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Human betaherpesvirus 7

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Human betaherpesvirus 7
SpecialtyInfectious disease
Human betaherpesvirus 7
Virus classification Edit this 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

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]

Signs and symptoms

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,[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]

Complications with HHV-7 infection has been shown to be a factor in a great variety of transplant types.[9]

Virology

Structure

A mature virus particle measures about 170 nanometres (1,700 Å) in diameter.[17]

The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller,[18] 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]

Cellular effects

HHV-7 resides mostly in CD4+ T cells,[19] albeit only in certain strains of them.[20][21][22] To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glyoproteins to enter CD4+ T cells.[23] About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription,[24] which interferes with HIV-1 infection[25] but may reactivate HHV-6 infection.[26] It is however unclear exactly what effect HHV-7 has on HIV infection.[9]

HHV-7 also has a number of other effects on cells. Among these include membrane leaking, the presence of lytic syncytia,[27][28] occasional apoptosis,[29] the supporting of latent infection,[30] and increases and decreases in levels of certain cytokines.[31][32]

Detection and treatment

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. 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.[33] 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][34]

No treatment for HHV-7 infection exists, but no clinical situation where such treatment would be useful has yet been discovered.[9]

Epidemiology

Over 95% of adults have been infected and are immune to HHV-7,[35] and over three quarters of those were infected before the age of six.[36] 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.[37] 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.[38] 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.[39]

References

  1. ^ 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.
  2. ^ 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.
  3. ^ 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.
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  21. ^ Mirandola, P; Secchiero, P; Pierpaoli, S; Visani, G; Zamai, L; Vitale, M; Capitani, S; Zauli, G (2000). "Infection of CD34(+) hematopoietic progenitor cells by human herpesvirus 7 (HHV-7)". Blood. 96 (1): 126–131. doi:10.1182/blood.V96.1.126. PMID 10891440.
  22. ^ 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. doi:10.1128/JVI.71.2.1708-1712.1997. PMC 191236. PMID 8995705.
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  26. ^ Tanaka-Taya, K; Kondo, T; Nakagawa, N; Inagi, R; Miyoshi, H; Sunagawa, T; Okada, S; Yamanishi, K (2000). "Reactivation of human herpesvirus 6 by infection of human herpesvirus 7". Journal of Medical Virology. 60 (3): 284–9. doi:10.1002/(SICI)1096-9071(200003)60:3<284::AID-JMV6>3.0.CO;2-8. PMID 10630960.
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  38. ^ 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.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  39. ^ 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.{{cite journal}}: CS1 maint: unflagged free DOI (link)

Further reading

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