Background Coronavirus disease 2019 (COVID-19) is an emerging serious global health problem. Gastrointestinal symptoms are common in COVID-19 patients, and severe acute respiratory syndrome coronavirus 2 RNA has been detected in stool specimens. However, the relationship between the gut microbiome and disease remains to be established. Methods We conducted a cross-sectional study of 30 patients with COVID-19, 24 patients with influenza A(H1N1), and 30 matched healthy controls (HCs) to identify differences in the gut microbiota by 16S ribosomal RNA gene V3–V4 region sequencing. Results Compared with HCs, COVID-19 patients had significantly reduced bacterial diversity; a significantly higher relative abundance of opportunistic pathogens, such as Streptococcus, Rothia, Veillonella, and Actinomyces; and a lower relative abundance of beneficial symbionts. Five biomarkers showed high accuracy for distinguishing COVID-19 patients from HCs with an area under the curve (AUC) up to 0.89. Patients with H1N1 displayed lower diversity and different overall microbial composition compared with COVID-19 patients. Seven biomarkers were selected to distinguish the 2 cohorts (AUC = 0.94). Conclusions The gut microbial signature of patients with COVID-19 was different from that of H1N1 patients and HCs. Our study suggests the potential value of the gut microbiota as a diagnostic biomarker and therapeutic target for COVID-19, but further validation is needed.

Coronavirus disease 2019 (COVID-19) is a highly contagious infectious disease. Similar to H7N9 infection, pneumonia and cytokine storm are typical clinical manifestations of COVID-19. Our previous studies found that H7N9 patients had intestinal dysbiosis. However, the relationship between the gut microbiome and COVID-19 has not been determined. This study recruited a cohort of 57 patients with either general ( n = 20), severe ( n = 19), or critical ( n = 18) disease. The objective of this study was to investigate changes in the abundance of ten predominant intestinal bacterial groups in COVID-19 patients using quantitative polymerase chain reaction (q-PCR), and to establish a correlation between these bacterial groups and clinical indicators of pneumonia in these patients. The results indicated that dysbiosis occurred in COVID-19 patients and changes in the gut microbial community were associated with disease severity and hematological parameters. The abundance of butyrate-producing bacteria, such as Faecalibacterium prausnitzii , Clostridium butyricum , Clostridium leptum , and Eubacterium rectale , decreased significantly, and this shift in bacterial community may help discriminate critical patients from general and severe patients. Moreover, the number of common opportunistic pathogens Enterococcus (Ec) and Enterobacteriaceae (E) increased, especially in critically ill patients with poor prognosis. The results suggest that these bacterial groups can serve as diagnostic biomarkers for COVID-19, and that the Ec/E ratio can be used to predict death in critically ill patients.

Our work revealed that A. muciniphila attenuated APAP-induced liver injury by alleviating oxidative stress and inflammation in the liver, and its hepatoprotective effect was accompanied by activation of the PI3K/Akt pathway and mediated by regulation of the composition and metabolic function of the intestinal microbiota. This finding suggested that the microbial community is a non-negligible impact on drug metabolism and probiotic administration could be a potential therapy for drug-induced liver injury.

Prostate cancer is the second most common malignancy in men and androgen deprivation therapy is the first-line therapy. However, most cases will eventually develop castration-resistant prostate cancer after androgen deprivation therapy treatment. Enzalutamide is a second-generation androgen receptor antagonist approved by the Food and Drug Administration to treat patients with castrationresistant prostate cancer. Unfortunately, patients receiving enzalutamide treatment will ultimately develop resistance via various complicated mechanisms. This review examines the emerging information on these resistance mechanisms, including androgen receptor-related signalling pathways, glucocorticoid receptor-related pathways and metabolic effects. Notably, lineage plasticity and phenotype switching, gene polymorphisms and the relationship between microRNAs and drug resistance are addressed. Furthermore, potential therapeutic strategies for enzalutamideresistant castration-resistant prostate cancer treatment are suggested, which can help discover more effective and specific regimens to overcome enzalutamide resistance.