A signicant proportion of patients who recovered from SARCoV-2 infection develop chronic symptoms lasting weeks or months, referred as Long COVID. Though the exact etiology of Long COVID is unknown; however, one of major symptom experienced by these patients is chronic fatigue syndrome which is associated with several mitochondrial disorders or viral diseases. In this review, a systematic approach has been performed to explain Long COVID as possible outcome of mitochondrial dysfunction. The review highlights what is known in literature about the dysfunctional pathways which can develop in mitochondria and their relationship to viruses and associated mitochondrial disorders. It also identies potential areas which require urgent, further research in order to help clinical management and interventional studies for better long-term outcomes.

Studies suggest certain stimuli like apoptosis behind the aberrant expression of circulating specific auto-antibodies in Type-1 diabetic patients. In the present study, we investigated whether Streptozotocin (a diabetogenic compound) induced apoptosis in Rat RINm5f Insulinoma cells can expose immunogenic cryptic antigens. A time course treatment of RINm5f cells with 4 mM Streptozotocin revealed 6hrs as minimal time period to induce apoptosis without much effect on viability.Subsequent immunization of mice with the untreated and Streptozotocin treated RINm5f cells revealed highly reactive sera from 6hr STZ treated cells. Hybridoma technique showed a highly reactive clone named sup160which secretedIgG1 type monoclonal antibody.Parallely, we show that 6hr STZ-RINm5f challenged mice displayed both humoral and cellular immune response, as shown by increased presence of IgG1 / IgG2a subclass of antibodies and overexpression of IFNγ, IL-4 and TNFα in splenocytes. FACS and confocal imaging further established the reactivity of sup160 antibody with RINm5f cell surface antigen. The antigen was identified to be cytokeratin18 protein as detected by 2D gel electrophoresis and mass spectrometry. In conclusion, we have successfully established a novel xenogenic mice model system for identification of new auto-antigen in Type-1 diabetes, although further studies are warranted in human subjects.

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