IgG antibodies against Human Herpes Virus type 6 are being investigated. Clinically it appears as Exanthema subitum (Roseola infantum), or "sixth disease". Primary HHV-6B infection is acquired through direct contact of young children with infected older persons, most often through saliva. Vertical transmission of HHV-6 has also been proven, but it occurs in only 1-2% of all births. HHV-6 integrates into chromosomes in immunocompetent patients and this results in high levels of viral DNA in blood and serum. This fact should be taken into account when interpreting the laboratory results of molecular biological studies. The clinical manifestation is an initial toxic-infectious syndrome, an increase in temperature, enlargement of the cervical lymph nodes and rhinopharyngitis. Then a maculopapular rash appears on the body (excluding the limbs and face), which quickly disappears without leaving scars. HHV-6B infection in infants is the most common cause of temperature-induced seizures. In a prospective study involving children aged 1 month to 5 years, HHV-6B was found to be frequently associated with febrile status epilepticus (as was HHV-7, although to a lesser extent). HHV-6 infections are mostly uncomplicated and self-limiting. Asymptomatic forms have also been described. Rarely, HHV-6 infection can be fatal. Acute HHV-6 infection is rare in immunocompetent adults. Its clinical presentation is a mononucleosis-like illness with high fever, lymphadenopathy or hepatitis, and more rarely encephalitis, with negative virological indicators for CMV or EBV. After primary infection, HHV-6 remains latent in lymphocytes and monocytes and a low viral load is maintained in cells and tissues. In immunocompetent individuals, this persistent infection is usually of no clinical significance. In cases of immunocompromise, the virus reactivates, with HHV-6A being associated with a worse prognosis. This condition occurs in 33-48% of patients undergoing hematopoietic stem cell transplantation, and is often associated with reactivation of latent cytomegalovirus infection. Co-infection significantly aggravates the outcome of the disease. The clinical presentation is as hepatitis, pneumonia, bone marrow suppression, encephalitis, fever and rash, as well as the development of graft-versus-donor reaction (GVHD). Transmission of HHV-6 also occurs during transplantation of solid organs and hematopoietic stem cells. In HIV-infected patients, HHV-6 can regulate HIV replication and accelerate progression to AIDS. A sixth type of herpes virus has been shown to infect and destroy cells that produce myelin and is in the pathogenesis of HIV dementia.
- HHV-6 has been isolated from various tissues, cells and body fluids and is associated with the following conditions:
- lymphadenitis or lymphadenopathy
- lymphomas and lymphoproliferative diseases
- drug-induced hypersensitivity syndrome (DIHS) or drug reaction with eosinophilia and systemic symptoms (DRESS)
- Sjogren's syndrome, sarcoidosis, systemic lupus erythematosus
- chronic fatigue syndrome (CFS)
- Guillain-Barre syndrome multiple sclerosis (MS)
HHV-6 antigen has been detected in the nuclei of oligodendrocytes in the plaques of MS patients. A correlation has been demonstrated between anti-HHV-6 IgM antibodies and the onset of MS compared to healthy individuals and those with progressive multiple sclerosis.
The following panel of laboratory tests is recommended depending on the patient's clinical picture and immune status:
- CBC with DBC - leukopenia with relative leukocytosis
- assessment of renal function - in renal transplantation
- liver enzymes - in hepatitis and liver dysfunction
- serological studies - proof of specific anti-HHV-6 IgG antibodies
Virological test results should be interpreted in the context of the overall clinical picture. Positive values can mean disease, but also strained immunity.