Human herpesvirus 7
|Human herpesvirus 7|
|Classification and external resources|
|Human herpesvirus 7|
|Group:||Group I (dsDNA)|
Human herpesvirus 7 (HHV-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). HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to by their genus, Roseolovirus. HHV-7 was first isolated in 1990 from CD4+ T cells taken from peripheral blood lymphocytes.
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. 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, and febrile seizures, though most often no symptoms present at all.
There are indications that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome, encephalopathy, hemiconvulsion-hemiplegia-epilepsy syndrome, hepatitis infection, postinfectious myeloradiculoneuropathy, pityriasis rosea, and the reactivation of HHV-4, leading to "mononucleosis-like illness".
Complications with HHV-7 infection has been shown to be a factor in a great variety of transplant types.
A mature virus particle measures about 170 nanometres (1,700 Å) in diameter.
The genome of HHV-7 is very similar to that of HHV-6, although it is about 10% smaller, with a DNA genome of about 145,000 base pairs. 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.
HHV-7 resides mostly in CD4+ T cells, albeit only in certain strains of them. To enter CD4+ T cells, HHV-7, unlike HHV-6, uses CD4 and possibly some cell-surface glyoproteins to enter CD4+ T cells. About a week after HHV-7 has infected a cell, it begins to downregulate CD4 transcription, which interferes with HIV-1 infection but may reactivate HHV-6 infection. It is however unclear exactly what effect HHV-7 has on HIV infection.
HHV-7 also has a number of other effects on cells. Among these include membrane leaking, the presence of lityic syncytia, occasional apoptosis, the supporting of latent infection, and increases and decreases in levels of certain cytokines.
Detection and treatment
In adults, the effects of HHV-7 separate from HHV-6 have not been well-researched. 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. No reliable serological test has been developed yet for HHV-7 alone, but multiple are in the process of being developed. The use of PCR assays to test for HHV-7 is also being explored.
No treatment for HHV-7 infection exists, but no clinical situation where such treatment would be useful has yet been discovered.
Over 95% of adults have been infected and are immune to HHV-7, and over three quarters of those were infected before the age of six. 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.
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