Search

In 2019 in Wuhan province, China, an outbreak of atypical pneumonia was reported with similar symptoms to Severe Acute Respiratory Syndrome (SARS), an outbreak reported in 2003, and Middle East Respiratory Syndrome (MERS) reported in Saudi Arabia in 2012. This emerging disease was caused by a novel coronavirus "Severe Acute Respiratory Syndrome Coronavirus 2" (SARS-CoV-2) or also called COVID-19. Which causes severe respiratory problems and various extrapulmonary manifestations. At the moment, the high mortality of COVID-19 has been related to the male sex, older adults (>60 years), and preexisting comorbidities of diabetes, obesity, hypertension, and heart problems. Diabetes is a disease characterized by insulin resistance and loss of ß cell function in the pancreas, with an impaired immune system due to chronic inflammation. In patients with severe COVID-19 infection, altered secretion of pro-inflammatory cytokines has been observed, if this infection occurs in a diabetic patient who already has an inflammatory state per se, an exacerbated inflammation and multiorgan failure with fatal consequences can be triggered. Several authors hypothesis suggest that hyperglycemia increases the viral replication in patients "diabetic with COVID-19 infection" is necessary to keep adequate glycemic control. Treatments for COVID-19 had focused on decreasing symptoms, the use of antivirals, anti-inflammatory drugs, monoclonal antibodies and COVID-19 convalescent plasma has shown variable results. A vaccine is needed to control this viral infection, at the moment more than 150 candidates have been developed with efficiency ranges from 70 to 95%, however, the long-term immunity in vaccinated people is still unknown. This review focus on the characteristics of SARS-CoV-2 infection and the immune response in diabetic patients facing COVID-19. [ABSTRACT FROM AUTHOR]

In humans, coronaviruses can cause infections of the respiratory system, with damage of varying severity depending on the virus examined: ranging from mild-to-moderate upper respiratory tract diseases, such as the common cold, pneumonia, severe acute respiratory syndrome, kidney failure, and even death. Human coronaviruses known to date, common throughout the world, are seven. The most common—and least harmful—ones were discovered in the 1960s and cause a common cold. Others, more dangerous, identified in the early 2000s and cause more severe respiratory tract infections. Among these the SARS-CoV, isolated in 2003 and responsible for the severe acute respiratory syndrome (the so-called SARS), which appeared in China in November 2002, the coronavirus 2012 (2012-nCoV) cause of the Middle Eastern respiratory syndrome (MERS) from coronavirus, which exploded in June 2012 in Saudi Arabia, and actually SARS-CoV-2. On December 31, 2019, a new coronavirus strain was reported in Wuhan, China, identified as a new coronavirus beta strain ß-CoV from group 2B, with a genetic similarity of approximately 70% to SARS-CoV, the virus responsible of SARS. In the first half of February, the International Committee on Taxonomy of Viruses (ICTV), in charge of the designation and naming of the viruses (i.e., species, genus, family, etc.), thus definitively named the new coronavirus as SARS-CoV-2. This article highlights the main knowledge we have about the biomolecular and pathophysiologic mechanisms of SARS-CoV-2. [ABSTRACT FROM AUTHOR]