Dynamics of T follicular helper cells in patients with rheumatic diseases and subsequent antibody responses in a three-dose immunization regimen of CoronaVac.

Given increased acceptance of the CoronaVac, there is an unmet need to assess the safety and immunogenic changes of CoronaVac in patients with rheumatic diseases (RD). Here we comprehensively analysed humoral and cellular responses in patient with RD after a three-dose immunization regimen of CoronaVac. RD patients with stable condition and/or low disease activity (n = 40) or healthy controls (n = 40) were assigned in a 1:1 ratio to receive CoronaVac (Sinovac). The prevalence of anti-receptor binding domain (RBD) antibodies and neutralizing antibodies was similar between healthy control (HC) and RD patients after the second and the third vaccination. However, the titers of anti-RBD IgG and neutralizing antibodies were significantly lower in RD patients compared to HCs (p < 0.05), which was associated with an impaired T follicular helper (Tfh) cell response. Among RD patients, those who generated an antibody response displayed a significantly higher Tfh cells compared to those who failed after the first and the second vaccination (p < 0.05). Interestingly, subjects with a negative serological response displayed a similar Tfh memory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-derived peptides as their anti-RBD IgG positive counterpart, and all (4/4) of the non-responders in HCs, and 62.5% (5/8) of the non-responders in patients with RD displayed a positive serological response following the third dose. No serious adverse events were observed. In conclusion, our findings support SARS-CoV-2 vaccination in patients with RD with stable and/or low disease activity. The impaired ability in generating vaccine-specific antibodies in patients with RD was associated with a reduction in Tfh cells induction. The window of vaccination times still needs to be explored in future studies. Clinical trial registration: This trial was registered with ChiCTR2100049138.

Risk of Severe Illness and Risk Factors of Outcomes of COVID-19 in Hospitalized Patients with Chronic Liver Disease in a Major U. S. Hospital Network.

Methods: We studied 2731 patients with known CLD who were hospitalized at the Johns Hopkins Health System with COVID-19 between March 1, 2020, and December 15, 2021. The primary outcome was all-cause mortality, and secondary outcomes were MV and vasopressors. Multivariable Cox regression models were performed to explore factors associated with the outcomes. Results: Overall, 80.1% had severe COVID-19, all-cause mortality was 8.9%, 12.8% required MV, and 11.2% received vasopressor support. Older patients with underlying comorbidities were more likely to have severe COVID-19. There was association between elevated aminotransferases and total bilirubin with more severe COVID-19. Hepatic decompensation was independently associated with all-cause mortality (HR 2.94; 95% CI 1.23-7.06). Alcohol-related liver disease (ALD, HR 2.79, 95% CI, 1.00-8.02) was independently associated with increased risk for MV, and independent factors related to vasopressor support were chronic pulmonary disease and underlying malignancy. Conclusions: COVID-19 infection in patients with CLD is associated with poor outcomes. SARS-CoV-2 infection in patients with hepatic decompensation was associated with an increased risk of in-hospital mortality hazard, and ALD among patients with COVID-19 was associated with an increased hazard for MV.

Early identification of patients with severe COVID-19 at increased risk of in-hospital death: a multicenter case-control study in Wuhan.

BACKGROUND: Most evidence regarding the risk factors for early in-hospital mortality in patients with severe COVID-19 focused on laboratory data at the time of hospital admission without adequate adjustment for confounding variables. A multicenter, age-matched, case-control study was therefore designed to explore the dynamic changes in laboratory parameters during the first 10 days after admission and identify early risk indicators for in-hospital mortality in this patient cohort. METHODS: Demographics and clinical data were extracted from the medical records of 93 pairs of patients who had been admitted to hospital with severe COVID-19. These patients had either been discharged or were deceased by March 3, 2020. Data from days 1, 4, 7, and 10 of hospital admission were compared between survivors and non-survivors. Univariate and multivariate conditional logistic regression analyses were employed to identify early risk indicators of in-hospital death in this cohort. RESULTS: On admission, in-hospital mortality was associated with five risk indicators (ORs in descending order): aspartate aminotransferase (AST, >32 U/L) 43.20 (95% CI: 2.63, 710.04); C-reactive protein (CRP) greater than 100 mg/L 13.61 (1.78, 103.941); lymphocyte count lower than 0.6×109/L 9.95 (1.30, 76.42); oxygen index (OI) less than 200 8.23 (1.04, 65.15); and D-dimer over 1 mg/L 8.16 (1.23, 54.34). Sharp increases in D-dimer at day 4, accompanied by decreasing lymphocyte counts, deteriorating OI, and persistent remarkably high CRP concentration were observed among non-survivors during the early stages of hospital admission. CONCLUSIONS: The potential risk factors of high D-dimer, CRP, AST, low lymphocyte count and OI could help clinicians identify patients at high risk of death early in the hospital admission. This might assist with rationalization of health care resources.

Health Impact Assessment of PM2.5 attributable mortality from the September 2020 Washington State Wildfire Smoke Episode.

Major wildfires that started in the summer of 2020 along the west coast of the U.S. have made PM2.5 concentrations in cities in this region rank among the highest in the world. Regions of Washington were impacted by active wildfires in the state, and by aged wood smoke transported from fires in Oregon and California. This study aims to assess the population health impact of increased PM2.5 concentrations attributable to the wildfire. Average daily PM2.5 concentrations for each county before and during the 2020 Washington wildfire episode were obtained from the Washington Department of Ecology. Utilizing previously established associations of short-term mortality for PM2.5, we estimated excess mortality for Washington attributable to the increased PM2.5 levels. On average, PM2.5 concentrations increased 91.7 µg/m3 during the wildfire episode. Each week of wildfire smoke exposures was estimated to result in 87.6 (95% CI: 70.9, 103.1) cases of increased all-cause mortality, 19.1 (95% CI: 10.0, 28.2) increased cardiovascular disease deaths, and 9.4 (95% CI: 5.1, 13.5) increased respiratory disease deaths. Because wildfire smoke episodes are likely to continue impacting the Pacific Northwest in future years, continued preparedness and mitigations to reduce exposures to wildfire smoke are necessary to avoid this excess health burden.

Impacts of the COVID-19 responses on traffic-related air pollution in a Northwestern US city.

This study evaluates the COVID-19 impacts on traffic-related air pollution, including ultrafine particles (UFPs), PM2.5, black carbon (BC), NO, NO2, NOx, and CO in a Northwestern US city. Hourly traffic, air pollutants, and meteorological data on/near a major freeway in the downtown of Seattle, Washington, were collected for five weeks before and ten weeks after the Washington Stay Home Order (SHO) was enacted, respectively (February 17-May 31, 2020). The pollutants between pre- and post-SHO periods were compared, and their differences were statistically tested. Besides, first-order multivariate autoregressive (MAR(1)) models were developed to reveal the impacts specific to the change of traffic due to the COVID-19 responses while controlling for meteorological conditions. Results indicate that compared with those in the post-SHO period, the median traffic volume and road occupancy decreased by 37% and 52%, respectively. As for pollutants, the median BC and PM2.5 levels significantly decreased by 25% and 33%, relatively, while NO, NO2, NOx, and CO decreased by 33%, 29%, 30%, and 17%, respectively. In contrast, neither size-resolved UFPs nor total UFPs showed significant changes between the two periods, although larger particles (≥115.5 nm) decreased by 4-29%. Additionally, significant differences were found in meteorological conditions between the two periods. Based on the MAR(1) models, controlling for meteorological conditions, the COVID-19 responses were associated with significant decreases in median levels of traffic-related pollutants including 11.5-154.0 nm particles (ranging from -3% [95% confidence interval (CI): -1%, -4%] to -12% [95% CI: -10%, -14%]), total UFPs (-7% [95% CI: -5%, -8%]), BC (-6% [95% CI: -5%, -7%]), PM2.5 (-2% [95% CI: -1%, -3%]), NO, NO2, NOx (ranging from -3% [95% CI: -2%, -4%] to -10% [95% CI: -18%, -12%]), and CO (-4% [95% CI, -3%, -5%]). These findings illustrate that the conclusion of the COVID-19 impacts on urban traffic-related air pollutant levels could be completely different in scenarios whether meteorology was adjusted for or not. Fully adjusting for meteorology, this study shows that the COVID-19 responses were associated with much more reductions in traffic-related UFPs than PM2.5 in the Seattle region, in contrast to the reverse trend from the direct empirical data comparison.