Mucormycosis is a lethal human disease caused by fungi of the order Mucorales. Mucormycosis is caused by fungi mainly belonging to the genera Mucor, Rhizopus, and Lichtheimia, all of which belong to the order Mucorales. The number of individuals with mucormycosis-causing disorders has increased in recent years, hence, leading to the spread of mucormycosis. Throughout the coronavirus disease 2019 (COVID-19) pandemic, numerous cases of mucormycosis in COVID-19-infected patients have been reported worldwide, and the illness is now recognized as COVID-19-associated mucormycosis, with most of the cases being reported from India. Immunocompromised patients such as those with bone marrow sickness and uncontrolled diabetes are at a greater risk of developing mucormycosis. Genes, pathways, and other mechanisms have been studied in Mucorales, demonstrating a direct link between virulence and prospective therapeutic and diagnostic targets. This review discusses several proteins such as high-affinity iron permease (FTR1), calcineurin, spore coat protein (CotH), and ADP-ribosylation factors involved in the pathogenesis of mucormycosis that might prove to be viable target(s) for the development of novel diagnostic and therapeutic methods.

Neuropathological findings have been published from ∼900 patients who died with or from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, representing less than 0.01% of the close to 6.4 million deaths reported to the World Health Organization 2 years into the coronavirus disease 2019 (COVID-19) pandemic. In this review, we extend our prior work summarizing COVID-19 neuropathology by including information on published autopsies up to June 2022, and neuropathological studies in children, COVID-19 variants, secondary brain infections, ex vivo brain imaging, and autopsies performed in countries outside of the United States or Europe. We also summarize research studies that investigate mechanisms of neuropathogenesis in nonhuman primates and other models. While a pattern of cerebrovascular pathology and microglial-predominant inflammation remains the primary COVID-19-associated neuropathological finding, there is no singular understanding of the mechanisms that underlie neurological symptoms in acute COVID-19 or the post-acute COVID-19 condition. Thus, it is paramount that we incorporate microscopic and molecular findings from brain tissue into what we know about the clinical disease so that we attain best practice guidance and direct research priorities for the study of the neurological morbidity of COVID-19.