Liver enzyme abnormalities in patients with COVID-19 are associated with disease severity. Patients with liver enzyme abnormalities have higher A-aDO2 and GGT, lower albumin and decreased circulating CD4+ T cells and B lymphocytes. SARS-CoV-2 is able to infect the liver and cause conspicuous hepatic cytopathy. Massive apoptosis and binuclear hepatocytes were the predominant histological features of SARS-CoV-2-infected liver.
BACKGROUND. Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), has become a pandemic. This study addresses the clinical and immunopathological characteristics of severe COVID-19. METHODS. Sixty-nine patients with COVID-19 were classified into severe and nonsevere groups to analyze their clinical and laboratory characteristics. A panel of blood cytokines was quantified over time. Biopsy specimens from 2 deceased cases were obtained for immunopathological, ultrastructural, and in situ hybridization examinations. RESULTS. Circulating cytokines, including IL-8, IL-6, TNF-α, IP10, MCP1, and RANTES, were significantly elevated in patients with severe COVID-19. Dynamic IL-6 and IL-8 were associated with disease progression. SARS-CoV-2 was demonstrated to infect type II and type I pneumocytes and endothelial cells, leading to severe lung damage through cell pyroptosis and apoptosis. In severe cases, lymphopenia, neutrophilia, depletion of CD4 + and CD8 + T lymphocytes, and massive macrophage and neutrophil infiltrates were observed in both blood and lung tissues. CONCLUSIONS. A panel of circulating cytokines could be used to predict disease deterioration and inform clinical interventions. Severe pulmonary damage was predominantly attributed to both cytopathy caused by SARS-CoV-2 and immunopathologic damage. Strategies that prohibit pulmonary recruitment and overactivation of inflammatory cells by suppressing cytokine storm might improve the outcomes of patients with severe COVID-19.
Mining activity for rare earth elements (REEs) has caused serious environmental pollution, particularly for soil ecosystems. However, the effects of REEs on soil microbiota are still poorly understood. In this study, soils were collected from abandoned sites of a REEs mine, and the structure, diversity, and co-occurrence patterns of soil microbiota were evaluated by Illumina high-throughput sequencing targeting 16S rRNA genes. Although microbiota developed significantly along with the natural restoration, the microbial structure on the site abandoned for 10 years still significantly differed from that on the unmined site. Potential plant growth promoting bacteria (PGPB) were identified by comparing 16S sequences against a self-constructed PGPB database via BLAST, and it was found that siderophore-producing and phosphorus-solubilizing bacteria were more abundant in the studied soils than in reference soils. Canonical correspondence analysis indicated that species richness of plant community was the prime factor affecting microbial structure, followed by limiting nutrients (total carbon and total nitrogen) and REEs content. Further co-occurring network analysis revealed nonrandom assembly patterns of microbiota in the studied soils. These results increase our understanding of microbial variation and assembly pattern during natural restoration in REE contaminated soils.
A begomovirus isolated from Malvastrum coromandelianum and tomato originating from Yunnan province (China) was shown to be representative of a new begomovirus species, for which the name tomato leaf curl Yunnan virus (TLCYnV) is proposed. TLCYnV has high levels of sequence identity to tomato yellow leaf curl China virus (TYLCCNV) across the whole genome, except for sequences encompassing the C4 gene. Agrobacterium-mediated inoculation showed TLCYnV to be highly infectious to a range of plant species but poorly infectious to M. coromandelianum. In contrast to TYLCCNV, TLCYnV was shown to infect tomato in the absence of a betasatellite. In field-collected samples, TLCYnV was identified most frequently in tomato in which it was not associated with a betasatellite. Transgenic expression in Nicotiana benthamiana showed that the C4 protein of TYLCCNV did not induce developmental abnormalities, whereas the C4 of TLCYnV induced severe developmental abnormalities, reminiscent of virus symptoms. The genome of TLCYnV was shown to be significantly less methylated in plants than that of TYLCCNV and the C4 protein of TLCYnV was shown to suppress post-transcriptional gene silencing and transcriptional gene silencing more effectively than the C4 of TYLCCNV. The results indicate that TLCYnV evolved from TYLCCNV by recombination, acquiring a more virulent C4, allowing it to dispense with the requirement for a betasatellite. The implications of these findings in relation to the evolution of monopartite begomoviruses are discussed.
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