Non-Polio enterovirus infections pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: {Sujaya}}

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.

• 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.

• 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.

Template:WikiDoc Sources