Roseola pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Primary infection with HHV-6 had been shown to be the cause of exanthema subitum (roseola) in infants and can also result in an infectious mononucleosis-like illness in adults. | |||
==Pathophysiology== | ==Pathophysiology== |
Revision as of 16:01, 25 May 2017
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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 had been shown to be the cause of exanthema 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 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.