重庆市九龙坡区2005—2007年麻疹流行病学分析

目的了解九龙坡区麻疹的流行病学特征，为更好地制定有针对性的控制措施提供依据。方法利用办公软件Excel2003对九龙坡区2005—2007年麻疹疫情资料和监测资料进行分析。结果2005—2007年九龙坡区麻疹年平均发病率为10．59／10万。发病地区有明显的聚集趋势，发病时间有一定的季节性，男女性别比为1．30：发病以0-6岁儿童为主，占病例总数的76．36％，无免疫史病例占67．83％。结论无麻疹疫苗免疫史是麻疹发病的最主要危险因素．以后应减少〈8个月婴儿的暴露机会，加强≥8个月龄婴儿麻疹疫苗的及时和有效接种，加强麻疹疫情监测，完善流动儿童的计划免疫管理，减少免疫空白，保护易感人群。     

东莞市常平镇2005—2007年麻疹疫情分析及防制对策探讨

目的了解东莞市常平镇麻疹流行规律，预测流行趋势，制定防制对策，降低发病率，保护易感人群。方法收集2005—2007年东莞市常平镇的麻疹发病资料进行统计分析。结果2005—2007年东莞市常平镇共报告麻疹病例369例，年均报告发病率为29．46／10万，年均发病率外来暂住人口显著高于本地人口（x^2=10．354，P〈0．01）；麻疹发病有明显的周期性，3-8月份发病例数占全年总数的87．2％，流行模式为散发和爆发并存,以散发为主；发病年龄向低年龄组（〈8个月）和高年龄组（〉14岁）转移；2005年以来麻疹疫苗基础免疫年平均接种率为90．2％，本地儿童高于外来流动儿童。结论外来暂住人口中的散居儿童和工厂员工是东莞市常平镇麻疹发病的主要对象，外来暂住人口数影响当地麻疹发病率。建议采取以加强外来流动儿童麻疹常规免疫和外来青工麻疹免疫为主的综合防制措施。     

广州市2002-2005年麻疹流行病学特征及控制措施探讨

目的通过分析近年来广州市麻疹流行病学特征,为探讨麻疹控制措施提供理论依据。方法对2002-2005年麻疹发病情况进行描述性流行病学分析。结果广州市2002-2005年国家法定传染病报告系统共报告麻疹病例数5014例,报告年发病率分别为2.16/10万、3.58/10万、29.10/10万、22.33/10万;期间发生16起麻疹暴发疫情;发病数前5位的区按先后排序为白云区、番禺区、海珠区、花都区、天河区,以上5区病例数占全市病例数的81.41%;3～7月为高发季节,占全年总病例数的74.09%;14岁以下为高发年龄,占总病例数的69.37%;病例以流动人口为主,占总病例数77.26%;有明确免疫史病例仅占总病例数12.98%。结论广州麻疹发病有回升趋势,疫情形势严峻,应采取加强学校验证入学、麻疹疫苗查漏补种、强化疫点处理等综合防控措施。     

宿州市2005-2008年麻疹流行特征分析及消除对策探讨

目的研究宿州市2005-2008年麻疹的流行特征,探讨消除麻疹的措施。方法采取描述性流行病学方法 ,对麻疹监测系统的数据进行统计分析。结果 2005-2008年宿州市麻疹年均发病率为5.18/10万,2005年发病率最高;以小年龄组发病为主,5岁以下的小年龄组发病呈逐年上升趋势,尤其是〈1岁组儿童发病上升明显。对184例8月龄至5岁的麻疹病例进行麻疹疫苗（MV）免疫接种史情况分析,0剂次者占39.13%,1剂次者占35.33%,接种剂次不详者占22.28%。结论开展MV强化免疫活动,做好常规免疫接种工作,提高MV接种率和及时接种率,加强麻疹疑似病例的监测,预防医院内感染等是宿州市实现控制和消除麻疹目标的关键。     

广州市2007年与2008年麻疹流行特征比较

目的分析2008年与2007年麻疹的流行特征,比较两年间流行特征的异同,为2008年后半年麻疹的控制重点提供依据。方法利用《麻疹疫情监测系统数据》中麻疹的个案资料,抽取广州市2007年3-9月的2809例麻疹病例,及2008年1-5月的1003例病例,对其免疫史情况、发病年龄构成、户籍性质分布等进行比较分析。结果两年间麻疹病例的平均年龄差异无统计学意义（P〉0．05）;2008年上半年,相比2007年8月龄-14岁麻疹免疫目标人群发病所占比例下降（P〈0．05）,未到初免年龄（8月龄）病例中6-8月龄占了绝大部分比例;两年中免疫空白病例仍然是发病的重点人群;流动人口仍然是发病的主要人群。结论麻疹免疫目标人群的麻疹控制较2007年取得了一定的成绩,非目标人群（8月龄-14岁以外人群）、免疫空白人群及流动人口是麻疹控制的重点。     

广州市海珠区2007-2010年麻疹、风疹检测结果分析

目的分析广州市海珠区2007-2010年麻疹、风疹流行特征,为麻疹、风疹的预防和控制提供可靠依据。方法对辖区内2007-2010年的麻疹、风疹病例的实验室检测结果进行统计分析。结果辖区内2007-2010年间麻疹年平均发病率为15.61/10万;风疹年平均发病率为2.57/10万。麻疹病例多集中在婴幼儿及中青年人群;风疹病例以10～25岁青少年为主,且麻疹、风疹的病例发生具有明显的季节性。结论要达到消除麻疹、控制风疹发病率的目标,应继续做好计划免疫工作,提高免疫覆盖率,严密监测,预防暴发。     

北京市2007-2010年风疹病原学监测

目的 对北京地区风疹病原学进行监测.方法 收集风疹疑似病例血清标本和尿液和(或)咽拭子,用于血清学检测和病毒分离.病毒分离物和临床标本中的核酸利用real-time PCR方法进行检测.结果 2007-2010年,共收集99个风疹疑似病例血清标本和临床标本,血清学确诊55个病例(56%),病毒分离确诊51个病例(52%).回顾性检测疑似风疹病例及尿液和(或)咽拭子核酸,共确诊72个风疹病例(73%).分离的风疹病毒基因型主要为1E基因型.结论 北京地区主要流行的风疹病毒为1E基因型别.

Abstract：

Objective To clarify the pathogen for rubella in Beijing from 2007 to 2010. Methods Beijing Center for Disease Preventipn and Control ( CDC ) collected the specimens (including blood, urine and throat swab specimens) frqm clinically diagnosed rubella cases for serological test and virus isolation. The nucleic acid of rubella virus in clinical specimens and isolations was detected by real-time PCR. Results Fifty-five out of 99 blood specimens were positive for anti- rubella IgM. Fifty-one out of 99 clinically diagnosed rubella cases were confirmed as rubella cases by virus isolation. Seventy-two were confirmed as rubella virus infections with real-time PCR method for detecting the nucleic acid of rubella virus in clinical specimens. Compared with the sequences of reference strains of rubella virus, all of detected rubella virus belonged the IE gene type. Conclusion This study indicates that IE gene type virus was the predominant endemic rubella virus in Beijing.     

阳春市2000—2007年麻疹流行病学分析

目的分析阳春市2000—2007年麻疹流行病学特征,探讨麻疹的预防控制措施。方法采用描述流行病学的方法对2000—2007年阳春市麻疹监测资料进行统计分析。结果2000—2007年阳春市麻疹年均发病率为2．75／10万,2004年发病率最高（5．90／10万）,2005年开展了一次强化免疫和查漏补种工作后,2006发病率显著下降（0．28／10万）。每年3～7月为发病的高峰期;发病年龄主要集中在8月龄～15岁儿童,占总病例的97．01％;发病地区主要集中在春城、圭岗、永宁,占总病例的53．85％。结论2000—2007年阳春市麻疹疫情不稳定,呈现季节集中、年龄集中、地区集中的趋势,需进一步健全麻疹监测系统,加强麻疹免疫接种工作,并适时开展强化免疫活动。     

泉州市2009年麻疹监测结果分析

目的 分析泉州市2009年麻疹监测结果,为制定消除麻疹策略提供科学依据。方法 按国家麻疹监测方案开展监测工作,应用描述流行病学方法和Excel 2003软件对2009年麻疹监测结果进行分析。结果 2009年共有132例麻疹疑似病例纳入麻疹监测信息报告管理系统管理,确诊15例,发病率为0.19/10万,排除病例报告发病率﹥1/10万的县（市、区）占41.67%;48 h个案调查率为96.09%,7 d内血清检测结果及时报告率达到85.51%;血标本采集率为52.27%（69/132）,检测麻疹IgM阳性率为21.74%,检测风疹IgM阳性率为42.03%。73.33%的病例集中在晋江;53.33%的病例集中在1月份和4月份;66.67%的病例集中在0～7月龄小年龄组和﹥14岁的大年龄组;无免疫史和免疫史不详者占73.33%;66.67%的病例是流动人口;60%的病例在发病前7～21 d去过医院。结论 泉州市2009年麻疹监测的敏感性和特异性均较低;无MV免疫史和免疫史不详的人群是麻疹发病的高危人群。     

2007-2010年广州市海珠区疑似麻疹风疹病例血清学检测结果分析

目的分析广州市海珠区2007-2010年麻疹及风疹的流行特征。方法采用IgM抗体捕捉ELISA对广州市海珠区2007-2010年麻疹、风疹疑似病例血清标本进行IgM抗体检测。数据用SPSS13.0进行统计分析。结果麻疹IgM抗体总阳性率为44.30%,风疹IgM抗体总阳性率为13.09%,各年度麻疹、风疹的阳性率差异有统计学意义（χ2=171.708,P〈0.05;χ2=34.191,P〈0.05）。男女麻疹、风疹病例性别分布差异均无统计学意义。麻疹阳性病例年龄主要分布在8月龄～7岁及15～29岁,风疹阳性病例年龄主要分布在15～29岁。4年间麻疹、风疹阳性病例分别集中在3～7月、3～6月。结论海珠区2010年麻疹阳性率较前几年明显降低,说明防控措施有力,但2010年风疹的阳性率升高应引起足够的重视。麻疹的发病人群主要为学龄前儿童和青年,风疹的发病人群以青年为主。春季为麻疹、风疹的高发季节,应适时进行防控,避免暴发流行。     

Molecular surveillance of rubella viruses in Taiwan from 2005 to 2011

Rubella has been listed as a mandatory notifiable disease in Taiwan since 1988. Because of high coverage rates with an effective vaccine, rubella cases have decreased dramatically in Taiwan since 1994. However, rubella outbreaks still occur due to imported transmission. Five large clusters were detected in Taiwan from 2007 to 2011. In 2007, one cluster was caused by rubella genotype 1E viruses that were imported from Vietnam, whereas another cluster was caused by genotype 2B viruses and was untraceable. In 2008, two clusters were caused by different lineages of genotype 1E viruses that were imported from Malaysia. In 2009, a cluster that was caused by genotype 2B viruses was associated with imported cases from Vietnam. The rubella viruses from 124 confirmed cases from 2005 to 2011 were characterized, and the data revealed that these viruses were distributed in the following four genotypes: 1E (n = 56), 1h (n = 1), 1j (n = 4), and 2B (n = 63). Of these viruses, 93 (75%) were associated with imported cases, and 43 of 56 genotype 1E viruses were associated with imported cases from China, Vietnam, Malaysia, and Indonesia. One genotype 1h virus was imported from Belarus, and three of four genotype 1j viruses were imported from the Philippines. Of 63 rubella genotype 2B viruses, 46 were imported from Vietnam, Thailand, Malaysia, China, Germany, and South Africa. Molecular surveillance allows for the differentiation of circulating rubella viruses and can be used to investigate transmission pathways, which are important to identify the interruption of endemic virus transmission. J. Med. Virol. 85:745–753, 2013. © 2013 Wiley Periodicals, Inc.     

2010—2011年西城区（南区）手足口病原监测结果分析

目的对2010—2011年北京市两城区（_幸j区）手足口病患者进行肠道病毒病原体检测,分析肠道病毒病原学特征,为手足口病防控提供科学依据。方法采集医疗机构临床诊断为手足r1病患者咽拭子和粪便标本共418份,应用Realtime—PCR检测咽拭子标本病毒核酸;并对粪便标本进行病毒分离。结果418份标本中,肠道病毒总体检出率为53．59％（224／418）。2010年咽拭子标本未分型肠道病毒阳性枪出率（36．26％）高于2011年（16．89％）,结果差别有统计学意义（X^2=13．80,P〈0．005）;2011年咽拭子标本CoxA16型病毒阳性检出率（26．03％）高于2010年（10．99％）,差别有统计学意义（x^2=8．58,P〈0．005）。分别比较两年采集的咽拭子标本,发病3大内和3天以上采集的标本检出率差异均有统计学意义（2010年：x^2=5．85,P〈0．05;2011年：X^2=15．26,P〈0．005）。结论引起北京市西城区（南区）手足口病流行的主要肠道病原体,2010年为未分型肠道病毒,2011年为CoxA16。在发病3天内采集患者咽拭子标本,有助于提高病毒检出率。     

Measles virus hemagglutinin mediates monocyte aggregation and increased adherence to measles-infected endothelial cells

The effect of measles virus (MV) infection on monocyte adhesion was studied using human peripheral blood monocytes and monocytic and endothelial cell lines. The infection of monocytic U-937 cells led to the formation of large cellular aggregates. Aggregation was independent of intercellular adhesion molecule-1 (ICAM-1)/ lymphocyte function-associated antigen-1 (LFA-1), but could be inhibited by monoclonal antibodies (mAb) against the MV hemagglutinin glycoprotein (MV-H). mAb against the MV receptor, CD46, also blocked aggregation. No significant changes in the cell surface expression of adhesion molecules CD11a, CD11b, CD11c, CD18, CD54, CD44, CD49d (α4-integrin) and CD62L (L-selectin) were observed on MV-infected monocytes. Infection of a human endothelial cell line, EAhy 926 (HEC), with MV led to a two-fold increase in ICAM-1 expression and a two-fold increase in monocyte adherence to the HEC (from 22±1.6% to 42±4.8%). However, ICAM-1 mAb reduced monocyte adhesion to the control and MV-infected HEC to a similar degree, whereas anti-MV-H antibodies abolished the difference between binding to infected and control HEC. We conclude that MV hemagglutinin mediated both the homotypic aggregation in infected monocyte cultures and increased monocyte adherence to the infected endothelial cells. Received: 14 February 1996     

Measles virus attachment proteins with impaired ability to bind CD46 interact more efficiently with the homologous fusion protein

Fusion promotion by measles virus (MV) depends on an interaction between the hemagglutinin (H) and fusion (F) glycoproteins. Amino acid substitutions in MV H that drastically reduce hemagglutinating activity result in an increase in the amount of H (primarily the 74 kDa isoform) detectable in a complex with F at the cell surface. This is in direct contrast to the loss of the ability to detect a complex between the fusion protein of Newcastle disease virus and most attachment proteins that lack receptor binding activity. These opposing results provide support for the existence of different mechanisms for the regulation of fusion by these two paramyxoviruses.     

贵州独山、兴义不明原因发热病人登革病毒的分离和鉴定的初步研究

目的 对贵州独山、兴义两地夏秋季不明原因发热病人血清进行登革病毒(DEN)分离及鉴定,从病原学角度证实贵州省人群DEN的感染情况.方法 于2005年6至10月份收集贵州独山县、兴义市两地不明原因发热病人血清356份,并接种于生长良好的单层C6/36细胞盲传3代,观察细胞病变,用抗DEN1～4型单克隆抗体通过间接免疫荧光法进行型别鉴定;用DEN NSl基因区特异性通用引物进行RT-PCR检测分离的DEN毒株核酸,经序列测定并作系统发生树分析.结果 3份病人血清标本可使C6/36发生细胞病变,用单克隆抗体、RT-PCR扩增和序列测定,鉴定为DEN2;系统发生树分析证明,分离的病毒与DEN2-43、DEN2-44株系统进化关系最近.结论 贵州省独山、兴义两地人群中存在DEN感染.     

Measles virus-induced down-regulation of CD46 is associated with enhanced sensitivity to complement-mediated lysis of infected cells

CD46, the major component of the measles virus (MV) receptor complex and a member of the regulators of complement activity (RCA) gene cluster, is down-regulated in MV-infected cells. We investigated whether the reduction of surface CD46 correlates with enhanced sensitivity of lymphoid and monocytic cells to lysis by activated complement. On human U937 cells, acutely or persistently infected with MV-Edmonston (ED) vaccine strain, infection-dependent down-regulation of CD46 confers sensitivity to activated complement, regardless of the pathway of activation and the specificity of the activating antibodies. Interestingly, down-regulation of CD46 alone is sufficient to confer susceptibility of cells to complement lysis despite the continued surface expression of other RCA proteins such as CD35 and CD55. In primary cultures, both peripheral blood lymphocytes and macrophages are efficiently lysed in the presence of complement activated via the alternative pathway after MV infection. In contrast to the MV-ED infection, infection of cells with the lymphotropic MV wild-type strain WTF does not down-regulate CD46. Cells infected with MV-WTF do not exhibit enhanced susceptibility to complement lysis. These data suggest that MV strains similar to WTF that do not down-regulate CD46 may have an enhanced potential for replication and dissemination within the human host, whereas complement-mediated elimination of cells infected with CD46-down-regulating strains of MV, such as ED, may limit the spread of MV infection, and could thus represent an attenuating factor for MV.     

北京市房山区2006-2012年麻疹发病情况分析

目的 了解2006-2012年北京市房山区麻疹流行情况,为进一步采取有针对性的预防控制措施提供参考依据.方法 收集2006-2012年中国疾病预防控制信息系统报告的北京市房山区麻疹病例,运用SPSS13.0软件对收集的麻疹病例进行流行病学特征分析.结果 2006-2012年麻疹共报告457例,分年度发病率分别为14.078 /10万、8.486/10万、5.477/10万、6.119/10万、9.801/10万、0.439/10万、0.351/10万.8月龄以下儿童和15岁以上成人发病率较高.平原地区发病率高于丘陵地区和山区.发病高峰集中在3-6月份.结论 房山区2006-2012年麻疹发病率呈逐年下降趋势.2-6月为麻疹流行季.人口密度较大的平原地区及外来流动人口较大的地区为麻疹防控的重点地区.小于8月龄和大于45岁年龄段居民及民工群体为麻疹防控的重点人群.     

2007年山西省部分地区出生缺陷人群监测分析

目的了解2007年山西省围产儿出生缺陷发生情况。方法采用以人群为基础的监测方法收集资料,调查对象为监测点内孕28周至产后42天的围产儿。结果2007年全省出生缺陷发生率118.71/万;城镇发生率151.00/万,乡村发生率为95.64/万;男性出生缺陷发生率为117.65/万,女性为114.01/万。前五位缺陷种类依次为：先天性心脏病,多指（趾）,神经管缺陷,总唇裂,先天性脑积水。结论2007年山西省出生缺陷总发生率顺位前五位,与2006年全国监测顺位相同,发生率接近;城镇出生缺陷发生率明显高于乡村,男女发生率无明显差异。     

Measles virus V protein blocks Jak1-mediated phosphorylation of STAT1 to escape IFN-alpha/beta signaling

Viruses have evolved various strategies to escape the antiviral activity of type I interferons (IFN-alpha/beta). For measles virus, this function is carried by the polycistronic gene P that encodes, by an unusual editing strategy, for the phosphoprotein P and the virulence factor V (MV-V). MV-V prevents STAT1 nuclear translocation by either sequestration or phosphorylation inhibition, thereby blocking IFN-alpha/beta pathway. We show that both the N- and C-terminal domains of MV-V (PNT and VCT) contribute to the inhibition of IFN-alpha/beta signaling. Using the two-hybrid system and co-affinity purification experiments, we identified STAT1 and Jak1 as interactors of MV-V and demonstrate that MV-V can block the direct phosphorylation of STAT1 by Jak1. A deleterious mutation within the PNT domain of MV-V (Y110H) impaired its ability to interact and block STAT1 phosphorylation. Thus, MV-V interacts with at least two components of IFN-alpha/beta receptor complex to block downstream signaling.