HRV is a common etiology in CAP among China adults, especially in severe CAP. Clinicians should be vigilant considering of the poor outcome. Highly qualified multiplex PCR techniques with invasive sampling are needed to increase the detection rate.

Human rhinovirus (HRV) is an important causative agent of acute respiratory tract infections (ARTIs). The roles of specific HRV genotypes in patients suffering from ARTIs have not been well established. We recruited 147 adult inpatients with community-acquired pneumonia (CAP) and 291 adult outpatients with upper ARTIs (URTIs). Respiratory pathogens were screened via PCR assays. HRV was detected in 42 patients, with 35 species A, five B and two C. Seventeen genotypes were identified, and HRV-A21 ranked the highest (9/42, 21.4%). The HRV-A21-positive infections were detected in four patients with CAP and in five with URTIs, all without co-infections. The HRV-A21 genome sequenced in this study contained 12 novel coding polymorphisms in viral protein (VP) 1, VP2 EF loop, VP3 knob and 3D regions. The infections of HRV-A21 virus obtained in this study could not be neutralized by antiserum of HRV-A21 prototype strain (VR-1131), indicating remarkable antigenic variation. Metagenomic analysis showed the HRV-A21 reads were dominant in bronchoalveolar lavage fluid of the three HRV-A21-positive patients with severe CAP, in which two dead. Our results highlight an unexpected infection of genotype HRV-A21 in the clinic, indicating the necessity of precise genotyping and surveillance of HRVs to improve the clinical management of ARTIs.

A prospective study was undertaken to identify clinical, radiographical, haematological and biochemical profiles of severe acute respiratory syndrome (SARS) patients.A prediction rule, which demarcates low from high risk patients for SARS in an outbreak situation was developed. A total of 295 patients with unexplained respiratory illnesses, admitted to Queen Mary Hospital, Hong Kong SAR, China, in March to July 2003, were evaluated for clinical, radiological, haematological and alanine transaminase (ALT) data daily for 3 days after hospitalisation.In total, 44 cases were subsequently confirmed to have SARS by RT-PCR (68.2%) and serology (100%). The scoring system of attributing 11, 10, 3, 3 and 3 points to the presence of independent risk factors, namely: epidemiological link, radiographical deterioration, myalgia, lymphopenia and elevated ALT respectively, generated high and low-risk (total score 11-30 and 0-10, respectively) groups for SARS. The sensitivity and specificity of this prediction rule in positively identifying a SARS patient were 97.7 and 81.3%, respectively. The positive and negative predictive values were 47.8 and 99.5%, respectively.The prediction rule appears to be helpful in assessing suspected patients with severe acute respiratory syndrome at the bedside, and should be further validated in other severe acute respiratory syndrome cohorts.

Background To explore the role of circular RNA (circRNA) circZFR in tumorigenic capacity of lung cancer (LC). Methods Thirty primary LC tissues were used to detect circRNAs expression. CircZFR was silenced in two LC cell lines using lentivirus-mediated short hairpins RNAs. Quantitative real time PCR (qRT-PCR), northern blot and in situ hybridization (ISH) assay were used to measure the expression of circRNA. Results CircRNA circZFR was highly expressed in LC tumors. CircZFR deficiency significantly abrogated clone formation. CircZFR depletion substantially decreased tumor growth compared to WT control cells. CircZFR overexpression was dramatically increased cell growth in LC cell lines. Consequently, circZFR overexpression substantially promoted tumor propagation. Consistently, circZFR deficiency significantly reduced the expression of CCND1 and major cell cycle genes in LC cell lines. In contrast, circZFR depletion did not alter the expression of ZFR. Consequently, circZFR deficiency dramatically decreased H3K4me3 levels on the CCND1 promoter at −1,100 to −900 bp segment of CCND1 promoter. Conclusions CircZFR was related with LC growth in vitro and in vivo and tumorigenic capacity of LC. The possible mechanism was to regulating expression of CCND1 , indicating the circZFR/CCND1 signaling might be a promising therapeutic target for LC treatment.