Roseola pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]

Roseola has two phases, the febrile and the rash (maculopapular) phase. During the first phase, HHV6 replicates in salivary glands and is secreted as primary source of infection. After completes resolution of the febrile phase, due to the latency of the virus in the lymphocytes and monocytes, the rash phase begins.

Roseola has two phases:

1. The febrile phase
2. The rash phase

• HHV 6 virus is replicated in the salivary glands and secreted in saliva in the primary infection.^[1]
• Intrauterine transmission was suggested by polymerase chain reaction (PCR) positivity of uncultured cord blood mononuclear cells.^[2]

• CNS invasion is believed to occur in rare cases accounting for some of the CNS manifestations such as febrile seizures.^[3]

• In the second phase of the disease, the HHV 6 virus is found to remain latent in lymphocytes and monocytes and found in low levels in some tissues. CD4 positive T cells have been found to support the growth of roseola.^[1][4]

• Infection of the CD134 cells has been shown in some studies to be responsible for the reactivation of HHV 6 from latency in vitro.
• The human herpes virus infects the T cells, monocytes–macrophages, epithelial cells, and central nervous system cells resulting in a lifelong latency or persistence of virus at multiple sites. HHV-6 exists in a true state of viral latency in monocytes and macrophages.^[4]
• HHV-6 has tropism towards CD4 T cells and replicates in the T cells inducing a lifelong latent infection in humans.

Chromosomal integration of HHV-6A and HHV-6B is responsible for transmission of infection from the parents to the newborn and is observed in 1% of the population.

A more serious form of HHV 6 is seen in older children, immunocompromised adults and organ transplant patients.

There are no gross pathologic findings associated with roseola.

There are no microscopic findings associated with roseola.