Non-Polio enterovirus infections pathophysiology: Difference between revisions
Jump to navigation
Jump to search
| Line 14: | Line 14: | ||
===[[Rhinoviruses]]=== | ===[[Rhinoviruses]]=== | ||
* Exclusively affects the [[epithelial]] layer of the airways | |||
* The mechanisms of uptake into cell include [[endocytosis]] and [[pinocytosis]] depending on the host and the [[virus]] type. | |||
*On entry into the [[cell]], the [[virion]] induces a [[conformational]] change by lowering the [[pH]] of the [[endosome]] or altering the [[receptor]] [[binding]]. This results in the exposure of [[hydrophobic]] domains and pore-mediated release of the [[viral]] particles into the [[cytoplasm]] of the [[genome]], marking the beginning of [[viral]] [[polyprotein]] [[synthesis]] by the host [[cells]]. | |||
* They do not participate in direct [[cell]] destruction, instead disrupting the [[epithelial]] [[barriers]] by stimulating [[Reactive oxygen species]] during their [[replication]] and dissociating [[zona occludens-1]] from the [[tight junction]] complex. This triggers the release of [[cytokines]], that activate [[granulocytes]], [[monocytes]] and [[dendritic]] [[cells]]. [[IgG]] and [[IgA]] response takes about 1 to 2 weeks, usually after the [[virus]] has been eliminated but is crucial in preventing [[re-inoculation]]. Levels may remain high till a year after, but do not exhibit [[cross-reactivity]] among [[serotypes]]. On the contrary, [[viral]] load can indicate [[severity]] of the [[disease]]. | |||
* In infants, [[rhinoviruses]] damage the [[respiratory]] [[cells]] and damage the [[immune response]]. They are an independent risk factor for the development of [[asthma]] and recurrent [[wheezing]]. | |||
* In adults, they are the most common causes of [[acute]] [[exacerbations]] of [[COPD]], necessitating [[hospital]] stays. They also contribute to abut two-thirds of [[viral]] upper [[respiratory]] tract [[infections]]-associated [[asthma]] [[exacerbations]]. | |||
== References == | == References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 18:58, 4 February 2023
|
Non-Polio enterovirus infections Microchapters |
|
Differentiating Non-Polio enterovirus infections from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Non-Polio enterovirus infections pathophysiology On the Web |
|
American Roentgen Ray Society Images of Non-Polio enterovirus infections pathophysiology |
|
Non-Polio enterovirus infections pathophysiology in the news |
|
Directions to Hospitals Treating Non-Polio enterovirus infections |
|
Risk calculators and risk factors for Non-Polio enterovirus infections pathophysiology |
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.
Rhinoviruses
- Exclusively affects the epithelial layer of the airways
- The mechanisms of uptake into cell include endocytosis and pinocytosis depending on the host and the virus type.
- On entry into the cell, the virion induces a conformational change by lowering the pH of the endosome or altering the receptor binding. This results in the exposure of hydrophobic domains and pore-mediated release of the viral particles into the cytoplasm of the genome, marking the beginning of viral polyprotein synthesis by the host cells.
- They do not participate in direct cell destruction, instead disrupting the epithelial barriers by stimulating Reactive oxygen species during their replication and dissociating zona occludens-1 from the tight junction complex. This triggers the release of cytokines, that activate granulocytes, monocytes and dendritic cells. IgG and IgA response takes about 1 to 2 weeks, usually after the virus has been eliminated but is crucial in preventing re-inoculation. Levels may remain high till a year after, but do not exhibit cross-reactivity among serotypes. On the contrary, viral load can indicate severity of the disease.
- In infants, rhinoviruses damage the respiratory cells and damage the immune response. They are an independent risk factor for the development of asthma and recurrent wheezing.
- In adults, they are the most common causes of acute exacerbations of COPD, necessitating hospital stays. They also contribute to abut two-thirds of viral upper respiratory tract infections-associated asthma exacerbations.