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Human betaherpesvirus 7

Human betaherpesvirus 7 (HHV-7) is one of nine known members of the Herpesviridae family that infects humans. HHV-7 is a member of Betaherpesvirinae, a subfamily of the Herpesviridae that also includes HHV-6 and Cytomegalovirus (HHV-5 or HCMV).[2][3] HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to by their genus, Roseolovirus.[4] HHV-7 was first isolated in 1990 from CD4+ T cells taken from peripheral blood lymphocytes.[5]

Human betaherpesvirus 7
SpecialtyInfectious disease
Human betaherpesvirus 7
Virus classification
(unranked): Virus
Realm: Duplodnaviria
Kingdom: Heunggongvirae
Phylum: Peploviricota
Class: Herviviricetes
Order: Herpesvirales
Family: Orthoherpesviridae
Genus: Roseolovirus
Species:
Human betaherpesvirus 7
Synonyms[1]
  • Human herpesvirus 7

Signs and symptoms edit

Both HHV-6B and HHV-7, as well as other viruses, can cause a skin condition in infants known as exanthema subitum, although HHV-7 causes the disease less frequently than HHV-6B.[6] HHV-7 infection also leads to or is associated with a number of other symptoms, including acute febrile respiratory disease, fever, rash, vomiting, diarrhea, low lymphocyte counts,[7] and febrile seizures,[8] though most often no symptoms present at all.[9]

There are indications that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome (DIHS),[10] encephalopathy,[11] hemiconvulsion-hemiplegia-epilepsy syndrome,[12] hepatitis infection,[13] postinfectious myeloradiculoneuropathy,[14] pityriasis rosea,[15] and the reactivation of HHV-4, leading to "mononucleosis-like illness".[16] Drug reaction with eosinophilia and systemic symptoms (DRESS) is a specific type of DIHS that may be linked to HHV-7 as the condition may develop in response to herpesvirus antigens. In one study, 76% of the 40 examined patients with DRESS exhibited some reactivation of Epstein-Barr virus, HHV-6, or HHV-7. Additionally, HHV-7 is currently suspected as a causative agent of lichen planus. In one dermatologic study, 33 skin biopsies were performed and HHV-7 was found at higher rates in lichen planus lesions. Remission of lichen planus was also associated with lower levels of HHV-7.[17] HHV-7 was also detected in 79.3% of cervical tissue examined, indicating that sexual contact may be a route of transmission for HHV-7.[18]

Notably, HHV-7 and HHV-6 were detected in 56.3% of unspecified encephalopathy cases examined, with more HHV-7 positive cells in the gray matter of the frontal and temporal lobes HHV-7 is typically present in astrocytes and oligodendrocytes in the cerebral cortex, deep nuclei, and cerebellum.[19] HHV-7 infection, along with HSV1, VZV, and HHV6, was associated with increased risk of dementia.[20] However, further research is needed further elucidate the causative and correlative factors between HHV-7 and encephalopathy.[19]

Complications with HHV-7 infection has been shown to be a factor in a great variety of transplant types.[9] Specifically, HHV-7 infection has been linked to a reactivation of cytomegalovirus (CMV) infection in renal transplant patients and may be linked to graft-vs-host disease.[17]

Virology edit

Structure edit

A mature virus particle measures about 170 nanometres (1,700 Å) in diameter.[21]

The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller,[22] with a DNA genome of about 145,000 base pairs.[9] There are a number of key differences between the genome of HHV-7 and that of HHV-6, but the importance of them for viral DNA replication is not yet known.[9]

Additionally, the HHV-7 virion appears to share much structural similarity to the HHV-6 virion. Despite this, some morphological characteristics of the viruses differ.[21]

Cellular effects edit

HHV-7 resides mostly in CD4+ T cells,[23] albeit only in certain strains of them.[24][25][26] To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glycoproteins to enter CD4+ T cells.[27] Despite this, HHV-7 may be able to enter cells that do not express the CD46 receptor.[28] About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription,[29] which interferes with HIV-1 infection[30] but may reactivate HHV-6 infection.[31] It is however unclear exactly what effect HHV-7 has on HIV infection.[9]

There has been some inquiry into the relationship between HHV-7 and HIV-1 co-receptors CXCR4 and CCR5. During infection, HHV-7 causes a loss of CXCR4 in CD4+ T-cells in addition to lowering intracellular Ca2+ flux and chemotaxis in response to stroll cell-derived factor 1 (SDF-1). Additionally, a CXCR4 antagonist that was effective against HIV was shown to be ineffective at inhibiting HHV-7. This information indicates that CXCR4 and CCR5 are not essential receptor proteins for HHV-7 infection.[28]

The trademark indication of HHV-7 infection at the cellular level is the presence of aforementioned syncytia. It is thought that these cells form via polyploidization resulting from a dysregulation of cyclin dependent kinase cdc2 and cyclin B. Giant cells form when the cell cycle is disrupted and accumulate between the G2 and M phase.[28] However, syncytia formation is more complex than initially thought. Some research has shown that syncytia formation in betaherpesviruses can vary based on the type of envelop protein expressed by the virion as well as the particular type of cell that the virus is infecting.[32]

HHV-7 also notably activates IL-15 upon infection. Activation of IL-15 leads to an increased natural killer (NK) cell response. This is thought to be one of the immune system's main methods of responding to HHV-7 infection.[28]

HHV-7 also has a number of other effects on cells. Among these include membrane leaking, the presence of lytic syncytia,[33][34] occasional apoptosis,[35] the supporting of latent infection,[36] and increases and decreases in levels of certain cytokines.[37][38]

Entry edit

HHV-7, like many other herpesviruses, relies on glycoproteins for entry. Specifically, HHV-7 is known to encode glycoproteins B, H, and L, but not C or D. In terms of betaherpesvirus specifically, it is thought that gB, gH, and gL are required for infection.[32] Additionally, HHV-7 encodes a glycoprotein complex (gp82-105) that is unique to HHV-7 and HHV-6.[39]

Detection and treatment edit

In adults, the effects of HHV-7 separate from HHV-6 have not been well-researched.[2] One reason for this is because the detection of HHV-7 was at first difficult to do quickly, as the process for doing so involves a procedure that is difficult to do in commercial laboratories and because viral isolation and serological testing are long processes that do not lend themselves to finishing quickly. HHV-7 can be grown in various lymphocytes in vitro, but researchers have noted that the virus does not propagate well under laboratory conditions.[40] A process known as loop-mediated isothermal amplification (LAMP) has recently been applied to speed up detection of HHV-7, although a larger sample size of patients must be tested first to see if the test will still work across a broad range of subjects.[41] No reliable serological test has been developed yet for HHV-7 alone, but multiple are in the process of being developed.[9] The use of PCR assays to test for HHV-7 is also being explored.[9][42]

No HHV-7 infection-specific treatment exists.[9] While HHV-7 may not be linked to any specific diseases, some researchers emphasize that the virus is still clinically relevant as it causes significant complications in immunocompromised patients. Specific treatment options for HHV-6, 7, and 8 are currently in the early stages of development. Some research suggests that acyclovir and anti-CMV drugs such as cidofovir and foscarnet may have some therapeutic benefit in HHV-7 infection. Additionally, some experimental drugs, such as cyclotriazadisulfonamide, and 9-R-2-phosphonomethoxypropyladenine may be effective against HHV-7. There is a need for HHV-7 specific treatments, however, because broad-spectrum antivirals are typically toxic and thus unsuitable for prophylactic use.[17]

Epidemiology edit

Over 95% of adults have been infected and are immune to HHV-7,[43] and over three quarters of those were infected before the age of six.[44] Primary infection of HHV-7 among children generally occurs between the ages of 2 and 5, which means it occurs after primary infection of HHV-6.[45] A 2014 Washington University School of Medicine's analysis of 102 healthy adults sampled at as many as five major body habitats found that HHV-7 was present in 98% of them, especially in the mouth.[46] A 2017 study looking at the human blood virome in 8,240 humans between the ages of 2 months to 102 years found that 20.37% of them were positive for HHV-7.[47]

References edit

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Further reading edit

  • Arvin, Ann; Whitley, Richard (2007). "Part III.4 HHV-6A, 6B, and 7". Human herpesviruses : biology, therapy, and immunoprophylaxis. Cambridge: Cambridge University Press. ISBN 978-0-521-82714-0.
  • Caselli, E; Di Luca, D (2007). "Molecular Biology and Clinical Associations of Roseoloviruses Human Herpesvirus 6 and Human Herpesvirus 7". New Microbiologica. 30 (3): 173–187. PMID 17802896.
  • Dewhurst, S (2004). "Human Herpesvirus Type 6 and Human Herpesvirus Type 7 Infections of the Central Nervous System". Herpes: The Journal of the IHMF. 11 (Suppl 2): 105A–111A. PMID 15319097.
  • Kempf, W (2002). "Human Herpesvirus 7 in Dermatology: What Role Does It Play?". American Journal of Clinical Dermatology. 3 (5): 309–315. doi:10.2165/00128071-200203050-00002. PMID 12069636. S2CID 28402208.
  • De Araujo, T; Berman, B; Weinstein, A (2002). "Human Herpesviruses 6 and 7". Dermatologic Clinics. 20 (2): 301–306. doi:10.1016/S0733-8635(01)00008-0. PMID 12120443.
  • Jackson, MA; Sommerauer, JF (2002). "Human Herpesviruses 6 and 7". The Pediatric Infectious Disease Journal. 21 (6): 565–566. doi:10.1097/00006454-200206000-00016. PMID 12182383.
  • Clark, DA (2002). "Human Herpesvirus 6 and Human Herpesvirus 7: Emerging Pathogens in Transplant Patients". International Journal of Hematology. 76 (Suppl 2): 246–252. doi:10.1007/bf03165124. PMID 12430932. S2CID 27064788.

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Human betaherpesvirus 7 HHV 7 is one of nine known members of the Herpesviridae family that infects humans HHV 7 is a member of Betaherpesvirinae a subfamily of the Herpesviridae that also includes HHV 6 and Cytomegalovirus HHV 5 or HCMV 2 3 HHV 7 often acts together with HHV 6 and the viruses together are sometimes referred to by their genus Roseolovirus 4 HHV 7 was first isolated in 1990 from CD4 T cells taken from peripheral blood lymphocytes 5 Human betaherpesvirus 7SpecialtyInfectious disease Human betaherpesvirus 7 Virus classification unranked Virus Realm Duplodnaviria Kingdom Heunggongvirae Phylum Peploviricota Class Herviviricetes Order Herpesvirales Family Orthoherpesviridae Genus Roseolovirus Species Human betaherpesvirus 7 Synonyms 1 Human herpesvirus 7 Contents 1 Signs and symptoms 2 Virology 2 1 Structure 2 2 Cellular effects 2 3 Entry 3 Detection and treatment 4 Epidemiology 5 References 6 Further readingSigns and symptoms editBoth HHV 6B and HHV 7 as well as other viruses can cause a skin condition in infants known as exanthema subitum although HHV 7 causes the disease less frequently than HHV 6B 6 HHV 7 infection also leads to or is associated with a number of other symptoms including acute febrile respiratory disease fever rash vomiting diarrhea low lymphocyte counts 7 and febrile seizures 8 though most often no symptoms present at all 9 There are indications that HHV 7 can contribute to the development of drug induced hypersensitivity syndrome DIHS 10 encephalopathy 11 hemiconvulsion hemiplegia epilepsy syndrome 12 hepatitis infection 13 postinfectious myeloradiculoneuropathy 14 pityriasis rosea 15 and the reactivation of HHV 4 leading to mononucleosis like illness 16 Drug reaction with eosinophilia and systemic symptoms DRESS is a specific type of DIHS that may be linked to HHV 7 as the condition may develop in response to herpesvirus antigens In one study 76 of the 40 examined patients with DRESS exhibited some reactivation of Epstein Barr virus HHV 6 or HHV 7 Additionally HHV 7 is currently suspected as a causative agent of lichen planus In one dermatologic study 33 skin biopsies were performed and HHV 7 was found at higher rates in lichen planus lesions Remission of lichen planus was also associated with lower levels of HHV 7 17 HHV 7 was also detected in 79 3 of cervical tissue examined indicating that sexual contact may be a route of transmission for HHV 7 18 Notably HHV 7 and HHV 6 were detected in 56 3 of unspecified encephalopathy cases examined with more HHV 7 positive cells in the gray matter of the frontal and temporal lobes HHV 7 is typically present in astrocytes and oligodendrocytes in the cerebral cortex deep nuclei and cerebellum 19 HHV 7 infection along with HSV1 VZV and HHV6 was associated with increased risk of dementia 20 However further research is needed further elucidate the causative and correlative factors between HHV 7 and encephalopathy 19 Complications with HHV 7 infection has been shown to be a factor in a great variety of transplant types 9 Specifically HHV 7 infection has been linked to a reactivation of cytomegalovirus CMV infection in renal transplant patients and may be linked to graft vs host disease 17 Virology editStructure edit A mature virus particle measures about 170 nanometres 1 700 A in diameter 21 The genome of HHV 7 is very similar to that of HHV 6 although it is about 10 smaller 22 with a DNA genome of about 145 000 base pairs 9 There are a number of key differences between the genome of HHV 7 and that of HHV 6 but the importance of them for viral DNA replication is not yet known 9 Additionally the HHV 7 virion appears to share much structural similarity to the HHV 6 virion Despite this some morphological characteristics of the viruses differ 21 Cellular effects edit HHV 7 resides mostly in CD4 T cells 23 albeit only in certain strains of them 24 25 26 To enter CD4 T cells HHV 7 unlike HHV 6 uses CD4 and possibly some cell surface glycoproteins to enter CD4 T cells 27 Despite this HHV 7 may be able to enter cells that do not express the CD46 receptor 28 About a week after HHV 7 has infected a cell it begins to downregulate CD4 transcription 29 which interferes with HIV 1 infection 30 but may reactivate HHV 6 infection 31 It is however unclear exactly what effect HHV 7 has on HIV infection 9 There has been some inquiry into the relationship between HHV 7 and HIV 1 co receptors CXCR4 and CCR5 During infection HHV 7 causes a loss of CXCR4 in CD4 T cells in addition to lowering intracellular Ca2 flux and chemotaxis in response to stroll cell derived factor 1 SDF 1 Additionally a CXCR4 antagonist that was effective against HIV was shown to be ineffective at inhibiting HHV 7 This information indicates that CXCR4 and CCR5 are not essential receptor proteins for HHV 7 infection 28 The trademark indication of HHV 7 infection at the cellular level is the presence of aforementioned syncytia It is thought that these cells form via polyploidization resulting from a dysregulation of cyclin dependent kinase cdc2 and cyclin B Giant cells form when the cell cycle is disrupted and accumulate between the G2 and M phase 28 However syncytia formation is more complex than initially thought Some research has shown that syncytia formation in betaherpesviruses can vary based on the type of envelop protein expressed by the virion as well as the particular type of cell that the virus is infecting 32 HHV 7 also notably activates IL 15 upon infection Activation of IL 15 leads to an increased natural killer NK cell response This is thought to be one of the immune system s main methods of responding to HHV 7 infection 28 HHV 7 also has a number of other effects on cells Among these include membrane leaking the presence of lytic syncytia 33 34 occasional apoptosis 35 the supporting of latent infection 36 and increases and decreases in levels of certain cytokines 37 38 Entry edit HHV 7 like many other herpesviruses relies on glycoproteins for entry Specifically HHV 7 is known to encode glycoproteins B H and L but not C or D In terms of betaherpesvirus specifically it is thought that gB gH and gL are required for infection 32 Additionally HHV 7 encodes a glycoprotein complex gp82 105 that is unique to HHV 7 and HHV 6 39 Detection and treatment editThis section needs to be updated Please help update this article to reflect recent events or newly available information February 2022 In adults the effects of HHV 7 separate from HHV 6 have not been well researched 2 One reason for this is because the detection of HHV 7 was at first difficult to do quickly as the process for doing so involves a procedure that is difficult to do in commercial laboratories and because viral isolation and serological testing are long processes that do not lend themselves to finishing quickly HHV 7 can be grown in various lymphocytes in vitro but researchers have noted that the virus does not propagate well under laboratory conditions 40 A process known as loop mediated isothermal amplification LAMP has recently been applied to speed up detection of HHV 7 although a larger sample size of patients must be tested first to see if the test will still work across a broad range of subjects 41 No reliable serological test has been developed yet for HHV 7 alone but multiple are in the process of being developed 9 The use of PCR assays to test for HHV 7 is also being explored 9 42 No HHV 7 infection specific treatment exists 9 While HHV 7 may not be linked to any specific diseases some researchers emphasize that the virus is still clinically relevant as it causes significant complications in immunocompromised patients Specific treatment options for HHV 6 7 and 8 are currently in the early stages of development Some research suggests that acyclovir and anti CMV drugs such as cidofovir and foscarnet may have some therapeutic benefit in HHV 7 infection Additionally some experimental drugs such as cyclotriazadisulfonamide and 9 R 2 phosphonomethoxypropyladenine may be effective against HHV 7 There is a need for HHV 7 specific treatments however because broad spectrum antivirals are typically toxic and thus unsuitable for prophylactic use 17 Epidemiology editOver 95 of adults have been infected and are immune to HHV 7 43 and over three quarters of those were infected before the age of six 44 Primary infection of HHV 7 among children generally occurs between the ages of 2 and 5 which means it occurs after primary infection of HHV 6 45 A 2014 Washington University School of Medicine s analysis of 102 healthy adults sampled at as many as five major body habitats found that HHV 7 was present in 98 of them especially in the mouth 46 A 2017 study looking at the human blood virome in 8 240 humans between the ages of 2 months to 102 years found that 20 37 of them were positive for HHV 7 47 References edit Davison Andrew 27 January 2016 Rename species in the family Herpesviridae to incorporate a subfamily designation PDF International Committee on Taxonomy of Viruses ICTV Retrieved 13 March 2019 a b Other Herpesviruses HHV 6 HHV 7 HHV 8 HSV 1 and 2 VZV American Journal of Transplantation 4 Suppl 10 66 71 2004 doi 10 1111 j 1600 6135 2004 00697 x PMID 15504215 Widen B F Lowings J P Belak S Banks M August 1999 Development of a PCR system for porcine cytomegalovirus detection and determination of the putative partial sequence of its DNA polymerase gene Epidemiology and Infection 123 1 177 180 doi 10 1017 S0950268899002599 PMC 2810741 PMID 10487654 Ongradi JoZsef Kovesdi Valeria Kovats Eniko 2010 Az emberi 7 es herpeszvirus Orvosi Hetilap in Hungarian 151 16 645 51 doi 10 1556 OH 2010 28856 PMID 20353917 Frenkel N Schirmer EC Wyatt LS Katsafanas G Roffman E Danovich RM June CH 1990 Isolation of a new herpesvirus from human CD4 T cells Proceedings of the National Academy of Sciences of the United States of America 87 2 748 52 Bibcode 1990PNAS 87 748F doi 10 1073 pnas 87 2 748 PMC 53343 PMID 2153965 Cohen J 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of a Novel Heparin Binding Glycoprotein Encoded by Human Herpesvirus 7 Journal of Virology 74 10 4530 4540 doi 10 1128 JVI 74 10 4530 4540 2000 ISSN 0022 538X PMC 111973 PMID 10775589 Kempf Werner 2002 08 01 Human Herpesvirus 7 in Dermatology American Journal of Clinical Dermatology 3 5 309 315 doi 10 2165 00128071 200203050 00002 ISSN 1179 1888 PMID 12069636 S2CID 28402208 Yoshikawa Tetsushi Ihira Masaru Akimoto Shiho Usui Chie Miyake Fumi Suga Sadao Enomoto Yoshihiko Suzuki Ryota et al March 2004 Detection of Human Herpesvirus 7 DNA by Loop Mediated Isothermal Amplification Journal of Clinical Microbiology 42 3 1348 1352 doi 10 1128 JCM 42 3 1348 1352 2004 PMC 356854 PMID 15004116 Clark D A Kidd I M Collingham K E Tarlow M Ayeni T Riordan A Griffiths P D Emery V C Pillay D 1997 Diagnosis of primary human herpesvirus 6 and 7 infections in febrile infants by polymerase chain reaction Archives of Disease in Childhood 77 1 42 45 doi 10 1136 adc 77 1 42 PMC 1717251 PMID 9279150 Clark DA Freeland ML MacKie LK Jarrett RF Onions DE 1993 Prevalence of antibody to human herpesvirus 7 by age The Journal of Infectious Diseases 168 1 251 2 doi 10 1093 infdis 168 1 251 PMID 8390545 Cermelli C Fabio G Montorsi M Sabbatini AM Portolani M 1996 Prevalence of antibodies to human herpesviruses 6 and 7 in early infancy and age at primary infection New Microbiologica 19 1 1 8 PMID 8673847 Yoshikawa T 2003 Human Herpesvirus 6 and 7 Infections in Transplantation Pediatric Transplantation 7 1 11 17 doi 10 1034 j 1399 3046 2003 02094 x PMID 12581322 S2CID 32279697 Wylie Kristine M Mihindukulasuriya Kathie A Zhou Yanjiao Sodergren Erica Storch Gregory A Weinstock George M 2014 01 01 Metagenomic analysis of double stranded DNA viruses in healthy adults BMC Biology 12 71 doi 10 1186 s12915 014 0071 7 ISSN 1741 7007 PMC 4177058 PMID 25212266 Moustafa Ahmed Xie Chao Kirkness Ewen Biggs William Wong Emily Turpaz Yaron Bloom Kenneth Delwart Eric Nelson Karen E 2017 03 22 The blood DNA virome in 8 000 humans PLOS Pathogens 13 3 e1006292 doi 10 1371 journal ppat 1006292 ISSN 1553 7374 PMC 5378407 PMID 28328962 Further reading edit nbsp Wikispecies has information related to Human betaherpesvirus 7 Arvin Ann Whitley Richard 2007 Part III 4 HHV 6A 6B and 7 Human herpesviruses biology therapy and immunoprophylaxis Cambridge Cambridge University Press ISBN 978 0 521 82714 0 Caselli E Di Luca D 2007 Molecular Biology and Clinical Associations of Roseoloviruses Human Herpesvirus 6 and Human Herpesvirus 7 New Microbiologica 30 3 173 187 PMID 17802896 Dewhurst S 2004 Human Herpesvirus Type 6 and Human Herpesvirus Type 7 Infections of the Central Nervous System Herpes The Journal of the IHMF 11 Suppl 2 105A 111A PMID 15319097 Kempf W 2002 Human Herpesvirus 7 in Dermatology What Role Does It Play American Journal of Clinical Dermatology 3 5 309 315 doi 10 2165 00128071 200203050 00002 PMID 12069636 S2CID 28402208 De Araujo T Berman B Weinstein A 2002 Human Herpesviruses 6 and 7 Dermatologic Clinics 20 2 301 306 doi 10 1016 S0733 8635 01 00008 0 PMID 12120443 Jackson MA Sommerauer JF 2002 Human Herpesviruses 6 and 7 The Pediatric Infectious Disease Journal 21 6 565 566 doi 10 1097 00006454 200206000 00016 PMID 12182383 Clark DA 2002 Human Herpesvirus 6 and Human Herpesvirus 7 Emerging Pathogens in Transplant Patients International Journal of Hematology 76 Suppl 2 246 252 doi 10 1007 bf03165124 PMID 12430932 S2CID 27064788 Retrieved from https en wikipedia org w index php title Human betaherpesvirus 7 amp oldid 1188098236, wikipedia, wiki, book, books, library,

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