Causal associations between chronic hepatitis B and COVID-19 in East Asian populations.

BACKGROUND: The relationship between chronic hepatitis B (CHB) and Coronavirus disease 2019 (COVID-19) has been inconsistent in traditional observational studies. METHODS: We explored the total causal and direct causal associations between CHB and the three COVID-19 outcomes using univariate and multivariate Mendelian randomization (MR) analyses, respectively. Genome-wide association study datasets for CHB and COVID-19 were obtained from the Japan Biobank and the COVID-19 Host Genetics Initiative, respectively. RESULTS: Univariate MR analysis showed that CHB increased the risk of SARS-CoV-2 infection (OR = 1.04, 95% CI 1.01-1.07, P = 3.39E-03), hospitalized COVID-19 (OR = 1.10, 95% CI 1.06-1.13, P = 7.31E-08), and severe COVID-19 (OR = 1.16, 95%CI 1.08-1.26, P = 1.43E-04). A series of subsequent sensitivity analyses ensured the stability and reliability of these results. In multivariable MR analyses adjusting for type 2 diabetes, body mass index, basophil count, and smoking, genetically related CHB is still positively associated with increased risk of SARS-CoV-2 infection (OR = 1.06, 95% CI 1.02-1.11, P = 1.44E-03) and hospitalized COVID-19 (OR = 1.12, 95% CI 1.07-1.16, P = 5.13E-07). However, the causal link between CHB and severe COVID-19 was attenuated after adjustment for the above variables. In addition, the MR analysis did not support the causal effect of COVID-19 on CHB. CONCLUSIONS: This study provides evidence that CHB increases COVID-19 susceptibility and severity among individuals of East Asian ancestry.

Experimental study of the purification performance of a MopFan-based photocatalytic air cleaning system.

Severe acute respiratory syndrome coronavirus (SARS-CoV)-2, the virus that causes the coronavirus disease (COVID)-19, is primarily transmitted through respiratory droplets which linger in enclosed spaces, often exacerbated by HVAC systems. Although research to improve HVAC handling of SARS-CoV-2 is progressing, currently installed HVAC systems cause problems because they recirculate air and use ineffective filters against virus. This paper details the process of developing a novel method of eliminating air pollutants and suspended pathogens in enclosed spaces using Photocatalytic Oxidation (PCO) technology. It has been previously employed to remove organic contaminants and compounds from air streams using the irradiation of titanium dioxide (TiO2) surfaces with ultraviolet (UV) lights causing the disintegration of organic compounds by reactions with oxygen (O) and hydroxyl radicals (OH). The outcome was two functional prototypes that demonstrate the operation of PCO-based air purification principle. These prototypes comprise a novel TiO2 coated fibre mop system, which provide very large surface area for UV irradiation. Four commercially accessible materials were used for the construction of the mop: Tampico, Brass, Coco, and Natural synthetic. Two types of UV lights were used: 365 nm (UVA) and 270 nm (UVC). A series of tests were conducted that proved the prototype's functionality and its efficiency in lowering volatile organic compounds (VOCs) and formaldehyde (HCHO). The results shown that a MopFan with rotary mop constructed with Coco fibres and utilising UVC light achieves the best VOC and HCHO purification performance. Within 2 h, this combination lowered HCHO by 50% and VOCs by 23% approximately.

SARS-CoV-2 ORF3A interacts with the Clic-like chloride channel-1 (CLCC1) and triggers an unfolded protein response.

Understanding the interactions between SARS-CoV-2 and host cell machinery may reveal new targets to treat COVID-19. We focused on an interaction between the SARS-CoV-2 ORF3A accessory protein and the CLIC-like chloride channel-1 (CLCC1). We found that ORF3A partially co-localized with CLCC1 and that ORF3A and CLCC1 could be co-immunoprecipitated. Since CLCC1 plays a role in the unfolded protein response (UPR), we hypothesized that ORF3A may also play a role in the UPR. Indeed, ORF3A expression triggered a transcriptional UPR that was similar to knockdown of CLCC1. ORF3A expression in 293T cells induced cell death and this was rescued by the chemical chaperone taurodeoxycholic acid (TUDCA). Cells with CLCC1 knockdown were partially protected from ORF3A-mediated cell death. CLCC1 knockdown upregulated several of the homeostatic UPR targets induced by ORF3A expression, including HSPA6 and spliced XBP1, and these were not further upregulated by ORF3A. Our data suggest a model where CLCC1 silencing triggers a homeostatic UPR that prevents cell death due to ORF3A expression.

Pre-existing immunity to SARS-CoV-2 associates with strong T cell responses induced by inactivated COVID-19 vaccines.

Individuals with a recent common cold coronavirus infection, which leads to pre-existing immunity against SARS-CoV-2, displayed a less severe course of COVID-19. However, the relationship between pre-existing immunity against SARS-CoV-2 and the inactivated-vaccine-induced immune response is still unknown. Here, 31 healthcare workers who received standard two doses of inactivated COVID-19 vaccines (Weeks 0 and 4, respectively) were enrolled, vaccine-induced neutralization and T cell responses were detected, and the correlation between the pre-existing SARS-CoV-2-specific immunity was analyzed. We found the SARS-CoV-2-specific antibodies, pseudovirus neutralization test (pVNT) titers, and spike-specific interferon gamma (IFN-γ) production in CD4+ and CD8+ T cells were significantly elevated after two doses of inactivated vaccines. Interestingly, the pVNT titers after the second dose of vaccination displayed no significant correlation with the pre-existing SARS-CoV-2-specific antibodies or B cells, nor the pre-existing spike-specific CD4+ T cells. Notably, the spike-specific T cell response after the second dose of vaccination was positively correlated with the pre-existing receptor binding domain (RBD)-specific B cells and CD4+ T cells, which were documented by the frequencies of RBD-binding B cells, the breadth of RBD-specific B cell epitopes, and the frequency of IFN-γ-expressing RBD-specific CD4+ T cells. Overall, the inactivated-vaccine-induced T cell responses, not the inactivated-vaccine-induced neutralization, closely correlated with pre-existing immunity to SARS-CoV-2. Our results provide a better understanding of inactivated-vaccine-induced immunity and help predict the immunogenicity induced by inactivated vaccines in individuals.

East Asian summer monsoon enhanced by COVID-19.

Anthropogenic emissions decreased dramatically during the COVID-19 pandemic, but its possible effect on monsoon is unclear. Based on coupled models participating in the COVID Model Intercomparison Project (COVID-MIP), we show modeling evidence that the East Asian summer monsoon (EASM) is enhanced by 2.2% in terms of precipitation and by 5.4% in terms of the southerly wind at lower troposphere, and the amplitude of the forced response reaches about 1/3 of the standard deviation for interannual variability. The enhanced EASM during COVID-19 pandemic is a fast response to reduced aerosols, which is confirmed by the simulated response to the removal of all anthropogenic aerosols. The observational evidence, i.e., the anomalously strong EASM observed in 2020 and 2021, also supports the simulated enhancement of EASM. The essential mechanism for the enhanced EASM in response to COVID-19 is the enhanced zonal thermal contrast between Asian continent and the western North Pacific in the troposphere, due to the reduced aerosol concentration over Asian continent and the associated latent heating feedback. As the enhancement of EASM is a fast response to the reduction in aerosols, the effect of COVID-19 on EASM dampens soon after the rebound of emissions based on the models participating in COVID-MIP. Supplementary Information: The online version contains supplementary material available at 10.1007/s00382-022-06247-8.

Probiotics in Health and Disease: Distinct Roles of Different Strains in Natural Killer Cell Activation and Regulation.

Elucidating the role of probiotic bacteria in health and disease perhaps constitutes one of the most exciting and fastest growing fields in medicine as we uncover the beneficial roles of these bacteria in many disease processes including cancer. We and others have reported previously that probiotic bacteria play a significant role in the activation of many cells including the cancer fighting natural killer (NK) cells. NK cells are the key immune effectors which control tumor growth and metastasis due to their ability to mediate direct cytotoxicity and/or differentiation of cancer stem cells/undifferentiated tumors through secreted and membrane bound interferon-gamma and tumor necrosis factor-alpha. In this review, we present an overview of recent studies from our laboratory and those of the others on their beneficial effects on immune cell function in particular on NK cells. In addition, we also highlight the current understanding of the role of probiotics in enhancement of the effectiveness of cancer therapeutics. Moreover, we discuss the functional impairment of cancer patients' NK cells and the role of probiotics in reversal of such functional impairment. NK cell-based immuno-therapies in combination with well-selected strains of probiotic bacteria may probably represent one of the best adjunct therapeutic approaches to prevent and treat cancer in the future.