Depression, anxiety and PTSD symptoms before and during the COVID-19 pandemic in the UK (preprint)

Background: The COVID-19 pandemic is a novel population-level stressor. As such, it is important to examine pandemic-related changes in mental health and to identify which individuals are at greatest risk of worsening symptoms. Methods: Online questionnaires were administered to 34,465 individuals in the UK, recruited from existing cohorts or via social media. Around one third (n = 12,718) with prior diagnoses of depression or anxiety completed pre-pandemic mental health assessments, allowing prospective investigation of symptom change. We examined changes in depression, anxiety and PTSD symptoms using prospective, retrospective and global ratings of change assessments. We also examined the effect of key risk factors on changes in symptoms.Outcomes: Prospective analyses showed small decreases in depression (PHQ-9: - .43 points) and anxiety symptoms (GAD-7: -.33 points), and increases in PTSD symptoms (PCL-6: .22 points). Conversely, retrospective analyses demonstrated large significant increases in depression (2.40 points) and anxiety symptoms (1.97 points) and 55% reported worsening mental health since the beginning of the pandemic on a global change rating. Using both prospective and retrospective symptom measures, regression analyses demonstrated that worsening depression, anxiety and PTSD symptoms were associated with i) prior mental health diagnoses, ii) female gender; iii) young age, and iv) unemployed or student status.Interpretation: We highlight the effect of prior mental health diagnoses on worsening mental health during the pandemic and confirm previously-reported sociodemographic risk factors. Discrepancies between prospective and retrospective measures of changes in mental health may be related to recall bias underestimating prior symptom severity.

Factor V is an immune inhibitor that is expressed at increased levels in leukocytes of patients with severe Covid-19 (preprint)

Severe Covid-19 is associated with elevated plasma Factor V (FV) and increased risk of thromboembolism. We report that neutrophils, T regulatory cells (Tregs), and monocytes from patients with severe Covid-19 express FV, and expression correlates with T cell lymphopenia. In vitro full length FV, but not FV activated by thrombin cleavage, suppresses T cell proliferation. Increased and prolonged FV expression by cells of the innate and adaptive immune systems may contribute to lymphopenia in severe Covid-19. Activation by thrombin destroys the immunosuppressive properties of FV. Anticoagulation in Covid-19 patients may have the unintended consequence of suppressing the adaptive immune system.