Non-Polio enterovirus infections pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
[[Enteroviral]] [[diseases]] are more likely to be severe in the [[immunocompromised]], including [[patients]] with [[diabetes]], [[HIV]], [[ | [[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== | ==Pathophysiology== | ||
Revision as of 19:01, 4 February 2023
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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
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.