Roseola pathophysiology

	Roseola Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Roseola from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Roseola pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Roseola pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Roseola pathophysiology
CDC on Roseola pathophysiology
Roseola pathophysiology in the news
Blogs on Roseola pathophysiology
Directions to Hospitals Treating Type chapter name here
Risk calculators and risk factors for Roseola pathophysiology

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

Overview

Virus replicated in the salivary glands and secreted in saliva is the source of infection transmission.
Intrauterine transmission was suggested by polymerase chain reaction (PCR) positivity of uncultured cord blood mononuclear cells.

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.

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.