Human herpesvirus 7

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

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.^[4] 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,^[5] and febrile seizures,^[6] though most often no symptoms present at all.^[7]

There are indications that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome,^[8] encephalopathy,^[9] hemiconvulsion-hemiplegia-epilepsy syndrome,^[10] hepatitis infection,^[11] postinfectious myeloradiculoneuropathy,^[12] pityriasis rosea,^[13] and the reactivation of HHV-4, leading to "mononucleosis-like illness".^[14]

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

Virology

Structure

A mature virus particle measures about 170 nanometres (1,700 Å) in diameter.^[15]

The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller,^[16] with a DNA genome of about 145,000 base pairs.^[7] 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.^[7]

Cellular effects

HHV-7 resides mostly in CD4+ T cells,^[17] albeit only in certain strains of them.^[18] To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glyoproteins to enter CD4+ T cells.^[19] About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription,^[20] which interferes with HIV-1 infection^[21] but may reactivate HHV-6 infection.^[22] It is however unclear exactly what effect HHV-7 has on HIV infection.^[7]

HHV-7 also has a number of other effects on cells. Among these include membrane leaking, the presence of lityic syncytia,^[23] occasional apoptosis,^[24] the supporting of latent infection,^[25] and increases and decreases in levels of certain cytokines.^[26]

Detection and treatment

In adults, the effects of HHV-7 separate from HHV-6 have not been well-researched.^[27] 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.^[28] No reliable serological test has been developed yet for HHV-7 alone, but multiple are in the process of being developed.^[7] The use of PCR assays to test for HHV-7 is also being explored.^[7][29]

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

Epidemiological

Over 95% of adults have been infected and are immune to HHV-7,^[30] and over three quarters of those were infected before the age of six.^[31] 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.^[32]

References

Further reading