Bing du xue bao = Chinese journal of virology最新文献

Viruses "hijack" cellular metabolism to complete their proliferation. Glucose is an important source of energy and carbon in the synthesis of precursor molecules in host cells, and its metabolism is regulated dramatically during virus infection. Here, we reviewed the mechanism of virus infection that alters glucose transport, expression of glucose metabolism-related genes (glycolysis, pentose phosphate pathway, gluconeogenesis) in cells, as well as islet cells and insulin receptors. It provides references for study of virus-altering cellular glucose metabolism.

Hand, foot, and mouth disease(HFMD)is caused by mainly enterovirus 71(EV-A71)and coxsackievirus A16(CV-A16),and is a serious healthcare problem worldwide.EV-A71 infection is thought to progress readily to serious complications whereas CV-A16 infection, in general, results in mild symptoms and presents repeatedly. However, the underlying mechanisms leading to these differences are not known. We compared changes in expression of type-I interferon(IFN-I)-related genes in normal human bronchial epithelial(16HBE) cells. Gene-expression levels of TLR3,MAVS,MDA5,MyD88,IRF7,IFNαand IFNβwere elevated significantly after EVA71 infection.MDA5expression was increased markedly, and that of TLR3 and IRF3was decreased obviously after CV-A16 infection, but that of MAVS,MyD88,IFNαand IFNβdid not show significant differences. Viral copy number and viral titers suggested that CV-A16 replicates more efficiently than EV-A71 in 16HBE.These results suggest that IFN-I production pathway-related genes in response to infection by EV-A71 and CV-A16 have notable discrepancies. Such information could shine a light on the different manifestations caused by EV-A71 and CV-A16,and the mechanism of repeat infection by CV-A16.

Human adenoviruses cause respiratory diseases, conjunctivitis, gastroenteritis and even severe pneumonia. Specific antiviral drugs and vaccines are still unavailable. Animal models that support adenovirus infection and pathogenesis are critical for the study of these viruses and the development of prophylactic and therapeutic strategies. However, the receptors of some human adenoviruses have not yet been identified, most human respiratory adenoviruses cannot infect rodents, and human adenoviruses cannot replicate in rodents due to host restrictions.These factors hamper the establishment of animal models that support adenovirus pathogenesis. In this review, we discuss recent advances in research into human adenovirus receptors, host range restriction factors and animal models, and provide insights for the development of animal models supporting adenovirus infection or/and pathogenesis.

We used molecular-biology methods to identify the pathogens that caused an outbreak of viral encephalitis in Guazhou (Gansu province, China)during June-August 2015.We also undertook molecular characterizations of these pathogens. A total of 132samples(14cerebrospinal fluid(CSF)samples;25throat swabs;66serum samples;27fecal samples)were collected from 74 patients during the outbreak of viral encephalitis. For CSF and serum samples, enzyme-linked immunosorbent assay immunoglobulin-M tests were undertaken to detect Japanese encephalitis viruses, enteroviruses, herpes simplex viruses, mumps viruses, and adenoviruses. Real-time polymerase chain reaction was done to detect enteroviruses(including coxsackievirus A16 and enterovirus 71) and the RNA of human adenoviruses. Then, viral isolation was carried out using HEp-2 and RD cells, and the entire VP1 region of positive viral isolates was amplified and sequenced. Finally, molecular characterizations of these pathogens were completed. Seventy two samples were identified as enteroviruses from 132 samples. Among them,71 were identified as echovirus(ECHO)30using enterovirus molecular typing. Japanese encephalitis viruses,herpes simplex viruses, mumps viruses, and adenoviruses were not detected.ECHO30 was isolated from 46 samples out of 29 patients.Similarities in nucleic acids among these ECHO30 isolates were 99.2%-100.0%.ECHO30 from Gansu province and other ECHO30 strains isolated in China since 2011 belonged to a same evolutionary branch.ECHO30 was the pathogen that caused the outbreak of viral encephalitis in Guazhou in 2015.ECHO30 from and Gansu province and ECHO30 isolated in China since 2011 belonged to the same evolutionary branch.

To understand the epidemiological etiology characteristics of hand, foot and mouth disease(HFMD)in Guangdong province, and to explore the risk change trend of the whole province. By using the descriptive epidemiological methods, the whole province’s incidence trend, population distribution and pathogenic form of HFMD were analyzed with the HFMD surveillance data,population data and geographic information of Guangdong province from 2008 to 2015.The analysis results show: A total of 2,133,722 cases of HFMD, including 5,066 severe cases and 259 death cases were reported in Guangdong province from 2008 to 2015.All the cities of Guangdong had HFMD cases, especially the Pearl River Delta Regions, which were on high-risk areas. There were two peaks every year, with the main peak of incidence occurred in spring and summer, and the sub peak occurred in autumn.Most cases were children aged<5years old, the proportion of this group in overall infections, the severe and death cases were 90.58%,95.93%and 97.30%,respectively,while the proportion for the children less than 3years old were 77.32% and 81.85%,respectively. The incidence of this disease among men was higher than that of women. Dynamic changes were presented between different years and seasons:CV-A16 was more popular in 2009,and enterovirus that none EV-A71 and none CV-A16 were predominant strains in 2013 and 2015.Especially in 2015,the proportion of other EV ranged as high as 71.97%.Besides,EV-A71 was the absolute predominance pathogen within death cases and was important pathogen in severe cases. This study suggests that HFMD epidemiology and laboratory monitoring in Guangdong Province should be strengthened, and provides scientific data support for further improvement of HFMD prevention and control strategies in Guangdong Province.

To study the effect of interferon(IFN)against hepatitis B virus(HBV)by silencing phospholipid scramblase (PLSCR)1in HepG2 cells. siRNA specific for PLSCR1 was designed and transfected in HepG2 cells. The inhibitory effect of siRNA was determined using semi-quantitative polymerase chain reaction(PCR)and western blotting 48hpost-transfection.HepG2 cells treated with IFN were co-transfected with plasmids expressing HBV1.3and siRNA targeting PLSCR1.Total RNA of HepG2 cells was isolated and the mRNA level of PLSCR1 measured by reverse-transcription semi-quantitative PCR. The expression of HBsAg in culture supernatants was determined by enzyme-linked immunosorbent assay. Expression of PLSCR1 was inhibited by siRNA911 in HepG2cells.Compared with the control, the level of HBsAg decreased in the cell supernatants of cells transfected with HBV1.3plasmid or NC-siRNA + HBV1.3plasmid.Compared with cells not treated with IFN, the level of HBsAg did not change significantly in the supernatants of cells transfected with siRNA + HBV1.3plasmid and treated with IFN. Inhibition of PLSCR1 could decrease the antiviral activity of IFN against HBV. These data suggest that PLSCR1 has an important role in the inhibition of HBV replication due to IFN.

This study aims to research the effect of inter-lineage reassortment of type B influenza virus on its biological characteristics. The representative strains isolated in 2013~2015were selected, which included wild type viruses and inter-lineage reassortment viruses. We tested the growth curve of each virus based on the value of TCID50 at different time point. And further detected the Km value of virus to analysis the activity of neuraminidase of each virus. The growth curve of viruses in 2013 and 2014reached peak 48 hours after infection, maintained at high level until 72 hours, then the virus titer declined gradually, however the virus isolated in 2015 reached peak 24 hours after infection. The reassortment strain B/Fujian Tongan/1565/2013 has the similar growth characteristics with the wild type virus on the same year. Meanwhile the growth curve of other inter-lineage viruses in 2014 and 2015is lower than that of wild type viruses. We determined neuraminidase kinetic constants of all viruses. The reassortment strain B/Fujian Tongan/1565/2013 has the strongest affinity of neuraminidase. The results of 2014~2015virus suggest that the stronger affinity of neuraminidase of virus the better growth characteristics of virus. But the virus in 2013 is lack of such relationship between the growth characteristics and activity of neuraminidase. The neuraminidase activity and growth characteristics of inter-lineage reassortments due to surface protein gene exchange is not consistent, suggesting internal virus protein might have affected the growth characteristics of the viruses2013-2015,and pending further study.

To establish a method for measurement of the neutralizing activity of a monoclonal antibody against the rabies virus. Twenty-four rabies street virus-positive samples were isolated by the mouse inoculation test. Isolated rabies street viruses were cultured and the virus titer tested in N2A cells. We established a rabies street virus bank with viruses that could adapt to the growth of N2A cells with a high titer. Then repeatability was evaluated after three detections of the TRN006 monoclonal antibody. Of the 24 positive samples,15 strains of the virus could adapt to N2A cells and form fluorescent foci in cells.Finally,10 strains with a high titer were selected for the rabies street virus bank, which covered nine Provinces of China and four Chinese lineages. Three lineages were used for the neutralization test for the monoclonal antibody, and the Student’s t-test showed that it had good repeatability.

The human metapneumovirus (HMPV) is an important pathogen in respiratory-tract infections in children. We undertook genomic sequence analyses and described the genetic characteristics of an uncommon sub-genotype, the HMPV A1 strain, and provide useful data for further studies. The HMPV A1(BJ-1610)strain was identified from a nasopharyngeal aspirate collected from a 3-month-old female with bronchopneumonia. Gene fragments of BJ-1610 were amplified by reverse transcription-polymerase chain reaction(RT-PCR)and assembled by DNAStar software. Sequence alignment for BJ-1610 and other HMPV reference strains with four known genotypes available in the GenBank database was conducted by DNAStar. Phylogenetic trees were created using MEGA 6.06 software. The whole genome of BJ-1610 was 13406nt in length (GenBank accession number:KU821121).Compared with HMPV reference strains,BJ-1610 shared the highest similarities with HMPV/AUS/150229278/2003/A(KC562226)from Australia, which was classified into sub-genotype A1.The nucleotide identity of the full genome between BJ-1610 and KC562226was 98.4%.N,P,F,M2-2and L genes had great similarity with KC562226 compared with other reference strains, whereas SH and G genes shared higher similarities with other strains of sub-genotype A1.Phylogenetic analyses of the whole genome showed that BJ-1610 was clustered into sub-genotype A1 and was close to KC562226.The N,P,M,F,M2-1,M2-2and L genes of BJ-1610 showed the same genetic features as the whole genome, whereas the variable genes SH and G were closest to KC403980.The F protein of BJ-1610 showed high genetic conservation. The length of the SH protein of BJ-1610 changed from 552 bp to 567 bp due to mutations in the stop codon. The amino-acid mutations on protein G led to a decrease in the number of N-glycosylation sites. As an infrequently circulating genotype, sequence analyses of the whole genome of a HMPV A1strain(BJ-1610)will promote further studies on its epidemiology and pathogenicity, and aid the development of vaccines and antiviral drugs.

We investigated infection by canine parvovirus and genetic variation of the VP2 gene. We collected feces samples of 50 diarrheal dogs in Sichuan Province, China. Analyses polymerase chain reaction (PCRs), agarose gel electrophoresis, and amplification of the complete sequence of canine parvovirus were done. We observed 19PCR-positive samples. Sequencing analyses of 15PCR-positive samples based on amplification of the complete VP2 gene showed all to be CPV-2a,and to be polymerized with Sichuan isolates. These results suggest that the common epidemic strain in Sichuan Province is CPV-2a,and may originate from the same strain. Compared with reference strains, there were no significant variations in canine parvovirus in Sichuan Province, China.