Human herpesvirus 7

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Human herpesvirus 7
Classification and external resources
ICD-9-CM 058.12
DiseasesDB 5863
MeSH D016199
Human herpesvirus 7
Virus classification
Group: Group I (dsDNA)
Order: Herpesvirales
Family: Herpesviridae
Subfamily: Betaherpesvirinae
Genus: Roseolovirus
Species

Human herpesvirus 7 (HHV-7)

Human herpesvirus 7 (HHV-7) is one of nine known members of the Herpesviridae family that infects humans. HHV-7 is a member of Betaherpesviridae, a subfamily of the Herpesviridae that also includes HHV-6 and Cytomegalovirus (HHV-5 or HCMV).[1][2] HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to by their genus, Roseolovirus.[3] HHV-7 was first isolated in 1990 from CD4+ T cells taken from peripheral blood lymphocytes.[4]

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.[5] 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,[6] and febrile seizures,[7] though most often no symptoms present at all.[8]

There are indications that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome,[9] encephalopathy,[10] hemiconvulsion-hemiplegia-epilepsy syndrome,[11] hepatitis infection,[12] postinfectious myeloradiculoneuropathy,[13] pityriasis rosea,[14] and the reactivation of HHV-4, leading to "mononucleosis-like illness".[15]

Complications with HHV-7 infection has been shown to be a factor in a great variety of transplant types.[8]

Virology[edit]

Structure[edit]

A mature virus particle measures about 170 nanometres (1,700 Å) in diameter.[16]

The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller,[17] with a DNA genome of about 145,000 base pairs.[8] 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.[8]

Cellular effects[edit]

HHV-7 resides mostly in CD4+ T cells,[18] albeit only in certain strains of them.[19][20][21] To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glyoproteins to enter CD4+ T cells.[22] About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription,[23] which interferes with HIV-1 infection[24] but may reactivate HHV-6 infection.[25] It is however unclear exactly what effect HHV-7 has on HIV infection.[8]

HHV-7 also has a number of other effects on cells. Among these include membrane leaking, the presence of lityic syncytia,[26][27] occasional apoptosis,[28] the supporting of latent infection,[29] and increases and decreases in levels of certain cytokines.[30][31]

Detection and treatment[edit]

In adults, the effects of HHV-7 separate from HHV-6 have not been well-researched.[1] 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. A process known as loop-mediated isothermal amplification (LAMP) has recently been developed 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.[32] No reliable serological test has been developed yet for HHV-7 alone, but multiple are in the process of being developed.[8] The use of PCR assays to test for HHV-7 is also being explored.[8][33]

No treatment for HHV-7 infection exists, but no clinical situation where such treatment would be useful has yet been discovered.[8]

Epidemiological[edit]

Over 95% of adults have been infected and are immune to HHV-7,[34] and over three quarters of those were infected before the age of six.[35] 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.[36]

References[edit]

  1. ^ a b "Other Herpesviruses: HHV-6, HHV-7, HHV-8, HSV-1 and -2, VZV". American Journal of Transplantation. Blackwell Munksgaard. 4 Suppl 10: 66–71. 2004. doi:10.1111/j.1600-6135.2004.00697.x. PMID 15504215. 
  2. ^ 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. Cambridge University Press. 123 (1): 177–180. doi:10.1017/S0950268899002599. PMC 2810741free to read. PMID 10487654. 
  3. ^ Ongrádi, JóZsef; Kövesdi, Valéria; Kováts, Enikő (2010). "Az emberi 7-es herpeszvírus". Orvosi Hetilap (in Hungarian). 151 (16): 645–51. doi:10.1556/OH.2010.28856. PMID 20353917. 
  4. ^ 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 53343free to read. PMID 2153965. 
  5. ^ Cohen, J. I.; Fahle, G.; Kemp, M. A.; Apakupakul, K.; Margolis, T. P. (2010). "Human Herpesvirus 6-A, 6-B and 7 in Vitreous Fluid Samples". Journal of Medical Virology. 82 (6): 996–9. doi:10.1002/jmv.21751. PMC 2938775free to read. PMID 20419813. 
  6. ^ Suga, S; Yoshikawa, T; Nagai, T; Asano, Y (1997). "Clinical features and virological findings in children with primary human herpesvirus 7 infection". Pediatrics. 99 (3): E4. doi:10.1542/peds.99.3.e4. PMID 9099769. 
  7. ^ Clark, DA; Kidd, IM; Collingham, KE; Tarlow, M; Ayeni, T; Riordan, A; Griffiths, PD; Emery, VC; 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): 42–5. doi:10.1136/adc.77.1.42. PMC 1717251free to read. PMID 9279150. 
  8. ^ a b c d e f g h Tremblay, Cecile (January 2, 2008). Hirsch, Martin S; McGovern, Barbara H, eds. "Human herpesvirus 7 infection". UpToDate. 
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  12. ^ Hashida, T; Komura, E; Yoshida, M; Otsuka, T; Hibi, S; Imashuku, S; Imashuku, S; Ishizaki, T; et al. (1995). "Hepatitis in Association With Human Herpesvirus-7 Infection". Pediatrics. 96 (4 Pt 1): 783–785. PMID 7567349. 
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  14. ^ Chuh, A; Chan, H; Zawar, V (2004). "Pityriasis rosea--evidence for and against an infectious aetiology". Epidemiology and Infection. 132 (3): 381–390. doi:10.1017/S0950268804002304. PMC 2870116free to read. PMID 15188706. 
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  18. ^ Katsafanas, GC; Schirmer, EC; Wyatt, LS; Frenkel, N (1996). "In vitro activation of human herpesviruses 6 and 7 from latency" (PDF). Proceedings of the National Academy of Sciences of the United States of America. 93 (18): 9788–92. Bibcode:1996PNAS...93.9788K. doi:10.1073/pnas.93.18.9788. PMC 38507free to read. PMID 8790409. 
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  21. ^ Yasukawa, M; Inoue, Y; Ohminami, H; Sada, E; Miyake, K; Tohyama, T; Shimada, T; Fujita, S (1997). "Human herpesvirus 7 infection of lymphoid and myeloid cell lines transduced with an adenovirus vector containing the CD4 gene". Journal of Virology. 71 (2): 1708–1712. PMC 191236free to read. PMID 8995705. 
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  23. ^ Hall, CB (1997). "Human Herpesviruses at Sixes, Sevens, and More (editorial)". Annals of Internal Medicine. American College of Physicians. 127 (6): 481–3. doi:10.1059/0003-4819-127-6-199709150-00010 (inactive 2015-01-13). PMID 9313006. 
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  27. ^ 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 53343free to read. PMID 2153965. 
  28. ^ Secchiero, P; Flamand, L; Gibellini, D; Falcieri, E; Robuffo, I; Capitani, S; Gallo, RC; Zauli, G (1997). "Human Herpesvirus 7 induces CD4(+) T-cell death by two distinct mechanisms: necrotic lysis in productively infected cells and apoptosis in uninfected or nonproductively infected cells". Blood. 90 (11): 4502–12. PMID 9373261. 
  29. ^ Menegazzi, P; Galvan, M; Rotola, A; Ravaioli, T; Gonelli, A; Cassai, E; Di Luca, D (1999). "Temporal mapping of transcripts in human herpesvirus-7". Journal of General Virology. 80 (10): 2705–12. PMID 10573164. 
  30. ^ Atedzoe, BN; Menezes, J; D'Addario, M; Xu, J; Ongradi, J; Ahmad, A (1999). "Modulatory effects of human herpes virus-7 on cytokine synthesis and cell proliferation in human peripheral blood mononuclear cell cultures". Journal of Leukocyte Biology. 66 (5): 822–8. PMID 10577515. 
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  32. ^ 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 356854free to read. PMID 15004116. 
  33. ^ 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 1717251free to read. PMID 9279150. 
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Further reading[edit]