SARS-CoV-2 triggering autoimmune diseases.

Autoimmunity, hyperstimulation of the immune system, can be caused by a variety of reasons. Viruses are thought to be important environmental elements that contribute to the development of autoimmune antibodies. It seems that viruses cause autoimmunity with mechanisms such as molecular mimicry, bystander activation of T cells, transient immunosuppression, and inflammation, which has also been seen in post-Covid-19 autoimmunity. Infection of respiratory epithelium by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dysregulates the immune response, triggers both innate and acquired immunity that led to the immune system's hyperactivation, excessive cytokine secretion known as "cytokine storm," and finally acute respiratory distress syndrome (ARDS) associated with high mortality. Any factor in the body that triggers chronic inflammation can contribute to autoimmune disease, which has been documented during the Covid-19 pandemic. It has been observed that some patients produce autoantibody and autoreactive CD4+ and CD8+ T cells, leading to the loss of self-tolerance. However, there is a scarcity of evidence defining the precise molecular interaction between the virus and the immune system to elicit autoreactivity. Here, we present a review of the relevant immunological findings in Covid-19 and the current reports of autoimmune disease associated with the disease.

The impact of lymphoid memory cells in different ages of COVID-19 patients.

Coronaviruses are highly pathogenic and transmissible viruses. The SARS-CoV-2 virus that emerged in December 2019 is increasingly recognized as a serious, worldwide public health concern. Respiratory infections and the hyper-inflammatory response induced by SARS-CoV-2 play a key role in disease severity and death in infected COVID-19 patients. However, much uncertainty still exists about the pathogenesis and various effects of COVID-19 on immune system. It seems that memory T cells can reduce the severity of COVID-19 infection by inducing a protective immune response. Memory T cells along with protective antibodies are the main defenses and also protective barrier against recurrent COVID-19 infection. The role of Memory T cells varies in different ages and the severity of COVID-19 infection varies between children, adults and the elderly. Furthermore, the aim of this review is to evaluate the role of memory cells in mild, moderate and severe infected COVID-19 patients with different ages.