Diabetes as one of the long-term COVID-19 complications: from the potential reason of more diabetic patients' susceptibility to COVID-19 to the possible caution of future global diabetes tsunami.

According to recent researches, people with diabetes mellitus (type 1 and 2) have a higher incidence of coronavirus disease 2019 (COVID-19), which is caused by a SARS-CoV-2 infection. In this regard, COVID-19 may make diabetic patients more sensitive to hyperglycemia by modifying the immunological and inflammatory responses and increasing reactive oxygen species (ROS) predisposing the patients to severe COVID-19 and potentially lethal results. Actually, in addition to COVID-19, diabetic patients have been demonstrated to have abnormally high levels of inflammatory cytokines, increased virus entrance, and decreased immune response. On the other hand, during the severe stage of COVID-19, the SARS-CoV-2-infected patients have lymphopenia and inflammatory cytokine storms that cause damage to several body organs such as ß cells of the pancreas which may make them as future diabetic candidates. In this line, the nuclear factor kappa B (NF-κB) pathway, which is activated by a number of mediators, plays a substantial part in cytokine storms through various pathways. In this pathway, some polymorphisms also make the individuals more competent to diabetes via infection with SARS-CoV-2. On the other hand, during hospitalization of SARS-CoV-2-infected patients, the use of some drugs may unintentionally lead to diabetes in the future via increasing inflammation and stress oxidative. Thus, in this review, we will first explain why diabetic patients are more susceptible to COVID-19. Second, we will warn about a future global diabetes tsunami via the SARS-CoV-2 as one of its long-term complications.

Possible role of autophagy induced by COVID-19 in cancer progression, chemo-resistance, and tumor recurrence.

COVID-19 infection is a serious threat to patients with primary diseases, especially multiple cancers. Studies suggest that cancer patients are one of the most susceptible populations to experience severe COVID-19 and death. In addition, a number of studies suggest various mechanisms for SARS-CoV-2 in cancer progression. In this study, we discussed the role of SARS-CoV-2 in the induction of autophagy and we hypothesized that autophagy induced by COVID-19 not only can contribute to viral replication but also potentially can lead to cancer progression, chemo-resistance, and tumor recurrence in multiple cancer patients. Therefore, targeting autophagy-related signaling pathways and cellular and molecular processes could be a potentially promising therapeutic approach for cancer patients with COVID-19. Hence, this study can shed light on a new window on the management of such patients. However, more investigations in the future are required to understand other pathological effects of COVID-19 infection on cancer patients to provide new therapeutic strategies to combat these complications in these patients.