SARS-CoV-2 and pancreas: a potential pathological interaction?

The widespread extrapulmonary complications of coronavirus disease 2019 (COVID-19) have gained momentum; the pancreas is another major target for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we take a closer look into potential pathological interactions. We provide an overview of the current knowledge and understanding of SARS-CoV-2 infection of the pancreas with a special focus on pancreatic islets and propose direct, indirect, and systemic mechanisms for pancreas injury as result of the COVID-19-diabetes fatal bidirectional relationship.

Enteroviruses and T1D: Is It the Virus, the Genes or Both which Cause T1D.

Type 1 diabetes (T1D) is a chronic autoimmune disorder that results from the selective destruction of insulin-producing ß-cells in the pancreas. Up to now, the mechanisms triggering the initiation and progression of the disease are, in their complexity, not fully understood and imply the disruption of several tolerance networks. Viral infection is one of the environmental factors triggering diabetes, which is initially based on the observation that the disease's incidence follows a periodic pattern within the population. Moreover, the strong correlation of genetic susceptibility is a prerequisite for enteroviral infection associated islet autoimmunity. Epidemiological data and clinical findings indicate enteroviral infections, mainly of the coxsackie B virus family, as potential pathogenic mechanisms to trigger the autoimmune reaction towards ß-cells, resulting in the boost of inflammation following ß-cell destruction and the onset of T1D. This review discusses previously identified virus-associated genetics and pathways of ß-cell destruction. Is it the virus itself which leads to ß-cell destruction and T1D progression? Or is it genetic, so that the virus may activate auto-immunity and ß-cell destruction only in genetically predisposed individuals?