Human herpesvirus 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

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

Structure

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

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

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

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

Further reading