Fam72a enforces error-prone DNA repair during antibody diversification.

Efficient humoral responses rely on DNA damage, mutagenesis and error-prone DNA repair. Diversification of B cell receptors through somatic hypermutation and class-switch recombination are initiated by cytidine deamination in DNA mediated by activation-induced cytidine deaminase (AID) and by the subsequent excision of the resulting uracils by uracil DNA glycosylase (UNG) and by mismatch repair proteins. Although uracils arising in DNA are accurately repaired, how these pathways are co-opted to generate mutations and double-strand DNA breaks in the context of somatic hypermutation and class-switch recombination is unknown.

The syndemic burden of HIV/AIDS in Africa amidst the COVID-19 pandemic.

Introduction: The human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) has long affected millions of individuals across the globe. Historically, the prevalence of this disease is particularly noted within the African continent. Before the coronavirus disease 2019 (COVID-19) pandemic, many African countries struggled to effectively manage the increasing burden associated with HIV/AIDS.