Stop H5N1 influenza in US cattle now

The relentless march of a highly pathogenic avian influenza virus(HPAIV)strain,known as H5N1,to become an unprecedented panzootic continues unchecked.The leap of H5N1 clade 2.3.4.4b from Eurasia and Africa to North America in 2021 and its further spread to South America and the Antarctic have exposed new avian and mammalian populations to the virus and led to outbreaks on an unrivaled scale.The virus has infected wild birds across vast geographic regions and caused wildlife deaths in some of the world's most biodiverse ecosystems.

Dairy cows inoculated with highly pathogenic avian influenza virus H5N1

Highly pathogenic avian influenza(HPAI)H5N1 hemagglutinin clade 2.3.4.4b was detected in the United States in 2021.These HPAI viruses caused mortality events in poultry,wild birds,and wild mammals.On March 25,2024,HPAI H5N1 clade 2.3.4.4b was confirmed in a dairy cow in Texas in response to a multi-state investigation into milk production losses.1 Over 200 positive herds were identified in 14 U.S.states.The case description included reduced feed intake and rumen motility in lactating cows,decreased milk production,and thick yellow milk.2,3 The diagnostic investigation revealed viral RNA in milk and mammary tissue with alveolar epithelial degeneration and necrosis and positive immunoreactivity of glandular epithelium.A single transmission event,likely from birds,was followed by limited local transmission and onward horizontal transmission of H5N1 clade 2.3.4.4b genotype B3.13.4 We sought to experimentally reproduce infection with genotype B3.13 in Holstein yearling heifers and lactating cows.Heifers were inoculated by aerosol respiratory route and cows by intramammary route.Clinical disease was mild in heifers,but infection was confirmed by virus detection,lesions,and seroconversion.Clinical disease in lactating cows included decreased rumen motility,changes to milk appearance,and production losses.Infection was confirmed by high levels of viral RNA detected in milk,virus isolation,lesions in mammary tissue,and seroconversion.This study provides the foundation to investigate additional routes of infection,pathogenesis,transmission,and intervention strategies.

2022-2023年山东省A(H1N1)pdm09流感病毒HA、NA基因变异特征分析

目的 了解山东省2022-2023流感监测年度分离的A(H1N1)pdm09亚型流感病毒血凝素(hemagglutinin,HA)和神经氨酸酶(neuraminidase,NA)基因的变异特征,为流感的防控提供科学依据。方法 从流感监测网络实验室分离的流感毒株中按地市随机选取14株A(H1N1)pdm09亚型流感毒株,以WHO推荐的当季疫苗株为参考进行全基因组测序,并采用荧光法开展神经氨酸酶抑制(neuraminidase inhibition,NI)实验以评估药物敏感性。结果 山东省2022-2023年度分离的A(H1N1)pdm09流感病毒属于6B.1A分支中的5a.2a进化簇,核苷酸序列比对分析显示,HA和NA基因与2021-2023年度北半球疫苗株A/Victoria/2570/2019的亲缘关系较为接近,同源性分别为98.5%~98.7%和98.8%~99.1%。氨基酸序列分析显示,HA蛋白有20个位点发生了氨基酸序列变异,并发现1株病毒可能发生抗原漂移,有3株病毒发生了HA蛋白糖基化位点的缺失。NA酶相关重要位点未发生变异。NI实验显示,所测流感毒株均对抗流感病毒药物敏感。结论 所监测毒株与疫苗株整体同源性很高,但氨基酸存在一定程度变异,今后有必要持续开展流感病毒基因变异特征监测以了解流感流行的风险,以及评价基因变异对流感疫苗和治疗药物效果的影响。

射干止咳胶囊体内外抗甲型H1N1流感病毒作用初探

目的初步探讨射干止咳胶囊对甲型H1N1流感病毒的体内外抗病毒作用。方法通过细胞病变效应(cytopathic effect,CPE)结合MTT法考察射干止咳胶囊体外抑制甲型H1N1流感病毒活性的作用;采用小鼠滴鼻法感染甲型H1N1流感病毒为模型,观察射干止咳胶囊对甲型H1N1流感病毒的体内抗病毒作用。结果体外抗病毒试验结果显示,射干止咳胶囊对甲型H1N1流感病毒的最高抑制率为11.86%,提示在攻毒剂量为100TCID_(50)的条件下,射干止咳胶囊在体外对甲型H1N1流感病毒的抑制作用不明显。小鼠滴鼻感染5LD_(50)的甲型H1N1流感病毒,射干止咳胶囊低、中、高剂量组小鼠的死亡率分别为30%、10%、30%,死亡保护率达50%、70%、50%,平均生存天数分别为13 d、14 d、13 d,说明各给药组对攻毒小鼠具有较好的死亡保护作用。结论射干止咳胶囊体外抗甲型H1N1流感病毒的作用不显著,但射干止咳胶囊各剂量组对甲型H1N1流感病毒攻毒致小鼠死亡却具有明显的保护作用。

甲型流感病毒H1N1型灭活病毒标准物质研究

以人工培养真实病毒为原料,研制了一种甲型流感病毒H1N1型灭活病毒标准物质。该标准物质经化学灭活及灭活效果验证后,联合多家实验室采用数字PCR定量检测方法对拷贝数浓度进行定值,对标准物质的均匀性、稳定性及不确定度进行了评估。结果显示该标准物质均匀性良好,在-80~-70℃保存条件下稳定保存5个月,标准物质最终定值结果为(1384.5±249.3)copies/μL(k=2)。该标准物质可为H1N1型甲型流感病毒检测的全过程提供计量溯源和质量控制支撑,有助于提升相关核酸检测结果的准确性和可靠性。

感冒清热片防治甲型H1N1流感病毒感染的药效学研究

目的探讨感冒清热片防治甲型H1N1流感病毒感染的药效学情况。方法108例甲型H1N1流感病毒感染患者,随机分为观察组和对照组,每组54例。对照组使用磷酸奥司他韦治疗,观察组在对照组治疗基础上使用感冒清热片治疗。比较两组患者临床疗效、症状改善指标(起效时间、退热时间、止咳时间、痊愈时间)、以及治疗前后的中医证候(发热、咽痛、头痛、鼻塞流涕、咳嗽、乏力)积分、血清炎性因子[C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)]。结果观察组治疗总有效率96.30%高于对照组的77.78%(P<0.05)。治疗后,观察组患者发热、咽痛、头痛、鼻塞流涕、咳嗽、乏力评分分别为(0.83±0.24)、(1.12±0.30)、(1.07±0.29)、(1.03±0.32)、(1.05±0.33)、(1.09±0.28)分,均低于对照组的(1.46±0.37)、(2.31±0.58)、(2.14±0.52)、(2.25±0.63)、(2.36±0.61)、(2.42±0.65)分(P<0.05)。观察组起效时间(1.03±0.34)d、退热时间(1.56±0.40)d、止咳时间(4.35±0.68)d、痊愈时间(6.63±1.26)d均短于对照组的(2.32±0.57)、(2.63±0.74)、(7.24±1.16)、(9.38±1.72)d(P<0.05)。治疗后,观察组CRP(2.11±0.56)mg/L、TNF-α(19.34±2.20)μg/L、IL-6(4.02±0.54)ng/L均低于对照组的(4.83±0.69)mg/L、(25.89±2.73)μg/L、(6.13±0.62)ng/L(P<0.05)。结论感冒清热片防治甲型H1N1流感病毒感染的疗效显著,能有效缓解证候,加快症状缓解速度,提高抗炎作用。

2024年美国奶牛H5N1亚型高致病性禽流感疫情分析

2024年3月以来,美国报告了多例奶牛H5N1亚型高致病性禽流感病例,引发全球广泛关注。本文对本次疫情进行了系统梳理,分析了疫情流行情况和分布规律,提出了风险防范建议。现有数据表明,引发奶牛感染的H5N1亚型高致病性禽流感病毒属于2.3.4.4b分支,与美国同期在家禽和野禽中流行的毒株高度同源。初步分析表明,感染奶牛的病毒可能来源于野生候鸟。疫情发生后,美国采取了限制移动、调运检测等综合防控措施。本次疫情可能对美国奶牛产业造成一定程度的负面影响,但从目前来看对我国影响较小。建议持续进行国外疫情监视,国内加强野禽风险监测,强化家禽强制免疫,积极宣传引导,做好应急储备等,降低本次疫情对我国的影响。

2023年湖州市区pdm09 H1N1流感病毒NA基因特征分析

pdm09 H1N1流感病毒自2009年爆发引起全球大流行,目前已成为流感流行常见亚型之一[1]。该病毒包含由8个基因片段,其中神经氨酸酶(neuraminidase,NA)是嵌入流感病毒包膜表面的一种重要的功能糖蛋白[2]。主要负责成熟病毒从宿主细胞中释放,在感染下一个宿主细胞进行复制转录,最终使机体出现临床症状和体征[3]。

基于UPLC-Q-Exactive-Orbitrap-MS、网络药理学和实验验证探讨裸花紫珠抗H1N1活性成分及其作用机制

本实验首先对裸花紫珠的提取物进行萃取,得到不同的萃取部位,然后对各部位进行抗甲型流感病毒H1N1型(H1N1)活性筛选,确定裸花紫珠乙酸乙酯萃取部位(EACN)具有较好的体外抗H1N1的活性。采用超高效液相色谱-四级杆-静电场轨道阱联用(UPLC-Q-Exactive-Orbitrap-MS)技术对EACN进行定性分析。基于定性分析的结果,进一步使用数据挖掘和网络药理学,评估药物的活性成分、关键靶点和关键通路,最后使用H1N1感染BALB/c小鼠模型对预测结果进行验证。结果显示,在各个萃取部位中,乙酸乙酯部位体外抗H1N1效果最佳,半数抑制浓度(IC_(50))为51μg/mL,半数细胞毒浓度(CC_(50))为859.4μg/mL,选择指数(SI,CC_(50)/IC_(50))为16.85。从EACN中鉴定出34种化合物,在此基础上,利用网络药理学,筛选出和EACN抗H1N1相关的药物靶点67个,靶点共涉及生物过程491个,与抗H1N1相关的通路147个。H1N1感染BALB/c小鼠实验结果发现,EACN能改善H1N1感染引起的体重降低和肺指数的增加,降低小鼠肺组织的病毒载量,减轻小鼠肺组织的病理损伤,降低外周血血清中TNF-α、IFN-γ、IL-1β水平。实验结果提示EACN可能从直接抑制病毒、抗炎作用和免疫调节作用等多个途径发挥抗H1N1的作用。

The interaction between the 2009 H1N1 influenza A hemagglutinin and neuraminidase: mutations, co-mutations, and the NA stalk motifs

As the world is closely watching the current 2009 H1N1 pandemic unfold, there is a great interest and need in understanding its origin, genetic structures, virulence, and pathogenicity. The two surface proteins, hemagglutinin (HA) and neuraminidase (NA), of the influenza virus have been the focus of most flu research due to their crucial biological functions. In our previous study on 2009 H1N1, three aspects of NA were investigated: the mutations and co-mutations, the stalk motifs, and the phylogenetic analysis. In this study, we turned our attention to HA and the interaction between HA and NA. The 118 mutations of 2009 H1N1 HA were found and mapped to the 3D homology model of H1, and the mutations on the five epitope regions on H1 were identified. This information is essential for developing new drugs and vaccine. The distinct response patterns of HA to the changes of NA stalk motifs were discovered, illustrating the functional dependence between HA and NA. With help from our previous results, two co-mutation networks were uncovered, one in HA and one in NA, where each mutation in one network co-mutates with the mutations in the other network across the two proteins HA and NA. These two networks residing in HA and NA separately may provide a functional linkage between the mutations that can impact the drug binding sites in NA and those that can affect the host immune response or vaccine efficacy in HA. Our findings demonstrated the value of conducting timely analysis on the 2009 H1N1 virus and of the integrated approach to studying both surface proteins HA and NA together to reveal their interdependence, which could not be accomplished by studying them individually.

Genetic Characteristics of 2009 Pandemic H1N1 Influenza A Viruses Isolated from China's Mainland

A total of 100 H1N1 flu real-time-PCR positive throat swabs collected from fever patients in Zhejiang, Hubei and Guangdong between June and November 2009, were provided by local CDC laboratories. After MDCK cell culture, 57 Influenza A Pandemic （H1N1） viruses were isolated and submitted for whole genome sequencing. A total of 39 HA sequences, 52 NA sequences, 36 PB2 sequences, 31 PB1 sequences, 40 PA sequences, 48 NP sequences, 51 MP sequences and 36 NS sequences were obtained, including 20 whole genome sequences. Sequence comparison revealed they shared a high degree of homology （96%-99%） with known epidemic strains （A/Califomia/04/2009（H1N1）. Phylogenetic analysis showed that although the sequences were highly conserved, they clustered into a small number of groups with only a few distinct strains. Site analysis revealed three substitutions at loop 220 （221-228） of the HA receptor binding site in the 39 HA sequences： A/Hubei/86/2009 PKVRDQEG→PKVRDQEA, A/Zhejiang/08/2009 PKVRDQEG→PKVRDQER, A/Hubei/75/2009 PKVRDQEG→PKVRDQGG, the A/Hubei/75/2009 was isolated from an acute case, while the other two were from patients with mild symptoms. Other key sites such as 119, 274, 292 and 294 amino acids of NA protein,627 of PB2 protein were conserved. Meanwhile, all the M2 protein sequences possessed the Ser32Asn mutation, suggesting that these viruses were resistant to adamantanes. Comparison of these sequences with other H1N1 viruses collected from the NCBI database provides insight into H1N1 transmission and circulation patterns.

Clinical Predictors for Diagnosing Pandemic (H1N1) 2009 and Seasonal Influenza (H3N2) in Fever Clinics in Beijing,China

Objective Symptomatic predictors of influenza could assess risks and improve decisions about isolation and outpatient treatment. To develop such predictors, we undertook a prospective analysis of pandemic （HIN1） 2009 and seasonal influenza （H3N2） in patients attending fever clinics. Methods From 1 May 2009 to 1 January 2010, all adult patients admitted to fever clinics for suspected influenza, confirmed by real time RT-PCR, were enrolled. Predictors of influenza virus infection were selected with logistic regression models. Measures of sensitivity, specificity, positive and negative likelihood ratios （LRs） were calculated to identify the best predictors. Results The clinical features and routine blood test results of influenza （H1N1） 2009 and seasonal influenza were similar. The positive and negative LRs of current US CDC influenza-like illness （ILl） criteria were modest in predicting influenza infection. Our modified clinic predictors improved the ability of the positive and negative LRs to recognize pandemic （HIN1） 2009 and seasonal influenza. The revised criteria are： fever ~ 38 ~C accompanied by at least one of the following--cough, arthralgia or relative iymphopenia. Conclusion Patients with symptoms and signs that meet the new criteria are likely to have influenza and timely antiviral therapy may be appropriate. In addition, physicians should ascertain if influenza is circulating within the community or if there is a contact history of influenza and combine this information with the newly developed criteria to clinically diagnose influenza.

New mutational trends in the HA protein of 2009 H1N1 pandemic influenza virus from May 2010 to February 2011

As we enter the year of 2011, the 2009 H1N1 pandemic influenza virus is in the news again. At least 20 people have died of this virus in China since the beginning of 2011 and it is now the predominant flu strain in the country. Although this novel virus was quite stable during its run in the flu season of 2009-2010, a genetic variant of this virus was found in Singapore in early 2010, and then in Australia and New Zealand during their 2010 winter influenza season. Several critical mutations in the HA protein of this variant were uncovered in the strains collected from January 2010 to April 2010. Moreover, a structural homology model of HA from the A/Brisbane/10/2010(H1N1) strain was made based on the structure of A/California/04/2009 (H1N1). The purpose of this study was to investigate mutations in the HA protein of 2009 H1N1 from sequence data collected worldwide from May 2010 to February 2011. A fundamental problem in bioinformatics and biology is to find the similar gene sequences for a given gene sequence of interest. Here we proposed the inverse problem, i.e., finding the exemplars from a group of related gene sequences. With a clustering algorithm affinity propagation, six exemplars of the HA sequences were identified to represent six clusters. One of the clusters contained strain A/Brisbane/12/2010(H1N1) that only differed from A/Brisbane/10/2010 in the HA sequence at position 449. Based on the sequence identity of the six exemplars, nine mutations in HA were located that could be used to distinguish these six clusters. Finally, we discovered the change of correlation patterns for the HA and NA of 2009 H1N1 as a result of the HA receptor binding specificity switch, revealing the balanced interplay between these two surface proteins of the virus.

Gene Expression Profiles Comparison between 2009 Pandemic and Seasonal H1N1 Influenza Viruses in A549 Cells

Objective To perform gene expression profiles comparison so that to identify and understand the potential differences in pathogenesis between the pandemic and seasonal A （H1N1） influenza viruses. Methods A549 cells were infected with A/California/07/09 （H1N1） and A/GuangdongBaoan/51/08 （H1N1） respectively at the same MOI of 2 and collected at 2, 4, 8, and 24 h post infection （p.i.）. Gene expression profiles of A549 cells were obtained using the 22 K Human Genome Oligo Array, and differentially expressed genes were analyzed at selected time points. Results Microarrays results indicated that both of the viruses suppressed host immune response related pathways including cytokine production while pandemic H1N1 virus displayed weaker suppression of host immune response than seasonal H1N1 virus. Observation on similar anti-apoptotic events such as activation of apoptosis inhibitor and down-regulation of key genes of apoptosis pathways in both infections showed that activities of promoting apoptosis were different in later stage of infection. Conclusion The immuno-suppression and anti-apoptosis events of pandemic H1N1 virus were similar to those seen by seasonal H1N1 virus. The pandemic H1N1 virus had an ability to inhibit biological pathways associated with cytokine responses, NK activation and macrophage recognition .

福建省2009年甲型HIN1流感122例流行病学特征分析

目的了解新出现的甲型H1N1流感在福建省的流行病学特征,为防控提供依据。方法从中国疾病预防控制系统和福建省卫生厅网站收集福建省各地发现的甲型H1N1流感病例的相关信息,用Excel建立病例的个案信息库,用SPSS软件进行统计分析。结果2009年5月23日至7月13日,福建省共发现122例甲型H1N1流感确诊病例,无重症或死亡病例;其中107例为境外输入病例,2例为省外输入病例,13例为输入病例引发的本土续发病例,续发率为2.2%。53.3%(65/122)病例由卫生部门主动监测发现。未出现感染来源不明的本土病例,未发生社区暴发流行。结论福建省甲型H1N1流感疫情以输入性为主,由于防控得力,未造成疫情大面积传播;病例临床症状温和。

2009年新型甲型H1N1流感病毒血凝素基因进化分析

目的:探讨2009年新型甲(A)型H1N1流感病毒血凝素(HA)基因与世界各地不同年代分离的A/H1N1代表株HA基因的进化关系。方法:从NCBI数据库下载2009年新型A/H1N1亚型流感病毒的HA基因序列以及以往流行的人、猪和禽的A/H1N1亚型流感病毒参考序列,采用Molecular Evolutionary Genetics Analysis version 4.0(MEGA4.0)软件进行序列比对和构建系统进化树,并分别比较2009年新型甲型H1N1流感病毒HA基因与北美地区、欧洲地区、亚洲地区A/H1N1流感病毒HA基因编码蛋白的氨基酸序列。结果:不同时期人A/H1N1亚型流感病毒代表株HA基因进化分析显示:2009年新型A/H1N1流感病毒HA基因与1976～2007年北美地区分离的7株人A/H1N1亚型流感病毒具有较高的同源性,与欧洲和亚洲地区的同源性较低。不同种属间A/H1N1亚型流感病毒HA基因进化分析显示:2009年新型A/H1N1流感病毒HA基因与1998和2007年北美地区分离的A/H1N1猪流感病毒的HA基因进化关系较近,与欧洲及亚洲地区分离的A/H1N1猪流感病毒及A/H1N1禽流感病毒进化关系较远。氨基酸比对结果显示2009年新型A/H1N1流感病毒HA基因的重要抗原位点与北美地区分离的A/H1N1猪流感病毒相近,与欧洲和亚洲地区分离的A/H1N1猪流感病毒及人类流感病毒疫苗株相比变化较大。结论:2009年新型甲型H1N1流感病毒HA基因可能是北美地区甲型H1N1猪流感病毒长期进化并与该地区人A/H1N1流感病毒部分基因片段重排的结果,对人H1N1甲型流感病毒疫苗可能并不敏感。

重庆市2009年6～10月甲型H1N1流感疫情特征分析

目的分析重庆市甲型H1N1流感疫情特征，提出防控措施建议。方法运用描述性流行病学方法，对重庆市2009年6～10月甲型H1N1流感疫情特征进行分析。结果6～10月共确诊甲型H1N1流感病例1531例，其中6～8月确诊22例，以散发的输入性病例为主，9～10月确诊1509例，以本土聚集性病例为主。疫情分布在除城口之外的39个区县，病例数居前几位的集中在主城区。10-20岁年龄组占病例总数的82．36％，性别比男：女=1．52：1，学生占病例总数的94．70％。6～10月哨点医院送检的3397份流感样病例标本中，流感阳性标本463份，其中甲型H1N1流感256份，占55．29％。结论进入9月份之后，尤其是国庆长假后，重庆市甲型H1N1流感疫情呈增速发展趋势，且由散发的输入性病例为主转为以本土聚集性病例为主。疫情从城市向农村逐渐扩散，城乡差距越来越小，未来一段时间农村地区甲型H1N1流感的防控形势严峻。随着疫情形势的不断加重，甲型H1N1流感防控存在两个重点，一是加强学校重点场所的防控力度，减少暴发疫情的发生；二是加强院内感染和高危人群的防控工作，防止重症和死亡病例的发生。

2009年上海市甲型H1N1流感大流行的特征分析

目的分析上海市甲型H1N1流感(甲流)疫情的流行特征,为制定流感的预防控制策略提供参考。方法调查和收集上海市2009年5月至2010年4月期间确诊的全部甲流病例等疫情数据,对确诊病例的流行病学特征进行描述和分析。结果上海市2009年5月25日发现首例输入性甲流确诊病例,截至2010年4月30日,全市共报告甲流确诊病例3678例,其中住院病例331例,死亡10例。根据病情严重程度归类,轻症病例3 551例,重症病例98例,危重病例29例。所有确诊病例中有234例属境外输入病例。76.6%的甲流确诊病例为30岁以下的青壮年,并且以学生为主。重症病例以10岁以下儿童和50岁以上中老年人居多,男女性别比为2.38∶1。结论上海市甲流的流行经历了由输入性到本土流行两个阶段,有明显的季节性特征,在社会各方的共同努力之下,疫情已得到有效的控制。

2009年新型甲型H1N1流感病毒神经氨酸酶基因进化分析

目的:探讨2009年新型甲型H1N1流感病毒神经氨酸酶(NA)基因的进化及NA基因编码蛋白抗原性、酶活性位点、糖基化位点变异情况。方法:从NCBI基因库检索获得43株不同年代不同地域甲型流感病毒NA基因序列,用Molecular Evolutionary Genetics Analysis version 4.0(MEGA4.0)软件进行基因进化分析和氨基酸序列分析。结果:2009年新型甲型H1N1流感病毒与禽H5N1流感病毒NA基因的同源性达到85%,潜在抗原位点氨基酸分布相同;所有毒株的酶活性中心位点高度保守,但糖基化位点有变异。结论:2009年新型甲型H1N1流感病毒的NA基因可能来源于禽H5N1流感病毒;神经氨酸酶抑制剂治疗有效。

2009年新型甲型H1N1流感病毒全基因组序列重组分析

目的:分析2009年流行的新型甲型流感病毒(A/H1N1)全序列的基因重组现象。方法:从NCBI基因数据库下载2009年新型甲型流感病毒(A/H1N1)全基因组序列,采用Molecular Evolutionary Genetics Analysis version 4.0(MEGA4.0)软件对8条基因序列进行拼接和比对,分析2009年爆发株与历史流行株序列间的同源性;同时采用Simplot3.5.1软件分析新型流感病毒A/H1N1基因重组现象。结果:2009年3月以来爆发的新型A/H1N1病毒株聚合酶B1(polymerase B1,PB1)基因来自于人H3N2,其同源性为93.7%;聚合酶B2(polymerase B2,PB2)和聚合酶A(polymerase A,PA)与禽H5N1同源性较高,同源性分别为89.0%、89.9%;血凝素(hemagglutinin,HA)、核蛋白(nucleoprotein,NP)和非结构蛋白(non-structural protein,NS)与北美地区猪H1N1同源性较高,同源性分别为91.7%、93.1%和93.1%;神经氨酸酶(neuraminidase,NA)和基质蛋白(matrixprotein,MP)与欧洲地区猪H1N1同源性较高,同源性分别为90.5%、95.5%。全基因序列同源性分析发现2009年新型A/H1N1病毒与北美地区猪H1N1病毒同源性最高,为83.9%。结论:2009年新型甲型H1N1流感病毒可能是人H3N2、北美地区猪H1N1、欧洲地区猪H1N1、禽H5N1的基因重排病毒。