Replication of SARS CoV2 in Pancreatic Cells via ACE2 Cell Surface Receptors

Abstract

Earlier studies have reported that Diabetes mellitus (DM) increases the complications of Severe acute respiratory syndrome coronavirus 2 (SARS CoV2) or Coronavirus disease 2019 (COVID19), and patients are more likely to experience severe symptoms that could lead to mortality. One hypothesis states that hyperglycemic conditions facilitate the virus entry into the cell since the virus and the Angiotensin-Converting Enzyme 2 (ACE2) both require glucose for their function. However the exact interaction between the two has not been clearly defined from the cell biology point of view. The underlying mechanism for this differential effect in individuals with and without diabetes is not clearly understood. The reason for this could be due to the preexisting pathological pathways in patients with poorly controlled diabetes, which increases the risk of infectivity and are responsible for the higher levels of tissue injury and death in patients with diabetes [1]. However in this article we have focused mainly on COVID-19 induced diabetes as this area has lacuna. The diabetes specialists point out that many key metabolic tissues in the body, including pancreatic beta cells (b-cell) in the pancreas, adipose (fat storage) tissue, the small intestine, and kidneys, contain ACE2 receptors. They believe that when these viruses bind to ACE2 receptors, they may trigger changes in glucose metabolism that worsen preexisting diabetes or cause the condition to develop diabetes for the first time.

COVID-19 Outbreaks in Co-Morbid Patients: A Pursuit for Biomarkers

“…The Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), is a single-stranded RNA virus and is the cause of the ongoing COVID-19 disease 1 .…”