Roseola pathophysiology

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

Overview

Primary infection with HHV-6 has been shown to be the cause of exanthem subitum (roseola) in infants and can also result in an infectious mononucleosis-like illness in adults.

Pathophysiology

Transmission of infection

• HHV 6 virus is replicated in the salivary glands and secreted in saliva in the primary infection.
• Intrauterine transmission was suggested by polymerase chain reaction (PCR) positivity of uncultured cord blood mononuclear cells.
• CNS invasion is believed to occur accounting for some of the CNS manifestations such as febrile seizures.

• 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.

Pathogenesis

• The pathogenesis of roseola is unknown. However, in a prospective study of 38 children with roseola, human herpesvirus 6 (HHV-6) was detected in a blood sample in all of the children during the period of high fever .
• The human herpes virus infects the T cells, monocytes-macrophages, epithelial cells, and central nervous system cells resulting in a chronic infection.
• HHV-6 has tropism towards CD4 T cells and replicates in the T cells inducing a lifelong latent infection in humans.
• The pathogenicity of HHV-7 is not well understood.

Genetics

• 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.

Associated conditions

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

Gross pathology

Maculopapular rash as seen in an infant.