A genome-wide association study using data from thousands of patients in the US and abroad has identified a genetic risk factor of the loss of taste or smell that sometimes accompanies SARS-CoV-2 infection. In the study, which appears in this week's Nature Genetics, a team led by scientists from 23andMe analyzed online survey data from 69,841 individuals in the UK and US, identifying a genome-wide significant locus in the vicinity of the UGT2A1 and UGT2A2 genes. Both genes are expressed in the olfactory epithelium and play a role in metabolizing odorants, the researchers write. "Notably, the variant identified in this study also appears to be associated with general ability to smell, which may suggest that those with heightened smell or taste sensitivity may be more prone to notice a loss of these senses resulting from a SARS-CoV-2 infection." GenomeWeb has more on this, here.
Combining tissue samples with transcriptomic data, a team led by investigators from Stanford University have gained new insights into human-specific pathobiology in tuberculosis that may help in predicting infection outcome. TB in humans is characterized by the formation of immune-rich granulomas in infected tissues, the architecture and composition of which are thought to affect disease outcome. Yet not much is known about the spatial relationships that control human granulomas. To investigate, a group led by researchers from Stanford University used multiplexed ion beam imaging by time of flight to examine 37 proteins in tissues from patients with active TB, charting granuloma composition across eight computationally defined spatial tissue microenvironments. As reported in this week's Nature Immunology, the scientists find features of highly localized immune modulation in granulomas, while a follow-on transcriptomic meta-analysis of peripheral blood from patients with TB reveals immunoregulatory trends mirror those identified by granuloma imaging. The data indicate that there are local spatially coordinated immunoregulatory programs in TB granulomas with systemic manifestations that define active TB, which has implications for developing host-directed immunotherapies and understanding the immunologic basis of failed immunity in TB, the authors write.