OBJECTIVETo identify the enterovirus from stool samples of patients with hand, foot and mouth disease(HFMD) in Guangzhou from 2010 to 2012 and to perform phylogenetic analysis of the VP1 gene sequences of coxsackievirus A4 and coxsackievirus A10.

METHODSA total of 5 484 samples of suspected cases of HFMD which Guangzhou Center for Disease Control received from 2010 to 2012 were collected.Virus RNA was tested by nested RT-PCR method as human enterovirus 71, coxsackievirus A16, coxsackievirus A4, coxsackievirus A10 and other enteroviruses positive, and 4 111 samples were positive. Phylogenetic tree was constructed by partial VP1 gene sequences of coxsackievirus A4 and coxsackievirus A10 to perform phylogenetic analysis.

RESULTSIn 4 111 enterovirus-positive samples, the positive rate of EV71, CoxA16, CoxA10 and CoxA4 was 35.1% (1 443/4 111) , 30.7% (1 261/4 111) , 2.0% (82/4 111),0.8% (31/4 111) respectively. Different enterovirus-positive rate was statistically significant (χ(2) = 148.34, P < 0.05) .Incidences of coxsackievirus A4 positive was highest in 3-year old children as 1.3% (7/534) , and that of coxsackievirus A10 positive was highest in 0-year old children as 3.7% (34/914) . The highest positive rate of diagnosed coxsackievirus A4 positive cases was admitted in April(2.6%, 12/460) , and the highest positive rate of diagnosed coxsackievirus A10 positive cases was admitted in August 4.3% (12/278). Phylogenetic analysis indicated that all the CoxA4 stains were divided into subtype A and subtype B, and the CoxA10 stains were divided into subtypes A, subtype B and subtype C. The VP1 gene nucleotide sequences of CoxA4 and CoxA10 this study measured both belonged to subtype A.

CONCLUSIONSThe VP1 gene nucleotide sequences of CoxA4 and CoxA10 in Guangzhou from 2010 to 2012 both belonged to subtype A.

Child ; China ; epidemiology ; Enterovirus A, Human ; Hand, Foot and Mouth Disease ; Humans ; Molecular Epidemiology ; Phylogeny ; Polymerase Chain Reaction ; RNA, Viral

Mast cells are crucial effector cells in allergic reactions,where IgE is the most notably mechanism to trigger their degranulation and release large amounts of allergic mediators.However,IgE is not the only way to stimulate these cells to degranulate.There is a lot of stimuli,such as complement,neuropeptides,cytokines and other inflammatory products,which can directly trigger mast cell degranulation,and cause selective release of mediators.These mediators are closely related to many allergic and inflammatory diseases.The paper will focus on the activation of non-IgE stimulated human mast cells,and describe the allergic and inflammatory diseases briefly,and provide the theoretical basis for clinical detection,diagnosis and treatment.