Non-Polio enterovirus infections pathophysiology: Difference between revisions
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{{Non-Polio enterovirus infections}} | {{Non-Polio enterovirus infections}} | ||
{{CMG}} | {{CMG}} {{AE}} {Sujaya}} | ||
==Overview== | ==Overview== | ||
[[Enteroviral]] [[diseases]] are more likely to be severe in the [[immunocompromised]], including [[patients]] with [[diabetes]], [[HIV]], [[neoplasms]], or [[post-transplant]] status.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<ref name="pmid29523062">{{cite journal| author=Nikonov OS, Chernykh ES, Garber MB, Nikonova EY| title=Enteroviruses: Classification, Diseases They Cause, and Approaches to Development of Antiviral Drugs. | journal=Biochemistry (Mosc) | year= 2017 | volume= 82 | issue= 13 | pages= 1615-1631 | pmid=29523062 | doi=10.1134/S0006297917130041 | pmc=7087576 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29523062 }} </ref><ref name="pmid26761027">{{cite journal| author=Royston L, Tapparel C| title=Rhinoviruses and Respiratory Enteroviruses: Not as Simple as ABC. | journal=Viruses | year= 2016 | volume= 8 | issue= 1 | pages= | pmid=26761027 | doi=10.3390/v8010016 | pmc=4728576 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26761027 }} </ref><ref name="pmid26610549">{{cite journal| author=Huang HI, Shih SR| title=Neurotropic Enterovirus Infections in the Central Nervous System. | journal=Viruses | year= 2015 | volume= 7 | issue= 11 | pages= 6051-66 | pmid=26610549 | doi=10.3390/v7112920 | pmc=4664993 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26610549 }} </ref><ref name="pmid23297263">{{cite journal| author=Jacobs SE, Lamson DM, St George K, Walsh TJ| title=Human rhinoviruses. | journal=Clin Microbiol Rev | year= 2013 | volume= 26 | issue= 1 | pages= 135-62 | pmid=23297263 | doi=10.1128/CMR.00077-12 | pmc=3553670 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23297263 }} </ref>== | ||
===[[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]]. | |||
== References == | == References == | ||
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[[Category:Disease]] | [[Category:Disease]] | ||
[[Category: | [[Category:Viruses]] | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
Latest revision as of 19:04, 4 February 2023
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Non-Polio enterovirus infections Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: {Sujaya}}
Overview
Enteroviral diseases are more likely to be severe in the immunocompromised, including patients with diabetes, HIV, neoplasms, or post-transplant status.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[1][2][3][4]
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.
References
- ↑ Nikonov OS, Chernykh ES, Garber MB, Nikonova EY (2017). "Enteroviruses: Classification, Diseases They Cause, and Approaches to Development of Antiviral Drugs". Biochemistry (Mosc). 82 (13): 1615–1631. doi:10.1134/S0006297917130041. PMC 7087576 Check
|pmc=value (help). PMID 29523062. - ↑ Royston L, Tapparel C (2016). "Rhinoviruses and Respiratory Enteroviruses: Not as Simple as ABC". Viruses. 8 (1). doi:10.3390/v8010016. PMC 4728576. PMID 26761027.
- ↑ Huang HI, Shih SR (2015). "Neurotropic Enterovirus Infections in the Central Nervous System". Viruses. 7 (11): 6051–66. doi:10.3390/v7112920. PMC 4664993. PMID 26610549.
- ↑ Jacobs SE, Lamson DM, St George K, Walsh TJ (2013). "Human rhinoviruses". Clin Microbiol Rev. 26 (1): 135–62. doi:10.1128/CMR.00077-12. PMC 3553670. PMID 23297263.