
{{Virusbox
| image = Herpesviridae EM PHIL 2171 lores.jpg
| taxon = Herpesviridae
| subdivision_ranks = Subfamilies and genera
| subdivision = See text
}}

'''''Herpesviridae''''' is a large [[family (biology)|family]] of [[DNA virus]]es that cause infections and certain diseases in animals, including humans.<ref name="Sherris">{{cite book |editor = Ryan KJ |editor2 = Ray CG |title = Sherris Medical Microbiology |edition = 4th |publisher = McGraw Hill |year = 2004 |isbn = 0-8385-8529-9 }}</ref><ref name="sobrino9">{{cite book |chapter-url=http://www.horizonpress.com/avir|author=Mettenleiter |year=2008 |chapter=Molecular Biology of Animal Herpesviruses |title=Animal Viruses: Molecular Biology |publisher=Caister Academic Press |website= www.horizonpress.com |isbn=978-1-904455-22-6 |display-authors=etal}}</ref><ref name="Sandri">{{cite book |veditors = Sandri-Goldin RM |title = Alpha Herpesviruses: Molecular and Cellular Biology |publisher = Caister Academic Press |year = 2006 |url=http://www.horizonpress.com/ahv |website = www.horizonpress.com |isbn = 978-1-904455-09-7}}</ref> The members of this family are also known as '''herpesviruses'''. The family name is derived from the Greek word [[wikt:ἕρπειν|ἕρπειν]] ({{transl|grc|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]]).<ref>{{cite journal | vauthors = Beswick TS |title=The Origin and the Use of the Word Herpes |journal=Med Hist |volume=6 |date=1962 |issue=3 |pages=214–232 |doi=10.1017/S002572730002737X |pmid=13868599 |pmc=1034725 }}</ref> In 1971, the [[International Committee on the Taxonomy of Viruses]] (ICTV) established ''Herpesvirus'' as a genus with 23 viruses among four groups.<ref>{{cite journal | vauthors = Wildy P |title=Classification and nomenclature of viruses. First report of the International Committee on Nomenclature of Viruses. |journal=Monographs in Virology |date=1971 |volume=5 |pages=1–81 |oclc=333944}}</ref> As of 2020, 115 species are recognized, all but one of which are in one of the three subfamilies.<ref name=ictv1 >{{cite web |title=Virus Taxonomy: 2020 Release |url=https://ictv.global/taxonomy |publisher=International Committee on Taxonomy of Viruses (ICTV) |date=March 2021 |access-date=10 May 2021}}</ref> Herpesviruses can cause both [[Virus latency|latent]] and [[Lytic cycle|lytic]] infections.

Nine herpesvirus types are known to primarily infect humans,<ref name="John" /> at least five of which are extremely widespread among most human populations, and which cause common diseases: [[herpes simplex virus|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|orolabial]] and [[genital herpes]]), [[varicella zoster virus|varicella zoster]] (or HHV-3; the cause of [[chickenpox]] and [[herpes zoster|shingles]]), [[Epstein–Barr virus|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|latent form]] of the virus remains in almost all humans who have been infected.<ref name="Peds09">{{cite journal | vauthors = Chayavichitsilp P, Buckwalter JV, Krakowski AC, Friedlander SF | title = Herpes simplex | journal = Pediatrics in Review | volume = 30 | issue = 4 | pages = 119–29; quiz 130 | date = April 2009 | pmid = 19339385 | doi = 10.1542/pir.30-4-119 | s2cid = 34735917 }}</ref><ref name="CDC – Epstein–Barr Virus and Infectious Mononucleosis">[https://www.cdc.gov/ncidod/diseases/ebv.htm In the United States, as many as 15% of adults between 35 and 72 years of age have been infected.] {{Webarchive|url=https://web.archive.org/web/20120420113839/http://www.cdc.gov/ncidod/diseases/ebv.htm |date=20 April 2012 }} National Center for Infectious Diseases</ref><ref>{{cite journal | vauthors = Staras SA, Dollard SC, Radford KW, Flanders WD, Pass RF, Cannon MJ | title = Seroprevalence of cytomegalovirus infection in the United States, 1988–1994 | journal = Clinical Infectious Diseases | volume = 43 | issue = 9 | pages = 1143–51 | date = November 2006 | pmid = 17029132 | doi = 10.1086/508173 | doi-access = free }}</ref> Other human herpesviruses are [[human herpesvirus 6|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-associated herpesvirus]].<ref name="John">{{cite book |title=Virology, Principles and Applications |publisher=John Wiley & Sons |isbn=978-0-470-02386-0 |author1=John Carter |author2=Venetia Saunders |date=15 August 2007 }}</ref> HHV here stands for "Human Herpesvirus".

In total, more than 130 herpesviruses are known,<ref>{{cite journal | vauthors = Brown JC, Newcomb WW | title = Herpesvirus capsid assembly: insights from structural analysis | journal = Current Opinion in Virology | volume = 1 | issue = 2 | pages = 142–9 | date = August 2011 | pmid = 21927635 | pmc = 3171831 | doi = 10.1016/j.coviro.2011.06.003 }}</ref> some of them from mammals, birds, fish, reptiles, amphibians, and molluscs.<ref name="John" /> Among the animal herpesviruses are [[pseudorabies virus]] causing [[Aujeszky's disease]] in pigs, and [[bovine herpesvirus 1]] causing [[bovine infectious rhinotracheitis]] and [[pustular vulvovaginitis]].

== Taxonomy ==
* Subfamily ''[[Alphaherpesvirinae]]''
** ''[[Iltovirus]]''
** ''[[Mardivirus]]''
** ''[[Scutavirus]]''
** ''[[Simplexvirus]]''
** ''[[Varicellovirus]]''
* Subfamily ''[[Betaherpesvirinae]]''
** ''[[Cytomegalovirus]]''
** ''[[Muromegalovirus]]''
** ''[[Proboscivirus]]''
** ''[[Quwivirus]]''
** ''[[Roseolovirus]]''
* Subfamily ''[[Gammaherpesvirinae]]''
** ''[[Bossavirus]]''
** ''[[Lymphocryptovirus]]''
** ''[[Macavirus]]''
** ''[[Manticavirus]]''
** ''[[Patagivirus]]''
** ''[[Percavirus]]''
** ''[[Rhadinovirus]]''

Additionally, the species ''[[Iguanid herpesvirus 2]]'' is currently unassigned to a genus and subfamily.<ref name=ictv1 />

See [[Herpesvirales#Taxonomy]] for information on taxonomic history, phylogenetic research, and the nomenclatural system.

== Structure ==
[[File:Herpesviridae virion.jpg|thumb|Schematic drawing of a ''Herpesviridae'' virion]]
All members of the ''Herpesviridae'' share a common structure; a relatively large, monopartite, double-stranded, linear [[DNA]] [[genome]] encoding 100–200 [[gene]]s encased within an [[icosahedron|icosahedral]] protein cage (with T=16 symmetry) called the [[capsid]], which is itself wrapped in a protein layer called the [[Viral tegument|tegument]] containing both viral proteins and viral mRNAs and a [[lipid bilayer]] membrane called the [[Envelope (biology)|envelope]]. This whole particle is known as a [[virion]].
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. There is tegument around. Tegument contains filaments, each 7&nbsp;nm wide. It is an amorphous layer with some structured regions. Finally, it is covered with a lipoprotein envelope. There are spikes made of glycoprotein protruding from each virion. These can expand the diameter of the virus to 225&nbsp;nm. The diameters of virions without spikes are around 186&nbsp;nm. There are at least two unglycosylated membrane proteins in the outer envelope of the virion. There are also 11 glycoproteins. These are gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL and gM. Tegument contains 26 proteins. They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation. The icosahedral nucleocapsid is similar to that of tailed bacteriophage in the order [[Caudovirales]]. This capsid has 161 capsomers consisting of 150 hexons and 11 pentons, as well as a portal complex that allows entry and exit of DNA into the capsid.<ref>Liu, Y., Jih, J., Dai, X. et al. Cryo-EM structures of herpes simplex virus type 1 portal vertex and packaged genome. Nature 570, 257–261 (2019). https://doi.org/10.1038/s41586-019-1248-6</ref><ref>Das, D., & Hong, J. (2019). Herpesvirus Polymerase Inhibitors. In Viral Polymerases (pp. 333–356). Elsevier. https://doi.org/10.1016/B978-0-12-815422-9.00012-7</ref>

== Life cycle ==
All herpesviruses are nuclear-replicating—the viral [[DNA]] is [[transcription (genetics)|transcribed]] to [[mRNA]] within the infected cell's [[nucleus (biology)|nucleus]].{{citation needed|date=September 2022}}

Infection is initiated when a viral particle contacts a cell with specific types of [[Transmembrane receptors|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 (genetics)|transcription]] of viral genes occurs.{{citation needed|date=September 2022}}

During symptomatic infection, infected cells transcribe [[lytic cycle|lytic]] viral genes. In some host cells, a small number of viral genes termed [[HHV LAT|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.{{citation needed|date=September 2022}}

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.<ref>{{cite journal | vauthors = Hu M, Depledge DP, Flores Cortes E, Breuer J, Schang LM | title = Chromatin dynamics and the transcriptional competence of HSV-1 genomes during lytic infections | journal = PLOS Pathogens | volume = 15 | issue = 11 | pages = e1008076 | date = November 2019 | pmid = 31725813 | pmc = 6855408 | doi = 10.1371/journal.ppat.1008076 | doi-access = free }}</ref>

Reactivation of latent viruses has been implicated in a number of diseases (e.g. [[Herpes Zoster|shingles]], [[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 symptom]]s, such as low-grade fever, headache, sore throat, [[malaise]], and rash, as well as clinical signs such as swollen or tender [[lymph node]]s and immunological findings such as reduced levels of [[natural killer cell]]s.{{citation needed|date=September 2022}}

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.<ref>{{cite journal | vauthors = Grinde B | title = Herpesviruses: latency and reactivation – viral strategies and host response | journal = Journal of Oral Microbiology | volume = 5 | issue = 1 | pages = 22766 | date = October 2013 | pmid = 24167660 | pmc = 3809354 | doi = 10.3402/jom.v5i0.22766 }}</ref>

{| class="wikitable sortable" style="text-align:center"
|-
! Genus !! Subfamily !! Host details !! Tissue tropism !! Entry details !! Release details !! Replication site !! Assembly site !! Transmission
|-
|''Iltovirus''|| α || Birds: galliform: psittacine||None||Cell receptor endocytosis||Budding||Nucleus||Nucleus||Oral-fecal, aerosol
|-
|''Proboscivirus''|| β ||Elephants||None||Glycoproteins||Budding||Nucleus||Nucleus||Contact
|-
|''Cytomegalovirus''|| β ||Humans; monkeys||Epithelial mucosa, hematopoietic (blood) lineage cells||Glycoproteins||Budding||Nucleus||Nucleus||Urine, saliva
|-
|''Mardivirus''|| α ||Chickens; turkeys; quail||None||Cell receptor endocytosis||Budding||Nucleus||Nucleus||Aerosol
|-
|''Rhadinovirus''|| γ ||Humans; mammals||B-lymphocytes||Glycoproteins||Budding||Nucleus||Nucleus||Sex, saliva
|-
|''Macavirus''|| γ ||Mammals||B-lymphocytes||Glycoproteins||Budding||Nucleus||Nucleus||Sex, saliva
|-
|''Roseolovirus''|| β ||Humans||T-cells; B-cells; NK-cell; monocytes; macrophages; epithelial||Glycoproteins||Budding||Nucleus||Nucleus||Respiratory contact
|-
|''Simplexvirus'' || α ||Humans; mammals||Epithelial mucosa||Cell receptor endocytosis||Budding||Nucleus||Nucleus||Sex, saliva
|-
|''Scutavirus''|| α ||Sea turtles||None||Cell receptor endocytosis||Budding||Nucleus||Nucleus||Aerosol
|-
|''Varicellovirus''|| α ||Mammals||Epithelial mucosa||Glycoproteins||Budding||Nucleus||Nucleus||Aerosol
|-
|''Percavirus''|| γ ||Mammals||B-lymphocytes||Glycoproteins||Budding||Nucleus||Nucleus||Sex, saliva
|-
|''Lymphocryptovirus''|| γ ||Humans; mammals||B-lymphocytes||Glycoproteins||Budding||Nucleus||Nucleus||Saliva
|-
|''Muromegalovirus''|| β ||Rodents||Salivary glands||Glycoproteins||Budding||Nucleus||Nucleus||Contact
|}

== Evolution ==
The three mammalian subfamilies – ''Alpha''-, ''Beta''- and ''Gamma''-''herpesviridae'' – arose approximately 180 to 220 [[Year#Abbreviations yr and ya|mya]].<ref name="McGeoch1995">{{cite journal | vauthors = McGeoch DJ, Cook S, Dolan A, Jamieson FE, Telford EA | title = Molecular phylogeny and evolutionary timescale for the family of mammalian herpesviruses | journal = Journal of Molecular Biology | volume = 247 | issue = 3 | pages = 443–58 | date = March 1995 | pmid = 7714900 | doi = 10.1006/jmbi.1995.0152 }}</ref> The major sublineages within these subfamilies were probably generated before the mammalian radiation of 80 to 60 mya. Speciations within sublineages took place in the last 80 million years probably with a major component of cospeciation with host lineages.{{citation needed|date=September 2022}}

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.{{citation needed|date=September 2022}}

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.<ref name="McGeoch2006">{{cite journal | vauthors = McGeoch DJ, Rixon FJ, Davison AJ | title = Topics in herpesvirus genomics and evolution | journal = Virus Research | volume = 117 | issue = 1 | pages = 90–104 | date = April 2006 | pmid = 16490275 | doi = 10.1016/j.virusres.2006.01.002 }}</ref>

== Immune system evasions ==
{{missing information|section|latency mechanisms beyond CMV, e.g. HSV LAT and ICP-47; whether there is a common mechanism in the family|date=November 2021}}
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-10) and another is by downregulation of the [[major histocompatibility complex]] II (MHC II) in infected cells.

=== cmvIL-10 ===
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. There is, however, much similarity in the functions of hIL-10 and cmvIL-10. Both have been shown to down regulate [[IFN-γ]], [[IL-1α]], [[GM-CSF]], [[Interleukin 6|IL-6]] and [[TNF-α]], which are all pro-inflammatory cytokines. They have also been shown to play a role in downregulating MHC I and MHC II and up regulating [[HLA-G]] (non-classical MHC I). These two events allow for immune evasion by suppressing the cell-mediated immune response and [[natural killer cell]] response, respectively. The similarities between hIL-10 and cmvIL-10 may be explained by the fact that hIL-10 and cmvIL-10 both use the same cell surface receptor, the hIL-10 receptor.  One difference in the function of hIL-10 and cmvIL-10 is that hIL-10 causes human peripheral blood mononuclear cells ([[PBMC]]) to both increase and decrease in proliferation whereas cmvIL-10 only causes a decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells.<ref>{{cite journal | vauthors = Spencer JV, Lockridge KM, Barry PA, Lin G, Tsang M, Penfold ME, Schall TJ | title = Potent immunosuppressive activities of cytomegalovirus-encoded interleukin-10 | journal = Journal of Virology | volume = 76 | issue = 3 | pages = 1285–92 | date = February 2002 | pmid = 11773404 | pmc = 135865 | doi = 10.1128/JVI.76.3.1285-1292.2002 }}</ref>

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|PKB]] (Akt). PKB may then activate [[mTOR]], which may target Stat3 for phosphorylation on the S727 residue.<ref>{{cite journal | vauthors = Spencer JV | title = The cytomegalovirus homolog of interleukin-10 requires phosphatidylinositol 3-kinase activity for inhibition of cytokine synthesis in monocytes | journal = Journal of Virology | volume = 81 | issue = 4 | pages = 2083–6 | date = February 2007 | pmid = 17121792 | pmc = 1797587 | doi = 10.1128/JVI.01655-06 | url = http://repository.usfca.edu/cgi/viewcontent.cgi?article=1015&context=biol_fac }}
</ref>

=== MHC downregulation ===
Another one of the many ways in which herpes viruses evade the immune system is by down regulation of [[MHC I]] and [[MHC II]]. This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the [[endoplasmic reticulum]] (ER). 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]]. The ER protein [[Transporter associated with antigen processing|TAP]] also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of the MHC and therefore the MHC does not reach the cell surface.<ref>{{cite journal | vauthors = Lin A, Xu H, Yan W | title = Modulation of HLA expression in human cytomegalovirus immune evasion | journal = Cellular & Molecular Immunology | volume = 4 | issue = 2 | pages = 91–8 | date = April 2007 | pmid = 17484802 }}</ref>

== Human herpesvirus types ==
Below are the nine distinct viruses in this family known to cause disease in humans.<ref>{{cite journal | vauthors = Adams MJ, Carstens EB | title = Ratification vote on taxonomic proposals to the International Committee on Taxonomy of Viruses (2012) | journal = Archives of Virology | volume = 157 | issue = 7 | pages = 1411–22 | date = July 2012 | pmid = 22481600 | doi = 10.1007/s00705-012-1299-6 | pmc = 7086667 | doi-access = free }}</ref><ref name="Baron">{{cite book | author = Whitley RJ | title =  Herpesviruses. ''in:'' Baron's Medical Microbiology| editor = Baron S| display-editors = etal| edition = 4th | publisher = Univ of Texas Medical Branch | year = 1996 | url = https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.chapter.3567 | isbn = 0-9631172-1-1 }}</ref><ref name="Elsevier">{{cite book |vauthors=Murray PR, Rosenthal KS, Pfaller MA | title = Medical Microbiology | edition = 5th | publisher = Elsevier Mosby | year = 2005 | isbn = 978-0-323-03303-9 }}</ref>

{| class = "wikitable" style = "float:left; font-size:100%; margin-left:15px width:65%"
|+'''Human herpesvirus (HHV) classification'''<ref name="Sherris"/><ref name="Baron"/>
|-
! Name !! Synonym !! Subfamily !! Primary Target Cell !! Syndrome !! Site of Latency !! Means of Spread
|-
| HHV‑1 || [[Herpes simplex virus]]-1 (HSV-1) || α (Alpha) || Mucoepithelial || [[Oral herpes|Oral]] and/or [[genital herpes]], [[herpetic gingivostomatitis]], [[pharyngitis]], [[eczema herpeticum]], [[herpetic whitlow]], [[herpes simplex keratitis]], [[erythema multiforme]], [[encephalitis]], as well as other [[herpes simplex]] infections|| [[Neuron]] (sensory ganglia) || Close contact (oral or [[sexually transmitted infection]])
|-
| HHV-2 || [[Herpes simplex virus]]-2 (HSV-2) || α || Mucoepithelial || Oral and/or [[genital herpes]], [[herpetic gingivostomatitis]], [[pharyngitis]], [[eczema herpeticum]], [[herpetic whitlow]], [[herpes simplex keratitis]], [[erythema multiforme]], [[Mollaret's meningitis]], as well as other herpes simplex infections || Neuron (sensory ganglia) || Close contact (oral or [[sexually transmitted infection]])
|-
| HHV-3 || [[Varicella zoster virus]] (VZV) || α || Mucoepithelial || [[Chickenpox]] and [[Herpes zoster|shingles]] || Neuron (sensory ganglia) || Respiratory and close contact (including [[sexually transmitted infection]])
|-
| HHV-4 || [[Epstein–Barr virus]] (EBV) ''Lymphocryptovirus'' || γ (Gamma) || [[B cell]]s and [[epithelial cell]]s || [[Epstein-Barr virus-associated lymphoproliferative diseases#Severe mosquito bite allergy|Severe mosquito bite allergy]], [[Epstein-Barr virus-associated lymphoproliferative diseases#Epstein-Barr virus-positive reactive lymphoid hyperplasia|Epstein-Barr virus-positive reactive lymphoid hyperplasia]], [[Infectious mononucleosis]], [[Burkitt's lymphoma]], [[Epstein-Barr virus-associated lymphoproliferative diseases#Epstein–Barr virus-positive Hodgkin lymphoma|Epstein–Barr virus-positive Hodgkin lymphoma]], [[extranodal NK/T cell lymphoma, nasal type]], [[Epstein-Barr virus-associated lymphoproliferative diseases#Epstein–Barr virus-associated aggressive NK cell leukemia|Epstein–Barr virus-associated aggressive NK cell leukemia]], [[Primary central nervous system lymphoma|CNS lymphoma]] in AIDS patients, [[Post-transplant lymphoproliferative disorder|post-transplant lymphoproliferative syndrome]] (PTLD), [[nasopharyngeal carcinoma]], HIV-associated [[hairy leukoplakia]], [[multiple sclerosis]]|| B cell ||  Close contact, transfusions, tissue transplant, and congenital
|-
| HHV-5 || ''[[Human betaherpesvirus 5|Cytomegalovirus]]'' (CMV) || β (Beta) || [[Monocyte]]s and [[epithelial cell]]s || [[Infectious mononucleosis]]-like syndrome,<ref name="Bottieau_2006">{{cite journal | vauthors = Bottieau E, Clerinx J, Van den Enden E, Van Esbroeck M, Colebunders R, Van Gompel A, Van den Ende J | title = Infectious mononucleosis-like syndromes in febrile travelers returning from the tropics | journal = Journal of Travel Medicine | volume = 13 | issue = 4 | pages = 191–7 | year = 2006 | pmid = 16884400 | doi = 10.1111/j.1708-8305.2006.00049.x | doi-access = free }}</ref> [[retinitis]] || Monocyte, and ? ||Saliva, urine, blood, breast milk
|-
| [[Human herpesvirus 6|HHV-6A and 6B]]|| rowspan="2" | ''[[Roseolovirus]]''|| β || [[T cell]]s and ? || ''Sixth disease'' ([[roseola infantum]] or ''exanthem subitum'') || T cells and ? || Respiratory and close contact?
|-
| [[Human herpesvirus 7|HHV-7]]|| β || T cells and ? || drug-induced hypersensitivity syndrome, encephalopathy, hemiconvulsion-hemiplegia-epilepsy syndrome, hepatitis infection, postinfectious myeloradiculoneuropathy, pityriasis rosea, and the reactivation of HHV-4 (EBV), leading to "mononucleosis-like illness" || T cells and ? || ?
|-
| HHV-8 || [[Kaposi's sarcoma-associated herpesvirus]]<br /> (KSHV), a type of ''[[Rhadinovirus]]'' || γ || Lymphocyte and other cells || [[Kaposi's sarcoma]], [[primary effusion lymphoma]], some types of multicentric [[Castleman's disease]] || B cell || Close contact (sexual), saliva?
|-
|}
{{Clear}}

=== Zoonotic herpesviruses ===
In addition to the herpesviruses considered [[Endemic (epidemiology)|endemic]] in humans, some viruses associated primarily with animals may infect humans.  These are [[Zoonosis|zoonotic]] infections:

{| class = "wikitable" style = "float:left; font-size:100%; margin-left:15px width:65%"
|+'''Zoonotic herpesviruses'''
|-
! Species !! Type !! Synonym !! Subfamily !! Human Pathophysiology
|-
| [[Macaque monkey]] || CeHV-1 || ''Cercopithecine herpesvirus 1'', ([[monkey B virus]]) || α || Very unusual, with only approximately 25 human cases reported.<ref name="PMID1313312"/>  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.<ref name="PMID1313312">{{cite journal | vauthors = Weigler BJ | title = Biology of B virus in macaque and human hosts: a review | journal = Clinical Infectious Diseases | volume = 14 | issue = 2 | pages = 555–67 | date = February 1992 | pmid = 1313312 | doi = 10.1093/clinids/14.2.555 }}</ref><ref name="Huff_2003">{{cite journal | vauthors = Huff JL, Barry PA | title = B-virus (Cercopithecine herpesvirus 1) infection in humans and macaques: potential for zoonotic disease | journal = Emerging Infectious Diseases | volume = 9 | issue = 2 | pages = 246–50 | date = February 2003 | pmid = 12603998 | pmc = 2901951 | doi = 10.3201/eid0902.020272 }}</ref>  Symptom awareness and early treatment are important for laboratory workers facing exposure.<ref name="wustl_factsheet_1999">[http://dcminfo.wustl.edu/occhealth/factsheet_herpesb.html Herpes-B Fact Sheet<!-- Bot generated title -->] {{webarchive|url=https://web.archive.org/web/20080106224228/http://dcminfo.wustl.edu/occhealth/factsheet_herpesb.html |date=6 January 2008 }}</ref>
|-
| Mouse || MuHV-4 || ''[[Murid herpesvirus 68]]'' (MHV-68) || γ || [[Zoonotic]] infection more common in laboratory workers handling infected mice.<ref name="PMID18197737"/><ref name="Wang">{{cite journal | vauthors = Wang Y, Tibbetts SA, Krug LT |title=Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68 |journal=Annual Review of Virology |date=29 September 2021 |volume=8 |issue=1 |pages=349–371|doi-access=free |doi=10.1146/annurev-virology-011921-082615 |pmid=34586873 |pmc=9153731 |issn=2327-056X}}</ref> ELISA tests show factor-of-four (x4) [[false positive]] results, due to antibody cross-reaction with other herpesviruses.<ref name="PMID18197737">{{cite journal | vauthors = Hricová M, Mistríková J | title = Murine gammaherpesvirus 68 serum antibodies in general human population | journal = Acta Virologica | volume = 51 | issue = 4 | pages = 283–7 | year = 2007 | pmid = 18197737 }}</ref>
|-
|}
{{Clear}}

== Animal herpesviruses ==
In [[animal virology]], the best known herpesviruses belong to the subfamily ''[[Alphaherpesvirinae]]''. Research on [[pseudorabies virus]] (PrV), the causative agent of [[Aujeszky's disease]] in pigs, has pioneered animal disease control with genetically modified vaccines. 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''.<ref name="sobrino9"/><ref name="Sandri"/>

== Research ==
{{Main|Herpes simplex research}}

Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. These include:{{cn|date=December 2024}}

{{div col|colwidth=18em}}
* [[Alzheimer's disease]]
* [[atherosclerosis]]
* [[cholangiocarcinoma]]
* [[chronic fatigue syndrome]]
* [[Crohn's disease]]{{cn|date=December 2024}}
* [[dysautonomia]]
* [[fibromyalgia]]
* [[Irritable bowel syndrome]]{{cn|date=December 2024}}
* [[labile hypertension]]
* [[lupus]]
* [[Ménière's disease]]
* [[multiple sclerosis]]
* [[pancreatic cancer]]
* [[pancreatitis]]
* [[pityriasis rosea]]
* [[Type II Diabetes]]
{{Div col end}}

== See also ==
* [[Acciptrid herpesvirus 1]]
* [[Agua Preta virus]], a potential herpesvirus

== References ==
{{Reflist|30em}}

== External links ==
{{Wikispecies|Herpesviridae}}
{{Commons category|Herpesviridae}}
* [https://web.archive.org/web/20150120190449/http://www.ictvonline.org/index.asp?bhcp=1 ICTV International Committee on Taxonomy of Viruses (official site)]
* [http://www.expasy.org/viralzone/all_by_species/176.html '''Viralzone''': Herpesviridae]
* [http://www.horizonpress.com/gateway/animal-viruses.html Animal viruses]
* [https://www.cdc.gov/ncidod/diseases/bvirus.pdf Article on Cercopithecine herpesvirus]
* [http://www.gsu.edu/bvirus National B Virus Resource Center]
* [http://www.aocd.org/skin/dermatologic_diseases/pityriasis_rosea.html Pityriasis Rosea overview]
* [https://www.wikigenes.org/e/art/e/61.html Herpes simplex: Host viral protein interactions.A database of Host/HSV-1 interactions] {{Webarchive|url=https://web.archive.org/web/20100812033023/https://www.wikigenes.org/e/art/e/61.html |date=12 August 2010 }}
* [http://www.viprbrc.org/brc/home.do?decorator=herpes Virus Pathogen Database and Analysis Resource (ViPR): Herpesviridae]

{{Herpesvirales}}
{{Diseases of the skin and appendages by morphology}}
{{Baltimore classification}}
{{Taxonbar|from=Q149348}}
{{Authority control}}

[[Category:Herpesviridae| ]]
[[Category:Animal virology]]
[[Category:Infectious causes of cancer]]
[[Category:Virus families]]
[[Category:Viral diseases]]

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