RESUMEN
Introduction: The COVID-19 pandemic has increased the global experience of anxiety and depression owing to social isolation and government-mandated quarantine for transmission reduction. To date, literature surrounding the mental health effects of COVID-19 for the U.S. population is limited. Methods: This is a retrospective study from a large metropolitan Detroit health system. Patient encounters between December 23, 2018 and June 22, 2021, with March 23, 2020 being the start of Michigan state-wide lockdown, were used to define pre- and post-COVID-19 encounters, respectively. The data were divided into Detroit and non-Detroit on the basis of patient ZIP code. All patients aged ≥13 years with a visit with a family medicine provider were included. Outcome variables included Patient Health Questionnaires-2 and -9 and General Anxiety Disorder-7 scores; diagnoses of depression, anxiety, adjustment, and grief disorders; antidepressant prescriptions; and behavioral health referrals. Logistic regression was used to determine the incidence of composite mood disorder, depression, and anxiety. Results: A total of 20,970 individuals were included in this study: 10,613 in the Detroit subgroup and 10,357 in the non-Detroit subgroup. A total of 88.2% of the Detroit population were Black, and 70% were female. Logistic regression shows that the incidence of composite mood disorder decreased with increasing age (OR=0.787, 0.608, 0.422, and 0.392; p<0.001). Male sex is a protective factor (OR=0.646, p<0.001). Federal insurance is the only factor presenting a statistically significant increased risk (OR=1.395, p<0.001). There was no statistical difference between residing in urban and suburban areas in the incidence of composite mood disorder (OR=0.996, p=0.953). Conclusions: This research demonstrates that residing in an urban setting did not increase the risk of developing a mental health disorder during the COVID-19 period.
RESUMEN
Human Vγ9Vδ2 T cells are well known for their rapid and potent response to infection and tumorigenesis when in the presence of endogenous or exogenous phosphoisoprenoids. However, the molecular mechanisms behind the activation of this γδ T cell population remains unclear. Evidence pointing to a role for the CD277/butyrophilin-3 (BTN3A) molecules in this response led us to investigate the structures of these molecules and their modifications upon binding to an agonist antibody (20.1) that mimics phosphoisoprenoid-mediated Vγ9Vδ2 activation and an antagonist antibody (103.2) that inhibits this reactivity. We find that the three BTN3A isoforms: BTN3A1, BTN3A2, and BTN3A3, have high structural homology to the B7 superfamily of proteins and exist as V-shaped homodimers in solution, associating through the membrane proximal C-type Ig domain. The 20.1 and 103.2 antibodies bind to separate epitopes on the BTN3A Ig-V domain with high affinity but likely with different valencies based on their binding orientation. These structures directly complement functional studies of this system that demonstrate that BTN3A1 is necessary for Vγ9Vδ2 activation and begin to unravel the extracellular events that occur during stimulation through the Vγ9Vδ2 T cell receptor.