Xiao-Ai Zhang

Beijing Institute of Microbiology and Epidemiology, Peping, Beijing, China

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Publications (12)57.5 Total impact

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    ABSTRACT: Severe Fever with Thrombocytopenia Syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus. Until recently, SFTSV-associated encephalitis remained largely uninvestigated.
    Journal of Infection 08/2014; · 4.07 Impact Factor
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    ABSTRACT: Enterovirus 118 (EV-118) within species HEV-C was detected in two 5-month-old boys with pneumonia in China. The EV-118 from both cases was genetically closer to ISR10 strain from Israel than to PER161 strain from Peru based on VP1 gene sequences. The complete genome of the detected EV-118 consists of 7,360 nucleotides, excluding the poly (A) tail. The 5'UTR contains 669 nucleotides, and 3'UTR consists of 73 nucleotides. A single open reading frame from base 670 to 7,287 that encodes a 2,206-amino-acid polyprotein was featured. The base composition of the full genome is 27.9 % A, 24.2 % C, 24.4 % G, and 23.6 % U. Phylogenetic analysis of the full genome sequences illustrated EV-118 was genetically closer to EV-109 and EV-105, and the Chinese strain differed from Peru strain. In summary, the presence of EV-118 was confirmed in pediatric pneumonia cases and complete genome sequences were identified for the first time in China.
    Virus Genes 02/2014; · 1.84 Impact Factor
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    ABSTRACT: Human rhinovirus-C (HRV-C) has been increasingly detected in patients with acute respiratory diseases (ARDs). Prolonged surveillance was performed on children with ARD to investigate the molecular epidemiology and clinical characteristics of HRV in Chongqing, China. Nasopharyngeal aspirates (NPA) were collected from hospitalized children with ARD during 2009-2012. HRV-C was genotyped by sequencing the VP4/VP2 coding region. Among the 1,567 NPAs obtained, 223 (14.2%) were HRV positive, and 75.3% of these 223 NPAs were co-infected with other viruses. HRV-A (54.7%) and HRV-C (39.9%) accounted for the majority of HRV infections. Logistic regression models demonstrated significant associations between HRV-A, HRV-C, and asthma attacks, as well as between HRV-C and wheezing. A phylogenetic tree showed that HRV-C2 was the predominant type of HRV-C, followed by HRV-C43, HRV-C1, and HRV-C17. Three novel genotypes were proposed on the basis of a low identity with the known HRVs. Our results showed that HRV-A and HRV-C were the predominant types of HRV infection, and HRV-C showed a high genetic variation in Chongqing, China. HRV infection was associated with asthma attacks and wheezing; furthermore, HRV infections played a minor role in causing severe pneumonia. This knowledge provides information for the prevention and control of HRV associated with ARDs.
    Scientific reports. 01/2014; 4:6686.
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    ABSTRACT: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease of which the clinical progression and factors related to death are still unclear. To identify the clinical progression of SFTS and explore predictors of fatal outcome throughout the disease progress. A prospective study was performed in a general hospital located in Xinyang city during 2011-2013. Confirmed SFTS patients were recruited and laboratory parameters that were commonly evaluated in clinical practice were collected. The clinical progression was determined based on analysis of dynamic profiles and Friedman's test. At each clinical stage, the laboratory features that could be used to predict fatal outcome of SFTS patients were identified by stepwise discriminant analysis. Totally 257 survivors and 54 deceased SFTS patients were recruited and the data of 11 clinical and laboratory parameters along their entire disease course were consecutively collected. Three clinical stages (day 1-5 post onset, day 6-11 post onset and day 12 to hospital discharge) were determined based on distinct clinical parameters evaluations. Multivariate discriminant analysis at each clinical stage disclosed the indicators of the fatal outcome as decreased platelet counts at early stage, older age and increased AST level at middle stage, and decreased lymphocyte percentage and increased LDH level at late stage. The significant indicators at three clinical stages could be used to assist identifying the patients with high risk of death. This knowledge might help to perform supportive treatment and avoid fatality.
    Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 10/2013; · 3.12 Impact Factor
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    ABSTRACT: Background. The wider distribution and high case fatality rate have made severe fever with thrombocytopenia syndrome (SFTS) a significant public health problem. The study is designed to identify the predictors of fatal outcome and to evaluate the effectiveness of antiviral therapy in treating the SFTSV infected patients. Method. A cross-sectional study was performed in a general hospital located in Xinyang city with largest SFTS patients number during 2011-2012. The primary outcome for the treatment effect analysis was death. Other outcomes included sequential platelet levels, and viral loads observed throughout the hospitalization, and the period in days for platelet count return to normal level after starting ribavirin therapy. Results. Totally 311 SFTSV infected cases were included in the study. The most frequent clinical presentations were fever, weakness, myalgia and gastrointestinal symptoms. Each patient had both or either of thrombocytopenia and leucopenia. The case fatality ratio (CFR) was 17.4% (95% CI: 13.1%-21.6%). Older age (OR, 1.061, 95%CI, 1.023-1.099, P=0.001), decreased level of consciousness (OR, 5.397, 95%CI, 2.660-10.948, P<0.001), elevated levels of LDH (>1200 U/L) (OR, 2.620, 95%CI, 1.073-6.399, P=0.035 ), and CK (>800 U/L) (OR, 2.328, 95%CI, 1.129-4.800, P=0.022) were significantly associated with fatal outcome. The CFRs were similar between patients who received ribavirin or received no ribavirin therapy. Ribavirin treatment showed no significant effect on either platelet counts or viral loads during the hospitalization in either fatal or non-fatal cases. Conclusions. These findings can improve the knowledge on the fatal outcome discrimination and the use of antiviral drug for SFTS patients.
    Clinical Infectious Diseases 08/2013; · 9.37 Impact Factor
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    ABSTRACT: The long-term immunogenicity after novel vaccine against A(H1N1)pdm09 administration or natural infection has not been well investigated. Six cohorts of subjects were followed up for over one year: one-dose A(H1N1)pdm09 vaccine recipient, A(H1N1)pdm09-seasonal trivalent vaccine recipients in different orders, confirmed A(H1N1)pdm09 patients without vaccination, with previous A(H1N1)pdm09 or seasonal influenza vaccination. Peripheral blood mononuclear cells and sera samples were collected at baseline and month 1, 2, 3, 7 and 14 after vaccination (infection). The immunogenicity was determined by hemagglutination-inhibition (HI) and B cell enzyme-linked immunospot (ELISPOT) assays. Single dose of A(H1N1)pdm09 vaccine elicited antibody titer of greater than 1:40 in 40% adults for 1 year and mean live of this adequate antibody was determined as 8.35 months. In contrast, responses after natural infections had lower peaking level and a relatively longer antibody duration, with estimated mean lives of 11.8 months. Pre-vaccination with the seasonal flu vaccine led to a significant reduction in HI titer to A(H1N1)pdm09 one month after vaccination, while pre-vaccination with A(H1N1)pdm09 had no effect on seasonal influenza vaccination. Seasonal flu vaccination followed by A(H1N1)pdm09 infection elicited boosting effect on antibody response against A(H1N1)pdm09. A similar memory B cell response was elicited from both vaccination and infection by ELISPOT assay. The long-term decay of immunity for A(H1N1)pdm09 vaccine and natural infection indicates the need of revaccination after the host lose protection acquired from either vaccination or infection. Prior infection, rather than the pre-vaccination with seasonal influenza could act on the host immunity to elicit boosting effect on the A(H1N1)pdm09.
    Vaccine 05/2012; 30(32):4785-9. · 3.77 Impact Factor
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    ABSTRACT: Coxsackieviruses A10 (CV-A10) and A6 (CV-A6) have been associated with increasingly occurred sporadic hand-foot-mouth disease (HFMD) cases and outbreak events globally. However, our understanding of epidemiological and genetic characteristics of these new agents remains far from complete. This study was to explore the circulation of CV-A10 and CV-A6 in HFMD and their genetic characteristics in China. A hospital based surveillance was performed in three heavily inflicted regions with HFMD from March 2009 to August 2011. Feces samples were collected from children with clinical diagnosis of HFMD. The detection and genotyping of enteroviruses was performed by real-time PCR and sequencing of 5'UTR/VP1 regions. Phylogenetic analysis and selection pressure were performed based on the VP1 sequences. Logistic regression model was used to identify the effect of predominant enterovirus serotypes in causing severe HFMD. The results showed 92.0% of 1748 feces samples were detected positive for enterovirus, with the most frequently presented serotypes as EV-71 (944, 54.0%) and CV-A16 (451, 25.8%). CV-A10 and CV-A6 were detected as a sole pathogen in 82 (4.7%) and 44 (2.5%) cases, respectively. Infection with CV-A10 and EV-71 were independently associated with high risk of severe HFMD (OR = 2.66, 95% CI: 1.40-5.06; OR = 4.81, 95% CI: 3.07-7.53), when adjusted for age and sex. Phylogenetic analysis revealed that distinct geographic and temporal origins correlated with the gene clusters based on VP1 sequences. An overall ω value of the VP1 was 0.046 for CV-A10 and 0.047 for CV-A6, and no positively selected site was detected in VP1 of both CV-A10 and CV-A6, indicating that purifying selection shaped the evolution of CV-A10 and CV-A6. Our study demonstrates variety of enterovirus genotypes as viral pathogens in causing HFMD in China. CV-A10 and CV-A6 were co-circulating together with EV-71 and CV-A16 in recent years. CV-A10 infection might also be independently associated with severe HFMD.
    PLoS ONE 01/2012; 7(12):e52073. · 3.53 Impact Factor
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    Emerging Infectious Diseases 05/2011; 17(5):932-4. · 6.79 Impact Factor
  • Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 11/2010; 49(3):225-6. · 3.12 Impact Factor
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    ABSTRACT: We followed a cohort of 773 individuals who received a monovalent vaccine against 2009 pandemic influenza A (H1N1). Approximately 6 weeks after vaccination, 12 persons developed the disease. Three groups of subjects were studied (12 patients who had or had not received previous monovalent vaccine and 1 group of 49 control subjects who had previously been immunized with the same vaccine). For all patients, clinical features were characterized and the causative viruses sequenced for possible mutations. Nasopharyngeal swabs, serum specimens, and peripheral blood monocyte cells (PBMCs) were collected at different time points up to 11 weeks after symptom onset to measure the virus load and humoral and cellular immune responses. Serum samples and PBMCs were also collected from 49 and 16 vaccinated control subjects, respectively. Both patient groups had similar clinical manifestations. No substantial viral mutations were detected. Compared with unvaccinated patients, viral loads in vaccinated patients were initially higher, but the levels decreased faster to undetectable levels. However, the virus became detectable again for 6 of them. Two weeks after infection, vaccinated and unvaccinated patients had similar neutralizing antibody levels as the vaccinated control subjects. Thereafter, the neutralizing antibody levels decreased markedly in vaccinated patients. During the acute phase, memory T cell counts and tumor necrosis factor-α levels were significantly higher in vaccinated than in unvaccinated patients. Although the clinical consequences of infection are comparable between vaccinated and unvaccinated patients, humoral and cellular immune responses in vaccinated patients are boosted for some weeks, indicating an additional benefit of vaccination against 2009 pandemic influenza A (H1N1) virus.
    Clinical Infectious Diseases 10/2010; 51(9):1028-32. · 9.37 Impact Factor
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    ABSTRACT: To identify the prevalence of Anaplasma phagocytophilum in both wild rodents and domestic animals and to make clear the genetic characteristics of the agents from different animals in China, a total of 105 livestock and 159 small rodents were analyzed by real-time-PCR and sequence analysis. The prevalence rate was 6.7% (7/105) and 14.5% (23/159), respectively. The nucleotide sequences of 16S rRNA (rrs) from the positive livestock and rodents were identical to each other. The phylogenetic analysis based on partial A. phagocytophilum p44ESup1 gene revealed that A. phagocytophilum identified in this study was placed on a separate clade distinct from those in other continents. These findings indicated A. phagocytophilum in rodents might be able to infect livestock and intensified the threats of anaplasmosis to livestock in the area. Further studies on public health significance of the agent are worth investigation in future.
    Veterinary Microbiology 08/2010; 144(3-4):405-8. · 3.13 Impact Factor
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    ABSTRACT: In early September 2009, an outbreak of influenza occurred at a college campus in Beijing, China, in which both pandemic H1N1 and seasonal H3N2 viruses were detected. Outbreak investigation was performed in the campus. Epidemiologic, clinical data were collected by interviewing patients and retrieving medical records. Individual contact tracing was performed for detailed contact information. Viruses were identified by reverse-transcription polymerase chain reaction assays followed by sequence analysis. The hemagglutination inhibition test was used to detect antibodies to both viruses for paired serum samples. Forty of 45 people with influenza-like illness had laboratory-confirmed influenza A infection; 22 of these 40 people were infected with pandemic H1N1 virus, 12 were infected with seasonal H3N2 virus, and 6 were coinfected with both viruses. In the subsequent generation of cases with mixed infection, we detected pandemic H1N1 virus infection more often than seasonal H3N2 virus infection. The clinical patterns were essentially similar for patients with different virus infections. No substantial differences in sequences were observed in either pandemic H1N1 or seasonal H3N2 virus between patients with mixed and single infection. Sequence analyses revealed that all of the detected viruses were susceptible to oseltamivir but resistant to adamantane. Hemagglutination inhibition tests of paired serum samples confirmed mixed infection in the outbreak. Cocirculation of pandemic H1N1 virus and seasonal H3N2 virus led to a mixed infection in patients. Pandemic H1N1 virus, however, took prevalence over seasonal influenza virus in the course of transmission. Therefore, competitive circulation of seasonal influenza A virus with the pandemic H1N1 virus seems less likely.
    Clinical Infectious Diseases 04/2010; 50(10):1359-65. · 9.37 Impact Factor