Mucormycosis is a rapidly progressive, invasive fungal infection that affects patients who are severely immunocompromised, as well as patients with diabetes and persons with immunocompetence who have major trauma. Mucormycosis manifests in several clinical forms, including sino-orbital, rhinocerebral, sinopulmonary, gastrointestinal, cutaneous, musculoskeletal, osteoarticular, and disseminated mucormycosis, as well as single-organ disease. Although mucormycosis is often lethal, early intervention reduces mortality. Successful treatment depends on early detection and staging of the disease, timely initiation of antifungal therapy, surgical resection of infected tissue, reversal of immunodeficiencies, and correction of metabolic abnormalities. Liposomal amphotericin B is the preferred agent for initial antifungal therapy, with oral triazoles as alternative agents. Research on rapid molecular diagnostic strategies, new antifungal agents, host-directed immune augmentation, antivirulence immune therapeutics, and risk-based stratification to inform management of disease may substantially improve outcomes in patients with this highly destructive mycosis.

Vaccine-induced immune thrombocytopenia and thrombosis (VITT) is a rare prothrombotic complication that occurs after adenoviral vector-based vaccination against coronavirus disease 2019; in rare cases, it can also occur after natural adenovirus infection. VITT is mediated by platelet-activating antibodies against the highly cationic protein platelet factor 4 (PF4). The underlying inciting antigen trigger and immunopathogenesis remain unknown.

Wild-type female Aedes aegypti mosquitoes that mate with male A. aegypti mosquitoes that have been infected with the wAlbB strain of Wolbachia pipientis bacteria produce nonviable offspring owing to cytoplasmic incompatibility. Repeated releases of wolbachia-infected males can potentially suppress wild-type mosquito populations and reduce the risk of dengue virus infection.

GM1 gangliosidosis, caused by biallelic variants in GLB1, results from deficiency of lysosomal β-galactosidase, which degrades GM1 ganglioside. This fatal neurodegenerative disease currently has no effective therapy.