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

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]



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]


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] 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.[37] 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.[38]


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Further reading[edit]