In 1990, four years after the isolation of HHV-6, another herpesvirus was discovered. Because of the similarities in genes HHV-6 and HHV-7 and the fact that HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to as Roseolovirus. HHV-7 has been found to cause at least some cases of exanthem subitum (roseola).
Antibodies to HHV-7 have been detected in 95% of the normal population. Over 75% were infected before six years of age. The primary infection of HHV-7 among children usually occurs between the ages of 2 and 5. This infers that the infection occurs after the primary infection of HHV-6, which is usually before 2 years of age.
It is believed that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome, hemiconvulsion-hemiplegia-epilepsy syndrome, encephalopathy, hepatitis, postinfectious myeloradiculoneuropathy, pityriasis rosea, and can reactive HHV-4, the Epstein-Barr Virus (EBV). Complications with HHV-7 infection have also been shown to be a factor in organ transplants.
There is no childhood disease or a definable syndrome that is associated with an acute HHV-7 infection. Both HHV-6B and HHV-7, as well as other viruses, can cause a rash roseola infantum in infants, but HHV-6B more than HHV-7. Even though there are usually no symptoms present with HHV-7, the infection is also associated with symptoms including acute febrile respiratory disease, fever, rash, vomiting, diarrhea, low lymphocyte counts, and febrile seizures.
The virus seems to be spread through saliva.
It has been established that HHV-7 infection is widespread among populations in the USA, Europe and Japan.
No reliable serological test has been developed yet for HHV-7 separate from HHV-6, but many are in the process of being developed.
No treatment for HHV-7 infection exists.