What is the pathophysiology of roseola infantum?

Updated: Oct 09, 2020
  • Author: Christopher R Gorman, MD; Chief Editor: William D James, MD  more...
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Answer

In the primary infection, replication of the virus occurs in the leukocytes and the salivary glands. HHV-6 is present in saliva. A study monitoring HHV-6 and HHV-7 DNA in saliva samples during the acute and convalescent phases demonstrated a significantly higher rate of detection in children aged 3-9 years versus adults, suggesting that children in the convalescent phase of roseola infantum are the more probable source of infection. [3] Early invasion of the CNS is believed to occur, thus accounting for seizures and other CNS complications. Evidence suggests that high serum levels of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinases 1 in infants infected with HHV-6 may lead to blood-brain barrier dysfunction, which may result in febrile seizures. [4] Study of cerebrospinal fluid levels of interleukin 1β and basic fibroblast growth factor may indicate a role in contributing to HHV-6B growth and the onset of encephalitis. [5] Although rare in the primary disease of infancy, generalized organ involvement has been reported with gastrointestinal, hematopathic syndromes; hepatitis; and hepatosplenomegaly.

Following the acute primary infection, HHV-6 remains latent in lymphocytes and monocytes and has been found in low levels in many tissues. Peripheral blood mononuclear cell cultures develop enlarged balloonlike cells. Cells supporting virus growth are CD4+ T lymphocytes. HHV-6 down-regulates the host immune response through several mechanisms, including molecular mimicry by production of functional chemokine and chemokine receptors.

The two variants of HHV-6 are A and B. The genomes of HHV-6A/B have been sequenced. HHV-6B, the main cause of roseola, consists of 97 unique genes. CD46 is the cell receptor for HHV-6, which imparts the virus' broad tissue tropism.

A possible association of HHV-6 and multiple sclerosis has been suggested but is still inconclusive. HHV-6 has been isolated in Kaposi sarcoma (caused by human herpesvirus 8), in which it may contribute to tumor progression. HHV-6 may facilitate oncogenic potential in lymphoma and has been associated with chronic fatigue syndrome.


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