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Objective:To investigate changes in the expression of Cosmc and T-synthase in peripheral B lymphocytes and in serum levels of galactose-deficient IgA1 (Gd-IgA1) in patients with Henoch-Sch?nlein purpura (HSP) .Methods:From January to August 2014, 56 patients with HSP were collected from outpatient or inpatient department of dermatology and venereology in the Second Hospital of Hebei Medical University, and were divided into 4 groups, including skin type group (22 cases) , joint type group (9 cases) , abdominal type group (12 cases) and renal type group (13 cases) . Twenty healthy volunteers served as healthy controls. Real-time fluorescence-based quantitative PCR was performed to determine the mRNA expression of Cosmc and T-synthase in peripheral B lymphocytes, and a lectin-based enzyme-linked immunosorbent assay (ELISA) to detect the serum level of Gd-IgA1. Comparisons among multiple groups were performed using one-way analysis of variance or Kruskal-Wallis H test, multiple comparisons were performed using least significant difference (LSD) - t test or Nemenyi test, and correlation analysis was performed using Spearman rank correlation analysis. Results:There was a significant difference in the duration from disease onset to the clinic visit ( χ2= 26.19, P < 0.05) among the skin type group (6.27 ± 3.09 d) , joint type group (5.56 ± 3.05 d) , abdominal type group (6.75 ± 3.75 d) , and renal type group (26.23 ± 14.12 d) , and the duration from disease onset to the clinic visit was significantly longer in the renal type group than in the other 3 groups (all P < 0.05) . The Cosmc mRNA expression significantly differed among the skin type group, joint type group, abdominal type group, renal type group and healthy control group (0.849 ± 0.239, 0.767 ± 0.181, 0.719 ± 0.183, 0.459 ± 0.121, 1.146 ± 0.232, F= 23.37, P < 0.05) , was significantly lower in the 4 patient groups than in the healthy control group ( P < 0.01) , and lower in the renal type group than in the other 3 patient groups (all P < 0.01) . There was no significant difference in the T-synthase mRNA expression in peripheral B lymphocytes among the patient groups and healthy control group ( F= 1.05, P > 0.05) . The serum level of Gd-IgA1 significantly differed among the skin type group, joint type group, abdominal type group, renal type group and healthy control group ( F= 7.06, P < 0.05) . Moreover, the Gd-IgA1 level was significantly higher in the patient groups than in the healthy control group (all P < 0.05) , and higher in the renal type group than in the other 3 patient groups (all P < 0.05) . The serum level of Gd-IgA1 in the HSP patients was significantly and negatively correlated with the mRNA expression of Cosmc ( rs=-0.50, P < 0.01) . Conclusion:Decreased mRNA expression of Cosmc and increased serum levels of Gd-IgA1 were observed in patients with HSP, and there was a negative correlation between the two indices.
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Objective@#To find out the source and the epidemic pattern of norovirus outbreak in July, 2016 to June, 2017 in Guangzhou.@*Methods@#The stool samples and clinical information of diarrhea cases were collected by the sentinel hospitals and CDCs; a real-time RT-PCR method was used to detect the norovirus nucleic acids from the samples, the positive ones were amplified and sequenced; the partial sequences of norovirus were aligned by an online BLAST alignment, and a phylogenetic tree was constructed by a neighbor-joining method .@*Results@#A total of 854 cases with infectious diarrhea were reported by Guangzhou diarrhea surveillance network from July, 2016 to June, 2017; the gender ratio (male versus female) was 1∶0.67; 78.33% of the cases were preschool children under the age of 7 years. Totally 220 samples were detected norovirus G II+ (25.76%, including 5 double-positive samples with G I+ ). GII.Pe-GII.4.Sydney_2012 was the prevalent genotype in the second half of 2016 (94.64%), which was replaced by GII.P16-GII.2 in the first half of 2017 (67.65%). Since September 2016, the reported number of norovirus-caused diarrhea epidemic was increased gradually; the peak of epidemic curve emerged in February to March of 2017, and the number started to decrease since April. In May to June there were only 2-3 epidemics reported monthly. All the endemics from September to November 2016 were caused by genotype GII.Pe-GII.4.Sydney_2012; the endemics from December 2016 to April 2017 were mainly caused by genotype GII.P16-GII.2. Some samples from kitchen workers and babysitters were detected GII+ , which was consistent with the result of the cases′ samples.@*Conclusions@#It was the first time that the novel GII.P16-GII.2 recombinant strain outbroke occurred in Guangzhou City and homology analysis also suggested that GII.P16-GII.2 was the main source of those epidemics in 2016 -2017 winter and spring season. Furthermore, The kitchen workers and babysitters may have played an important role in the spread of norovirus.
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Objective To understand the epidemiological and molecular characteristics of a norovirus-borne outbreak caused by GⅡ.4 Sydney 2012 in a university of Guangzhou to provide evidence for the prevention and control strategy on norovirus-caused epidemics.Methods A self-designed questionnaire was used to collect clinical information from the patients as well as other data related to the epidemic.Pathogen detections were performed through anal swab specimens from the patients,kitchen workers and samples from the environment.Positive samples were further sequenced for phylogenetic analysis.A case-control study was employed to identify the risk factors related to this outbreak.Results A total of 226 cases of norovirus-borne infection were identified between September 17 and 21,2017,including 223 students,with an attack rate of 0.73％ (223/30 711),and 3 kitchen workers.Students staying in the A dormitory area had the highest attack rate (1.73％,164/9 459).No clustering was found in different colleges or classes.Results from the case-control study revealed that people who ate at the canteen in A dormitory area during September 18 to 20 was at risk for the onset of illness (OR=10.75,95％CI:5.56-20.79).The highest risk was related to the dinner on September 18.Another significant risk factor (OR=3.65,95％ CI:1.92-6.94) was close personal contact in the same room of the dorm.The 3 norovirus infected kitchen workers were all from the canteen in A dormitory area where the positive rate of norovirus identified in kitchen workers was 26.67％ (12/45).Positive samples were sequenced and sub-typed with results showing that the GⅡ.4 Sydney 2012 variant and the nucleotide sequences of cases and kitchen workers were 100％ identical.Conclusions The outbreak was caused by norovirus GⅡ.4 Sydney 2012 variant at campus.Similar outbreaks had been seen since 2013,with the routes of transmission most likely due to food-borne or personal contact.
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Objective To understand the epidemiological and molecular characteristics of a norovirus-borne outbreak caused by GⅡ.4 Sydney 2012 in a university of Guangzhou to provide evidence for the prevention and control strategy on norovirus-caused epidemics.Methods A self-designed questionnaire was used to collect clinical information from the patients as well as other data related to the epidemic.Pathogen detections were performed through anal swab specimens from the patients,kitchen workers and samples from the environment.Positive samples were further sequenced for phylogenetic analysis.A case-control study was employed to identify the risk factors related to this outbreak.Results A total of 226 cases of norovirus-borne infection were identified between September 17 and 21,2017,including 223 students,with an attack rate of 0.73％ (223/30 711),and 3 kitchen workers.Students staying in the A dormitory area had the highest attack rate (1.73％,164/9 459).No clustering was found in different colleges or classes.Results from the case-control study revealed that people who ate at the canteen in A dormitory area during September 18 to 20 was at risk for the onset of illness (OR=10.75,95％CI:5.56-20.79).The highest risk was related to the dinner on September 18.Another significant risk factor (OR=3.65,95％ CI:1.92-6.94) was close personal contact in the same room of the dorm.The 3 norovirus infected kitchen workers were all from the canteen in A dormitory area where the positive rate of norovirus identified in kitchen workers was 26.67％ (12/45).Positive samples were sequenced and sub-typed with results showing that the GⅡ.4 Sydney 2012 variant and the nucleotide sequences of cases and kitchen workers were 100％ identical.Conclusions The outbreak was caused by norovirus GⅡ.4 Sydney 2012 variant at campus.Similar outbreaks had been seen since 2013,with the routes of transmission most likely due to food-borne or personal contact.
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<p><b>OBJECTIVE</b>To investigate the characteristics and dynamic changes of serum neutralizing antibody response in patients with primary infection of dengue virus type 1 (DENV-1).</p><p><b>METHODS</b>Serum samples were obtained from the same patients with primary infection of DENV-1 within 2 weeks after symptom onset in 2006 and in 2010. A group-specific DENV NS1 capture ELISA-based micro-neutralizing test (ELISA-MNT) capable of detecting neutralizing antibodies against all the 4 serotypes of DENV was used to test the neutralizing antibody titers against DENV in the serum samples. The neutralizing antibody titers against a standard strain and 2 clinically isolated strains of DENV-1 were detected in serum samples collected in 2010.</p><p><b>RESULTS</b>Cross-reactive neutralizing antibody response against all the 4 serotypes of DENV was found in both of the serum samples collected in 2006 and 2010, but the samples collected in 2006 showed stronger cross-reactive neutralizing antibody responses. The neutralizing antibody against DENV-2, rather than the anticipated DENV-1 antibody, had the highest titer in the samples collected in 2006, whereas the antibody against homologous DENV-1 had the highest titer in the samples obtained in 2010. The neutralizing antibody titers against the homologous DENV-1 was significantly higher in samples collected in 2010 (U=86.500, P=0.000), which also demonstrated significantly different neutralizing antibody titers against the 3 different strains of DENV-1 (Χ(2)=12.123, P=0.002).</p><p><b>CONCLUSION</b>The production of cross-reactive neutralizing antibodies between the 4 serotypes of DENV is a characteristic of DENV infection, particularly during early infection, but only the homologous neutralizing antibody increases obviously over time. The titers of the neutralizing antibodies against different strains, even of the same serotype, may differ distinctly.</p>