实验与检验医学
實驗與檢驗醫學
실험여검험의학
EXPERIMENTAL AND LABORATORY MEDICINE
2013年
6期
533-534,588
,共3页
胡芹%涂智杰%吴集才%魏建萍%张敏%曹健
鬍芹%塗智傑%吳集纔%魏建萍%張敏%曹健
호근%도지걸%오집재%위건평%장민%조건
手足口病%肠道病毒71型%VP1基因%基因型
手足口病%腸道病毒71型%VP1基因%基因型
수족구병%장도병독71형%VP1기인%기인형
Hand-foot-mouth disease%Enterovirus 71%VP1 gene%Genotype
目的:分析2011年景德镇地区两例临床症状不同的EV71手足口重症病例病毒株的分子生物学特征。方法采集2例临床症状不同的手足口病重症患者咽拭子标本,进行病毒分离和逆转录-聚合酶链反应(RT-PCR),并将其与GenBank已上传的其他EV71病毒株的VP1区进行相关生物信息学分析。结果两例临床症状不同的重症病例都由EV71病毒引起,他们都同属于C4a亚型,通过氨基酸序列比对发现它们在四个氨基酸的位点上存在变异引起不同临床症状,其中有神经症状的患儿出现第19位丙氨酸由缬氨酸取代(A→V),第106位酪氨酸由苯丙氨酸取代(Y→F);无神经症状的患儿出现第19位丙氨酸由半胱氨酸取代(A→C),第38位精氨酸由谷氨酰胺取代(R→Q),第293位丙氨酸由丝氨酸取代(A→S)。结论 EV71病毒是引起手足口重症病例的主要病原,临床症状的差异性主要体现在有无神经系统症状,通过基因分析发现不同位点氨基酸的突变可能成为临床症状差异性形成的生物学基础。
目的:分析2011年景德鎮地區兩例臨床癥狀不同的EV71手足口重癥病例病毒株的分子生物學特徵。方法採集2例臨床癥狀不同的手足口病重癥患者嚥拭子標本,進行病毒分離和逆轉錄-聚閤酶鏈反應(RT-PCR),併將其與GenBank已上傳的其他EV71病毒株的VP1區進行相關生物信息學分析。結果兩例臨床癥狀不同的重癥病例都由EV71病毒引起,他們都同屬于C4a亞型,通過氨基痠序列比對髮現它們在四箇氨基痠的位點上存在變異引起不同臨床癥狀,其中有神經癥狀的患兒齣現第19位丙氨痠由纈氨痠取代(A→V),第106位酪氨痠由苯丙氨痠取代(Y→F);無神經癥狀的患兒齣現第19位丙氨痠由半胱氨痠取代(A→C),第38位精氨痠由穀氨酰胺取代(R→Q),第293位丙氨痠由絲氨痠取代(A→S)。結論 EV71病毒是引起手足口重癥病例的主要病原,臨床癥狀的差異性主要體現在有無神經繫統癥狀,通過基因分析髮現不同位點氨基痠的突變可能成為臨床癥狀差異性形成的生物學基礎。
목적:분석2011년경덕진지구량례림상증상불동적EV71수족구중증병례병독주적분자생물학특정。방법채집2례림상증상불동적수족구병중증환자인식자표본,진행병독분리화역전록-취합매련반응(RT-PCR),병장기여GenBank이상전적기타EV71병독주적VP1구진행상관생물신식학분석。결과량례림상증상불동적중증병례도유EV71병독인기,타문도동속우C4a아형,통과안기산서렬비대발현타문재사개안기산적위점상존재변이인기불동림상증상,기중유신경증상적환인출현제19위병안산유힐안산취대(A→V),제106위락안산유분병안산취대(Y→F);무신경증상적환인출현제19위병안산유반광안산취대(A→C),제38위정안산유곡안선알취대(R→Q),제293위병안산유사안산취대(A→S)。결론 EV71병독시인기수족구중증병례적주요병원,림상증상적차이성주요체현재유무신경계통증상,통과기인분석발현불동위점안기산적돌변가능성위림상증상차이성형성적생물학기출。
Objective To analyze the molecular characterization of two enterovirus 71 (EV71) strains isolated from two severe hand foot mouth disease (HFMD) patients with different clinical symptoms in Jingdezhen City in 2011. Methods Throat swab specimens were collected from the two patients and EV71 were isolated for reverse transcription-polymerase chain reaction (RT-PCR) analysis. The differences of VP1 region genotype between the isolated virus and virus in GenBank were analyzed. Results Both patients with different severe clinical symptoms were caused by EV71 C4a subtype. Using amino acid sequence alignment, we found that there were four mutated amino acids and they would cause the different clinical symptoms. In EV71 isolated from pa-tient with neurologic symptoms, the 19th amino acid alanine was replaced by valine (A→V), the 106th amino acid tyrosine was re-placed by phenylalanine (Y→F). And in EV71 isolated from patient with no neurologic symptoms, the 19th amino acid alanine was replaced by cysteine (A→C), the 38th amino acid arginine was replaced by glutamine (R→Q), the 293rd amino acid alanine was replaced by serine (A→S). Conclusion EV71 is the main pathogen of severe HFMD. The differences of clinical symptoms mainly reflect in the presence of neurologic symptoms. Different locus mutation of amino acids in EV71 may be the biological basis of the different clinical symptoms.