Coronaviruses are a group of zoonotic viruses common among animals, which might spread

among humans as well. A new strand of this coronavirus, namely SARS-CoV-2, called
coronavirus disease 2019 (COVID-19) by the World Health Organization, was discovered in
early January of this year in Wuhan . During this pandemic, the SARS-CoV-2 contagiousness
rate has exceeded that of both the SARS and MERS viruses (though not mortality, with a rate of
5.58%), and the rate at which the infection is spreading is showing no signs of slowing down .
Several studies have elucidated the epidemic features of the infection, and others are underway,
aimed at identifying the specific biological traits of this virus. A longer incubation time
associated with the SARS-CoV-2 infection was reported and a shorter serial period in
comparison with SARS-CoV and MERS-CoV, which led to screening and control-policy
adjustments . The infection caused by the new virus in the corona family is still the subject of
numerous studies and investigations. Humankind is facing a pandemic affecting an ever-
increasing number of people, caused by a new viral agent that affects the immune system via
incompletely elucidated mechanisms. We analyzed 10 cases of Sars Cov 2 infection in patients
diagnosed with type I diabetes, who had moderate to severe forms of the disease. The symptoms
also included joint pain with various localizations. All patients presented imbalances of glycemic
values and persistent inflammatory syndrome. Diabetes and obesity induce a chronic
inflammation status in the body. We believe that Sars Cov 2 infection can trigger autoimmunity
phenomena due to chronic inflammation with various manifestations, including arthritis,
especially in patients who have joint manifestations during the infection. The long-term
consequences of this infection cannot be anticipated with certainty.We do not know (and
therefore cannot state with certainty) whether this SARS-CoV-2 infection will lead to
chronicization of certain inflammatory phenomena or activation of autoimmunity. We cannot
make indubitable statements related to the persistence of the virus within the body and its
potential to reactivate. We also do not know if the persistence of the virus in the body can
perpetuate inflammatory phenomena against the background of pre-existing inflammation in the
diabetic patient. We now know that when the virus reaches cells, it blocks infected cells’
capacity to respond and activate antiviral mechanisms. It appears that the immune response is
delayed due to a viral strategy.