Mycoplasma pneumoniae is one of the major respiratory bacterial pathogens that cause pneumonia in humans. Multiple-locus variable-number tandem-repeat analysis (MLVA) is currently the most discriminative method for typing M. pneumoniae strains. To better understand the epidemic of M. pneumoniae-related pneumonia in pediatric patients in Beijing, China, we performed MLVA analysis on 118 specimens collected during an epidemic from 2010–2012. Eleven distinct MLVA types were identified, including four novel types. There was no obvious association of macrolide resistance with any of the genotypes. Considering the instability of VNTR locus Mpn1, we propose an amended MLVA nomenclature system based on the remaining four VNTR loci.

Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Recent studies have shown that anti-silencing function 1B (ASF1B) might be used as a new proliferation marker for cancer diagnosis and prognosis. However, the expression and function of ASF1B in cervical cancer remain unclear. Here, we induced ASF1B knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established two murine models using stable ASF1B-shRNA HeLa cells or normal HeLa cells following AAV-shRNA-ASF1B administration to evaluate how suppression of ASF1B affects tumor growth. We showed that ASF1B functions as an oncogene in cervical cancer cells. Silence of ASF1B suppressed cervical cancer cell growth in vitro and in vivo, while, ASF1B overexpression accelerated cancer cell proliferation. Furthermore, ASF1B deficiency induced cell cycle arrest and apoptosis. Mechanistically, we found that ASF1B formed stable complexes with cyclin-dependent kinase 9 (CDK9), and positively regulated CDK9 stabilization. Taken together, tumorigenic ASF1B could be targeted to suppress cervical cancer tumor growth by inducing apoptotic cell death.

Objectives: To analyze the molecular and the clinical characteristics of Mycoplasma pneumoniae (Mp) pneumonia (MPP) and to explore the related factors predicting severe MPP (SMPP).Methods: A total of 423 pediatric cases of MPP were retrospectively analyzed, in 2013-2017, in Beijing, China. Clinical information was collected from the medical records. Mp-positive specimens were characterized using P1 typing and multiple locus variable-number tandem repeat analysis (MLVA). The macrolide resistanceassociated mutations were also detected.Results: The predominant genotype was P1-1 (88.2%) and M4-5-7-2 (87.5%), whereas percentages of type P1-2 and M3-5-6-2 increased across the 5-year period. The mutation rate of genotype M4-5-7-2 (365/370, 98.6%) was significantly higher than that of the genotype M3-5-6-2 (15/48, 32.25%; P = 0.000). Overall, 180 (42.6%) of the 423 Mp-positive patients were coinfected with other pathogens. Respiratory syncytial virus coinfection (24/180, 13.3%) was more common in cases typed M3-5-6-2 (4/23, 17.4%) than that of M4-5-7-2 (20/155, 12.9%; P = 0.038). Pleural effusion accounted for 52.6% (169/321) of the observed complications. In the mono-infection cases, cases typed M3-5-6-2 (56%, 14/25) were significantly (P = 0.020) associated with pleural effusion compared with those typed M4-5-7-2 (32.6%, 70/215); 84% (21/ 25) of specimens typed M3-5-6-2 were diagnosed as SMPP, whereas 63.7% (137/ 215) of specimens typed M4-5-7-2 were diagnosed as SMPP (P = 0.043). Conclusions:In our study, we proposed for the first time that the mono-infection patients with Mp typed M3-5-6-2 appear to have a higher risk for progressing to SMPP. MLVA typing can provide hints on the clinical characteristics of Mpp.

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M ycoplasma pneumoniae is a leading pathogen of respiratory infection, especially community-acquired pneumonia (CAP), in children and adults worldwide (1). M. pneumoniae can also cause extrapulmonary manifestations (especially cardiovascular, hematologic, and nervous system, as well as skin) and even death. M. pneumoniae can transmit from person to person through aerosolization. Epidemics occur at intervals of 3 to 7 years and may last up to 2 years each time, and M. pneumoniae is responsible for up to 25% of CAP (2, 3). Patients can carry M. pneumoniae from a few days to a few months. M. pneumoniae infection can result in great economic loss and social impact in families, schools, and militaries-even a whole society. Increasing scientists around the world have joined in the research on M. pneumoniae in recent years. From 1977 to the present (about 38 years), we have been continuously monitoring M. pneumoniae infections in children in Beijing, China. A total of seven epidemics were documented in seven different periods of time in