Non-Polio enterovirus infections pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===[[Non-polio]] [[non-rhinovirus]] [[enteroviruses]]=== | ===[[Non-polio]] [[non-rhinovirus]] [[enteroviruses]]=== | ||
* Replicate in the [[oropharyngeal]] [[mucosa]] and the [[intestines]], leading to their detection in [[oral]] [[secretions]] and [[stool]], the latter showing evidence of the [[pathogen]] months after resolution of the [[symptoms]]. | |||
* Targets the [[lymphatic]] [[tissues]] such as the [[Peyer's patches]] and the [[tonsils]], paving the way for [[lymphatic]] and [[hematogenous]] [[dissemination]] | |||
* Manifestations include [[myocarditis]], [[pancreatitis]] and often a second, stronger [[viremia]]. This can cause serious clinical illness and facilitate direct crossing of the [[blood-brain]] barrier to affect the [[central nervous system]]. | |||
* Alternative mechanisms include a "Trojan horse"entry model mediated by [[virus-infected]] [[leukocytes]]. | |||
*Once present in the [[CNS]], persistent [[infection]] is possible, likely by an [[immune]] response to the [[apoptosis]] and [[autophagy]] induced by this group of [[viruses]]. | |||
===[[Rhinoviruses]]=== | ===[[Rhinoviruses]]=== | ||
== References == | == References == |
Revision as of 18:36, 4 February 2023
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Differentiating Non-Polio enterovirus infections from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: {Sujaya}}
Overview
The cellular uptake of enteorviruses is mediated by receptor molecules such as, intracellular adhesion molecule-1 (ICAM-1), low-density lipoprotein receptor (LDL-R), and non-protein factors such as heparan sulfate and sialic acid. Incubation periods range from 12 hours to 5 days, with experimental volunteers reporting symptoms several hours after aritficial inoculation.
Pathophysiology
Non-polio non-rhinovirus enteroviruses
- Replicate in the oropharyngeal mucosa and the intestines, leading to their detection in oral secretions and stool, the latter showing evidence of the pathogen months after resolution of the symptoms.
- Targets the lymphatic tissues such as the Peyer's patches and the tonsils, paving the way for lymphatic and hematogenous dissemination
- Manifestations include myocarditis, pancreatitis and often a second, stronger viremia. This can cause serious clinical illness and facilitate direct crossing of the blood-brain barrier to affect the central nervous system.
- Alternative mechanisms include a "Trojan horse"entry model mediated by virus-infected leukocytes.
- Once present in the CNS, persistent infection is possible, likely by an immune response to the apoptosis and autophagy induced by this group of viruses.