Background The objectives of this study were to analyze the clinical features of coronavirus disease 2019 and evaluate the diagnosis and treatment. Methods A retrospective analysis of the clinical manifestation and auxiliary examination of 19 patients with COVID-19 from the Liyuan Hospital intensive care unit (ICU) between January 16, 2020 and February 20, 2020 was undertaken. Results There were 11 male and 8 female cases among the patients. The median (range) age was 73 (38-91) years. Of these patients, 8 (42.1%) had died and the median duration from ICU admission to death was 2 (interquartile range (IQR): 1-10.75) days. Seven of these 8 patients had underlying diseases. The auxiliary examination showed fever (68.4%), dry cough (15.8%), dyspnea (10.5%), and diarrhea (5.3%). All 19 cases showed ground-glass changes on chest computed tomography. Serum hypersensitive C-reactive protein (hs-CRP) and serum amylase A (SAA) were clearly increased in all of the cases. Among the 19 cases, there were 16 (84.2%) cases in which the total number of lymphocytes decreased, 12 cases (63%) had reduced liver function, and 11 cases (58%) had deviant results for fibrinogen (FIB) and D-dimer, in particular, the D-dimer level was significantly higher in the non-survivors compared with the survivors. Conclusion There were more men than women among critically ill patients. All of the cases showed ground-glass changes on chest computed tomography and the vast majority of patients displayed fever and dry cough. The clinical laboratory indices change significantly, especially the D-dimer level among non-survivors.

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Human papillomavirus (HPV) integration and high expression of HPV oncogenes (E6 and E7) are important mechanisms for HPV carcinogenesis in cervical cancer. However, the relationship between HPV integration and HPV E6 spliced transcripts, as well as the underlying mechanisms of HPV integration in carcinogenesis after HPV E6 splicing remains unclear. We analyzed HPV‐coiled‐coil domain containing 106 (CCDC106) integration samples to characterize the roles of HPV integration, E6 spliceosome I (E6*I), and high CCDC106 expression in cervical carcinogenesis. We found that E6 was alternatively spliced into the E6*I transcript in HPV‐CCDC016 integration samples with low p53 expression, in contrast to the role of E6*I in preventing p53 degradation in cervical cancer cells. In addition, CCDC106 was highly expressed after HPV‐CCDC106 integration, and interacted with p53, resulting in p53 degradation and cervical cancer cell progression in vitro and in vivo. Importantly, when E6*I was highly expressed in cervical cancer cells, overexpression of CCDC106 independently degraded p53 and promoted cervical cancer cell progression. In this study, we explored the underlying mechanisms of HPV‐CCDC106 integration in HPV carcinogenesis after HPV E6 splicing, which should provide insight into host genome dysregulation in cervical carcinogenesis.