Infectious diseases & immunity最新文献

In December 2019, a new coronavirus disease 2019 (COVID-19) emerged and rapidly spread globally, posing a worldwide health emergency. The pathogen causing this pandemic was identified as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). It is well known that SARS-CoV-2 transmits via respiratory droplets and close contact with infected individuals or contaminated items. In addition to these two major transmission routes, other modes of transmission have not been confirmed. Considering that some COVID-19 patients have presented with ocular discomforts and positive SARS-CoV-2 RNA in ocular surfaces, as well as the discovery of the SARS-CoV-2 receptors, angiotensin-converting enzyme 2, and transmembrane protease, serine 2, in the oculus, the ocular surface is now thought to be a possible alternative route of SARS-CoV-2 transmission and a replication site. This review summarizes the evidence connecting COVID-19 with ocular tissues, ocular symptoms during SARS-CoV-2 infection, the potential role of the conjunctiva in SARS-CoV-2 transmission, and the physiopathological mechanisms. Appropriate precautions in ophthalmology departments, including innovative complete and effective patient management plans, protective personal equipment, hand hygiene, and strict personal distance intervals, are essential to effectively minimize the spread of SARS-CoV-2 and control the pandemic.

Background: The ongoing global coronavirus disease 2019 (COVID-19) pandemic is posing a serious public health threat to nations worldwide. Understanding the pathogenesis of the disease and host immune responses will facilitate the discovery of therapeutic targets and better management of infected patients. Metabolomics technology can provide an unbiased tool to explore metabolic perturbation.

Methods: Twenty-six healthy controls and 50 COVID-19 patients with mild, moderate, and severe symptoms in the Fifth Medical Center of PLA General Hospital from January 22 to February 16, 2020 were recruited into the study. Fasting blood samples were collected and subject to metabolomics analysis by liquid chromatography-mass spectrometry. Metabolite abundance was measured by peak area and was log-transformed before statistical analysis. The principal component analysis, different expression analysis, and metabolic pathway analysis were performed using R package. Co-regulated metabolites and their associations with clinical indices were identified by the weighted correlation network analysis and Spearman correlation coefficients. The potential metabolite biomarkers were analyzed using a random forest model.

Results: We uncovered over 100 metabolites that were associated with COVID-19 disease and many of them correlated with disease severity. Sets of highly correlated metabolites were identified and their correlations with clinical indices were presented. Further analyses linked the differential metabolites with biochemical reactions, metabolic pathways, and biomedical MeSH terms, offering contextual insights into disease pathogenesis and host responses. Finally, a panel of metabolites was discovered to be able to discriminate COVID-19 patients from healthy controls, and also another list for mild against more severe cases. Our findings showed that in COVID-19 patients, citrate cycle, sphingosine 1-phosphate in sphingolipid metabolism, and steroid hormone biosynthesis were downregulated, while purine metabolism and tryptophan metabolism were disturbed.

Conclusion: This study discovered key metabolites as well as their related biological and medical concepts pertaining to COVID-19 pathogenesis and host immune response, which will facilitate the selection of potential biomarkers for prognosis and discovery of therapeutic targets.

Background: The development of severe coronavirus disease 2019 (COVID-19) is associated with systemic hyperinflammation, which drives multi-organ failure and death. Disease deterioration tends to occur when the virus is receding; however, whether other factors besides viral products are involved in the inflammatory cascade remains unclear.

Methods: Twenty-eight COVID-19 patients with laboratory-confirmed SARS-CoV-2 infection hospitalized at the Fifth Medical Center of Chinese PLA General Hospital from January 23 to February 20, 2020 and nine healthy donors during the same period were recruited in the study. COVID-19 patients were grouped as mild, moderate, severe based on disease severity. Plasma damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calprotectin (S100A8/A9), surfactant protein A (SP-A), cold-inducible RNA-binding protein (CIRBP), and Histone H4 were detected by ELISA assay, and analyzed in combination with clinical data. Plasma cytokines, chemokines and lymphocytes were determined by flow cytometry.

Results: Plasma levels of HMGB1 (38292.3 ± 4564.4 vs. 32686.3 ± 3678.1, P = 0.002), S100A8/A9 (1490.8 ± 819.3 vs. 742.2 ± 300.8, P = 0.015), and SP-A (6713.6 ± 1708.7 vs. 5296.3 ± 1240.4, P = 0.048) were increased in COVID-19 patients compared to healthy donors, while CIRBP (57.4 ± 30.7 vs. 111.9 ± 55.2, P = 0.004) levels decreased. Five DAMPs did not vary among mild, moderate, and severe patients. Moreover, SP-A levels correlated positively with inflammatory cytokines and negatively with time elapsed after symptom onset, whereas CIRBP showed an opposite pattern.

Conclusions: These findings suggest SP-A may involve in the inflammation of COVID-19, while CIRBP likely plays a protective role. Therefore, DAMPs represent a potential target in the prevention or treatment of COVID-19.