Roseola pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The human herpes virus infects the T cells, monocytes-macrophages, epithelial cells, and central nervous system cells resulting in a chronic infection. | *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. | *The pathogenicity of HHV-7 is not well understood. | ||
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===Microscopic pathology=== | ===Microscopic pathology=== | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 14:51, 23 May 2017
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Roseola Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Roseola pathophysiology On the Web |
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American Roentgen Ray Society Images of Roseola pathophysiology |
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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
Pathophysiology
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 newboen and is observed in 1% of the population.