Search

ObjectiveTo determine the epidemiological and etiological characteristics of hand，foot，and mouth disease （HFMD） in Pujiang County from 2008 through 2020， so as to provide scientific evidence for prevention and control measures.MethodsDescriptive epidemiological analysis was used to analyze HFMD cases retrieved in the Chinese Information System for Disease Control and Prevention in Pujiang County during 2008‒2020.ResultsFrom 2008 through 2020， a total of 9 393 cases were documented in Pujiang County， with an annual incidence of 182.3 per 100 000， showing a trend of alternating high-incidence and low-incidence years. The seasonal distribution was bimodal， and the incidence peaked in May-July and November-December. The incidence of HFMD in urban areas was significantly higher than that in rural areas， and the incidence was positively correlated with population density. Majority of cases （94.9%） were children under 5 years old， of which boys had higher incidence than girls. The number of documented cases was the highest among preschool children living in families and kindergartens， accounting for 97.3%. Totally， 558 cases were laboratory confirmed in Pujiang County in 2008-2020， of which severe cases were all caused by EV71 infection.ConclusionEnterovirus serotypes in HFMD have continually changed from 2008 through 2020 in Pujiang County. However， severe HFMD remains principally attributable to EV71 infection， suggesting that it is necessary to strengthen the surveillance on the etiology of HFMD. In addition， it warrants further promotion of EV71 vaccination.

Objective To analyze the relationship among the expression of CD4+T lymphocytes subset in the peripheral blood in different children with hand，foot and mouth disease (HFMD) infected by EV71 and the patients’ages as well as the severity degree of this disease. Methods We collected 138 peripheral blood samples derived from the confirmed cases with foot-and-mouth disease in the infectious disease department at Kunming children's Hospital between July and March in 2014， including 33 mild cases， 45 severe cases， and 60 critical cases. Patient ages were 9 months and 5 years. Using flow cytometry， we detected the expression of CD4+T lymphocyte subsets in different age groups and different conditions of HFMD groups. Results Compared to the reference value of CD4+T cells in normal healthy children， the percentages of CD4+T lymphocyte subsets in the peripheral blood were decreased evidently in all of these groups， in which the expression of CD4+T cells was lowest in 5-year-old severe and critical cases. Moreover， in these age groups， significantly differences were found between the mild and severe patients groups， and mild and critical cases (P<0.05). In addition， there was no correlation between the expressions of CD4+T cells in the mild type， severe and critical HFMD patients， but there was a statistically significant difference in the relative percentage of CD4+T cells in 15 months ~ 2 years and 2 ~ 5 years children in the critical type (P<0.05). Moreover， CD4+T cells at 15 months ~ 2 years old were significantly higher than those at ~ 5 years old， suggesting that the author should pay attention to distinguish different age groups of children when regularly monitoring the expressions of CD4+T cells in the peripheral blood of children with severe HFMD. Conclusion The aggravation of EV71 HFMD in children is closely related to the decreased expression of CD4+T cells in the peripheral blood， and the expressions of CD4+T cells in severe HFMD patients is related to age. We predicted that the cell immunity mediated by age related CD4+T cells might be inhibited or influenced by the immune escape mechanism of EV71， which could cause the aggravation of the disease. This might be the primary reason why EV71 can easily lead to severe HFMD in patients. [ABSTRACT FROM AUTHOR]

Objective To identify the role of RNA-editing enzyme ADAR1 (adenosine deaminase acting on RNA) in EV71 infection and virus mutation. Methods RNAi technology was applied to establish ADARl knock-down stable cell lines. Then the cells were served to evaluate the role of ADAR1 in EV71 infection by MTT assay for detecting virus-induced cell viability, virus plaque assay for quantification of the virus titer and the cellular susceptibility to the virus, and Western blot for virus protein expressions. ADAil-mediated RNA editing can resutt in the genetic A-G and T-C mutations. To further determine whether the effects of ADARl on EV7l infection were correlated with ADARl-mediated EV7l RNA editing and therefore increased the viral mutations during the infection， the characteristics of EV7l mutation were analyzed based on the different full-length viral genomes from epidemic regions. The viral genome was also sequenced from the infected ADARl knock-down cells. Results After ADA.R1 knock-down, the cell viability decreased quickly after the virus infection, and formed much more and larger sizes of plaques than the control cells. The virus capsid protein VPl expressions and virus titer in the cells culture media were both increased in ADARl knockdown cells. Statistic analysis showed that A-G and T-C mutations were the major mutations of EV71, which were believed to be the hot sites for RNA-editing. However, the results of viral RNA genomic sequencing data indicated that ADARl did not edit EV71 genome directly. Conclusions ADARl was a restriction factor for controlling EV71. However, ADARl does not directly edit EV71 genome. [ABSTRACT FROM AUTHOR]