Background We retrospectively analyzed 26 persistently asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) carriers. Methods Epidemiological and clinical characteristics from the 26 asymptomatic patients with positive results for SARS-CoV-2 ribonucleic acid testing were obtained. Results Twenty-two patients (84.6%) correlated with clustering occurrence. The median period from contact to diagnosis and the last positive nucleic acid test was 19 (8–24 days) and 21.5 days (10–36 days), respectively. The median period from diagnosis to negative nucleic acid test was significantly different between patients with normal or atypical chest computed tomography (CT) findings (n = 16, 61.5%; 7.5 days [2–20 days]) and patients with typical ground-glass or patchy opacities on CT (n = 10, 38.5%; 12.5 days [8–22 days]; P < .01). Seven patients (70.0%) with initial positive nucleic acid test results had a negative result simultaneously with improved CT findings. Obvious improvement in CT findings was observed in 3 patients (30.0%) despite positive nucleic acid test results. Conclusions In asymptomatic patients, changes in biochemical and inflammatory variables are small and changes on chest CT can occur. It is worth noting that the long existence of SARS-CoV-2 in some asymptomatic patients and false-negative results need to be considered in SARS-CoV-2 nucleic acid test.

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In China, hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC), which is called HBV-related HCC (HBV-HCC), but the pathogenesis has not been clearly elucidated. Long non-coding RNAs (lncRNAs) have been paid increasing attention to, as an important regulatory molecule involved in many biological processes, as well as a variety of diseases. This study examined lncRNA that might play an important role in HBV-HCC pathogenesis by conducting lncRNA and mRNA profile comparison between HBV-HCC and normal liver tissues. The differentially expressed lncRNA and mRNA profiles between HBV-HCC and normal liver tissues were analyzed by microarrays. The potential protein-encoding gene regulated by lncRNA, and the biological function (gene ontology, pathway analysis) of the target gene were investigated. The results showed that the expression levels of lncRNA and mRNA in HBV-HCC tissues were different from those in normal liver tissues. As compared with normal liver tissue, 837 (4.30%) lncRNAs exhibited more than two-fold change (P<0.05); 325 were up-regulated, and 512 were down-regulated; 991 (5.70%) mRNAs exhibited more than 2-fold change (P<0.05); 733 were up-regulated and 258 were down-regulated in HBV-HCC tissue. Besides, there were 7 lncRNAs with above 10-fold elevation, 6 lncRNAs with above 10-fold decrease, 18 mRNAs with above 10-fold elevation and 11 mRNAs with above 10-fold decrease. 444 (53.05%) lncRNAs had their corresponding mRNAs, some of which were adjacent to lncRNAs. The biological analysis showed that the target gene of differentially expressed lncRNAs took part in the important biological regulatory function. Target gene-related pathway analysis revealed the pathways in carcinoma and mitogen-activated protein kinase (MAPK) signaling pathways significantly changed in the HBV-HCC tissues as compared with normal liver tissues (P<0.05). It was suggested that as compared with normal liver tissues, the expression of lncRNAs in HBV-HCC tissues changed significantly, and lncRNAs played a key role in the pathogenesis of HBV-HCC probably by mainly regulating the carcinoma-related signaling pathway and MAPK signaling pathways.

Duration for carrying SARS-CoV-2 in COVID-19 patientsDear editor , We read with interest the report that written by Yu and colleagues. 1 This report retrospectively analyzed laboratory-confirmed novel coronavirus disease 2019 (COVID-19) pneumonia patients and summarized the clinical characteristics of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) reactivation. However, deep understanding of SARS-CoV-2 carrying duration, the time of infection, as well as its antiviral treatment period can contribute to the management and treatment for COVID-19.The COVID-19 caused by SARS-CoV-2 has transmitted quickly as a global public health emergency, with the characteristics of a high contagiosity, quick transmission and general susceptibility. 2 Previous studies mainly focused on the epidemiological, clinical characteristics, as well as prevention and control measures of COVID-19. 3 However, few studies demonstrated the duration for SARS-CoV-2 carrying in COVID-19 patients. Here, we collected the positive SARS-CoV-2 nucleic acid cases and examined the duration for SARS-CoV-2 carrying and its characteristics in different populations.From January 20, 2020 to March 1, 2020, inpatients with a specific SARS-CoV-2 epidemiological history and a positive SARS-CoV-2 nucleic acid test were collected in this retrospective study in Henan province. We compared the durations for carrying virus SARS-CoV-2 in different ages, gender, disease condition. The duration for SARS-CoV-2 carrying was defined as the time from a close contact with the source of infection to the last positive test for COVID-19 virus. Cases in this study were also divided into severe group and non-severe group to study. The definitions of severe group (including critically ill) and group of the non-severe type were in Table 1 .

Invasion and metastasis is the major cause of tumor recurrence, difficulty for cure and low survival rate. Excavating key transcription factors, which can regulate tumor invasion and metastasis, are crucial to the development of therapeutic strategies for cancers. PU.1 is a master hematopoietic transcription factor and a vital regulator in life. Here, we report that, compared to adjacent non-cancerous tissues, expression of PU.1 mRNA in metastatic hepatocellular carcinoma (HCC), but not primary HCC, was significantly down-regulated. In addition, levels of PU.1 mRNA in metastatic hepatoma cell lines MHCC97L and MHCC97H were much lower than in non-metastatic Hep3B cells. Transwell invasion assays after PU.1 siRNA transfection showed that the invasion of hepatoma cell lines was increased markedly by PU.1 knockdown. Oppositely, overexpression of PU.1 suppressed the invasion of these cells. However, knockdown and overexpression of PU.1 did not influence proliferation. Finally, we tried to explore the potential mechanism of PU.1 suppressing hepatoma cell invasion. ChIP-qPCR analysis showed that PU.1 exhibited a high binding capacity with miR-615-5p promoter sequence. Overexpression of PU.1 caused a dramatic increase of pri-, pre-and mature miR-615-5p, as well as a marked decrease of miR-615-5p target gene IGF2. These data indicate that PU.1 inhibits invasion of human HCC through promoting miR-615-5p and suppressing IGF2. These findings improve our understanding of PU.1 regulatory roles and provided a potential target for metastatic HCC diagnosis and therapy.