Human betaherpesvirus 7

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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 7
SpecialtyInfectious disease
Human betaherpesvirus 7
Virus classification e
(unranked): Virus
Realm: Duplodnaviria
Kingdom: Heunggongvirae
Phylum: Peploviricota
Class: Herviviricetes
Order: Herpesvirales
Family: Herpesviridae
Genus: Roseolovirus
Human betaherpesvirus 7
  • Human herpesvirus 7

Signs and symptomsEdit

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]



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 effectsEdit

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 treatmentEdit

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]


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]


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Further readingEdit