Diabetes mellitus: Lessons from COVID-19 for monkeypox infection.

BACKGROUND AND AIMS: Type 2 Diabetes Mellitus is known to be linked to malfunctioning antiviral defense; however, its association with the severity of monkeypox is poorly understood. In this review, we discuss key immunological mechanisms in the antiviral response affected by poor glucose control that could impact the susceptibility and severity of monkeypox infection, leading to a heightened emphasis on the use of the available antidiabetic drugs. METHODS: We searched PubMed and Google scholar for articles published from January 1985 to August 2022. No criteria for publication data were set, and all articles in English were included. RESULTS: Currently, there are no studies about the risk or consequences of monkeypox infection in the diabetic population. A high incidence of diabetes is reported in countries such as China, India, Pakistan, EUA, Indonesia, Brazil, Mexico, Bangladesh, Japan, and Egypt, where unfortunately imported cases of monkeypox have been reported and the infection continues to spread. CONCLUSIONS: High incidence of diabetes together with the cessation of smallpox vaccination has left large numbers of the human population unprotected against monkeypox. The best option for the population remains confined to the prevention of infection as well as the use of hypoglycemic agents that have also been shown to improve immune mechanisms associated with viral protection.

TREM-1 modulation during early stages of dengue virus infection.

Uncontrolled and intricate production of inflammatory factors is the characteristic feature of dengue infection. The triggering receptor expressed in myeloid cells-1 (TREM-1), expressed on the surface of monocytes and neutrophils, is capable of enhancing and regulating the inflammatory response via the production of different mediators in bacterial and viral infections. Here, both the expression of TREM-1 on human monocytes and neutrophils from peripheral blood of dengue infected individuals, as well as the levels of the soluble form of TREM-1 (sTREM-1) in the sera of these patients were compared against healthy controls. A significant reduction of TREM-1 expression was observed in neutrophils during the first days of infection, followed by a gradual recovery throughout the course of infection. Also, sera from DENV-infected patients exhibited significantly higher sTREM-1 levels than healthy individuals. The difference was more pronounced during the first 5 days after the onset of symptoms. These findings highlight the dynamic process of TREM-1 expression during DENV infection. We hypothesized that increment of free sTREM-1 could be a compensatory mechanism aiming to counteract the inflammatory process elicited during DENV infection.