Persistent coxsackievirus B infection and pathogenesis of ty
Enteroviruses are believed to trigger or accelerate islet autoimmunity in genetically susceptible individuals, thereby resulting in loss of functional insulin-producing -cells and type 1 diabetes mellitus (T1DM). Although enteroviruses are primarily involved in acute and lytic infections in vitro and in vivo, they can also establish a persistent infection. Prospective epidemiological studies have strongly associated the persistence of enteroviruses, especially coxsackievirus B (CVB), with the appearance of islet autoantibodies and an increased risk of T1DM. CVB can persist in pancreatic ductal and -cells, which leads to structural or functional alterations of these cells, and to a chronic inflammatory response that promotes recruitment and activation of pre-existing autoreactive T cells and -cell autoimmune destruction. CVB persistence in other sites, such as the intestine, blood cells and thymus, has been described; these sites could serve as a reservoir for infection or reinfection of the pancreas, and this persistence could have a role in the disturbance of tolerance to -cells.
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Markers of enterovirus infection (protein, RNA or antibodies) in the saliva, serum, stool, monocytes, gut mucosa and pancreas are more often detected in patients with type 1 diabetes mellitus (T1DM) than in control individuals.
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Persistent or recurrent enteroviral infections occur over long periods before the first detection of the islet autoantibodies in at-risk individuals and have been strongly associated with islet autoimmunity and an increased risk of developing T1DM.
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Coxsackievirus B (CVB) can persist in vitro and in vivo in animal and human systems, especially in pancreatic cells, which leads to structural or functional alterations of these cells.
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Persistent CVB infections might promote or enhance islet autoimmunity through various mechanisms.
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Some antiviral strategies (vaccines and drugs) are currently under investigation to prevent or clear persistent CVB infection.
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These strategies against enteroviral infections could be relevant for preventing or reducing the risk of developing T1DM and/or preserving -cell function in persistently infected at-risk individuals.

Source: https://www.nature.com/articles/s41574-022-00688-1
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