2010年广州市甲型H1N1流感病毒分离株HA基因变异分析

目的比较2010年广州市分离到的甲型H1N1流感病毒血凝素（HA）基因和2009年中国大陆甲型H1N1流感病毒HA基因的变异情况,为甲型H1N1流感的监测和防控提供理论依据。方法收集2010年广州市有发热和呼吸道症状病人的咽拭子标本,用H1N1流感特异性引物进行PCR检测,扩增分离到的H1N1病毒HA片段,测序后与2009年的H1N1毒株进行比对和分析,并用生物信息学方法对抗原位点和糖基化位点进行分析。结果共收集到426份标本,甲型流感阳性211份,其中H1N1流感4株,与2009年分离的甲型H1N1流感相比,有12个氨基酸碱基位点发生了有意义突变,其中6个位点位于抗原位点上;4株毒株HA基因145位氨基酸都发生了变异;其中2株毒株在第180位氨基酸位点的抗原位点发生了变异。进化分析表明4株毒株与2009年中国大陆分离的8株毒株进化关系较远。结论 2010年广州市甲型H1N1毒株与2009年相比发生了较大变异。HA基因145位和180位氨基酸位点变异对H1N1毒株抗原变异有重要意义。本文分离的A/Guangdong/ZS03/2010（H1N1）和A/Guangdong/ZS01/2010（H1N1）毒株可能已经发生了抗原性漂移。     

2016—2019年深圳市盐田区甲型H1N1流感病毒NA基因特征研究

目的分析深圳市盐田区2016—2019监测年度甲型H1N1流感病毒NA基因特征。方法选取35株盐田区分离的甲型H1N1流感病毒毒株进行NA基因序列分析、进化分析、抗原决定簇位点、耐药位点和糖基化改变的变异分析。结果进化树分析表明, 本研究所分析毒株分布在6B分支, 2016年上半年毒株分布在6B.2簇;2016年下半年及2017年度毒株分布在6B.1簇;2018—2019年度毒株分布在6B.1A簇。2016年核苷酸同源性为97.87%～98.09%, 氨基酸同源性为96.85%～96.89%, 2016年毒株与同年度疫苗株位于不同分支, 同源性较低。2017年核苷酸同源性为98.62%～99.35%, 氨基酸同源性为99.57%～99.78%;2018年核苷酸同源性为99.35%～99.86%, 氨基酸同源性为99.05%～99.12%;2019年核苷酸同源性为99.20%～99.86%, 氨基酸同源性为99.19%～99.78%。2017—2019年毒株与当年度疫苗株位于同一分支, 同源性较高。与各年度疫苗株相比, 盐田区流感毒株NA蛋白存在29个氨基酸位点变异。抗原决定簇区域:与疫...     

2011-2014年青岛地区甲型H3N2流感病毒基因进化分析

目的 了解2011-2014年青岛地区人群甲型H3N2流感病毒流行株基因进化及抗原变异趋势.方法 选取2011-2014年间青岛地区流行的甲型H3N2流感病毒64株,提取病毒RNA,应用逆转录聚合酶链反应(RT-PCR)扩增HA、NA、MP 3个基因片段,并进行序列测定,对各基因片段进行系统发育分析及基因和氨基酸位点变异分析.结果 HA进化树分析表明,甲型H3N2流感病毒基本上分为三大分支,并且每个分支与当年的疫苗株都不在同一分支上;HA1蛋白抗原决定簇共有8个位点发生了变化;NA蛋白酶活性中心及周围相关位点氨基酸组成保守,未检测到耐奥司他韦和扎那米韦的变异位点.M2蛋白均发生S31N突变.结论 2011-2014年青岛地区流行的H3N2流感病毒在持续不断地发生基因变异而产生抗原漂移;毒株全部为烷胺类药物耐药株,但对神经氨酸酶抑制剂敏感.     

2018-2019年辽宁省甲型流感病毒流行株HA基因进化与疫苗株匹配度分析

目的分析辽宁省2018-2019年甲型流感毒血凝素(hemagglutinin,HA)基因,计算并评估流行株与疫苗株的匹配度。方法选取2018-2019年49株甲型流感毒株进行测序,对HA基因进行进化分析;研究抗原表位、糖基化位点及受体结合位点变异情况;采用Pepitope模型对流行株与疫苗匹配度进行分析。结果2018-2019年流感流行季为11月份至次年3月份,主要流行型别为新甲型H1N1亚型。经进化分析,新甲型H1N1流行株属于6B.1分支,与当年疫苗株属于同一分支;季节性H3N2毒株分布在3C.2a分支上,与2018-2019年疫苗株处于同一分支,但2019-2020年疫苗株位于3C.3a分支。部分毒株在抗原表位及受体结合位点上发生了突变。若干毒株与疫苗株相比,糖基化位点发生了增加或缺失,并未出现新的糖基化位点。使用Pepitope模型对疫苗效力从分子水平进行评估,本年度新甲型H1N1流感疫苗效力及2019-2020年疫苗株预测效力均能达到较为理想的效果。但是季节性H3N2疫苗株与本年度流行株匹配度低,计算出的疫苗效力半数以上为负值。2019-2020年H3N2亚型疫苗株效力有待进一步观察。结论2018-2019年辽宁省甲型H1N1流行株发生了一定程度的变异,H3N2亚型流行株与2018-2019年疫苗株匹配度低。应密切关注流行株的基因变异情况并及时更新疫苗株。     

2015-2016年度中国甲型H1N1亚型流感病毒疫苗候选株的制备及鉴定CSCD

目的 为获得2015-2016年度中国流行的甲型H1N1亚型流感病毒疫苗候选株,制备流感病毒重配株并对其进行鉴定.方法 采用经典重配的方法,将H1N1亚型流感病毒流行株与H3N2亚型的鸡胚高产重配母本株（X-157株）在鸡胚上进行混合培养.用H3亚型的HA蛋白抗血清和X-157株全病毒抗血清对混合培养病毒进行阴性筛选.阴性筛选后HA滴度较高的病毒用Real-Time PCR法对表面蛋白基因型进行鉴定.对表面蛋白基因型正确的毒株用限制性内切酶酶切鉴定法鉴定其内部基因组成.进一步对HA和NA基因进行Sanger法测序,并用表面基因无氨基酸位点突变的毒株免疫雪貂,进行双向血凝抑制（Two-way hemagglutination inhibition test,HI）试验.结果 Real-Time PCR筛选出5株表面蛋白基因型正确的毒株.经内部基因鉴定其中4株为6＋2组成,1株为5＋3组成.5株重配株的HA和NA基因均未发生氨基酸位点突变.5株重配株HA滴度均维持在1 024以上.最终选取的12号重配株免疫原性良好,HI滴度达5 120,双向HI试验均通过.重配后疫苗株在鸡胚上的产量是重配前野毒株的64倍.结论 成功制备了2015-2016年度中国流行的甲型H1N1亚型流感病毒疫苗株,为疫苗贮备和疾病防控奠定了基础.     

2009年泉州市H1N1流感监测及基因特性分析

目的 了解2009年泉州地区H1N1流感监测情况,分析泉州市H1N1流感病毒的HA和NA基因特征,探讨该病毒的遗传变异及分子特性.方法 对泉州市H1N1流感监测期间的病人咽拭子采用real-time RT-PCR方法检测病毒核酸,MDCK细胞培养进行病毒分离、鉴定,并提取其中2株代表性毒株病毒RNA;采用RT-PCR扩增病毒HA和NA基因,纯化产物进行核苷酸序列测定;用DNAStar Megalign软件进行序列分析.结果 1020份咽拭子中有200份为H1N1流感病毒核酸阳性,70份季节性流感病毒核酸阳性,其中53份为H3N2亚型,14份为H1N1亚型,3份为B型,并分离到29株甲型H1N1流感病毒株.HA基因经核苷酸序列测定显示,该毒株与北美流行株高度同源,由HA基因核苷酸序列推导的氨基酸系列与疫苗株A/Brisbane/59/2007相比,有22个位于抗原决定簇的氨基酸位点发生变异,但受体结合特异性仍为人样受体.NA基因耐药性位点分析,显示对达菲药物依然敏感.结论 2009年泉州市H1N1流感流行毒株与北美流行株高度同源,相对于疫苗代表株出现了HA蛋白抗原性的改变.     

河北省2010—2020年甲型H3N2流感病毒HA基因抗原漂移分析

目的:分析河北省甲型H3N2流感病毒HA基因进化分支分布及抗原位点变异特征。方法:依据不同流行年度不同地区分布选取46株河北省H3N2毒株,MEGA建立HA基因进化树,BioEdit比对核苷酸和氨基酸序列在抗原决定簇及潜在糖基化位点变异情况,对2019—2020年流行3C.2a1b+T135K和3C.2a1b+T131...     

2009-2011年广东省甲型H1N1流感病毒血凝素基因的进化特征

目的 了解2009-2011年广东甲型H1N1流感病毒血凝素基因的HA1进化特征。方法 选取广东甲型H1N1流感病毒83株,提取病毒RNA,经RT-PCR反应扩增HA1并测序,测定的序列用生物信息软件分析,与GenBank中相关序列比较,并对推导的编码氨基酸序列进行进化分析。结果 2009-2011年广东甲型H1N1流感病毒HA1基因的进化速率是5.2× 10-3,高于人季节性H1N1病毒;变异氨基酸多数位于HA蛋白表面,其中部分位于抗原决定簇;在两例死亡病例分离株HA1的第222位氨基酸发生D222G/D222N变异。结论 遗传进化分析表明,甲型H1N1流感病毒发生了一定程度的变异,造成2011年初在广东的再次流行。HA1的第222位氨基酸变异可能与疾病的严重程度有关。     

河北省2010—2020年甲型H3N2流感病毒HA基因抗原漂移分析

目的分析河北省甲型H3N2流感病毒HA基因进化分支分布及抗原位点变异特征。方法依据不同流行年度不同地区分布选取46株河北省H3N2毒株, MEGA建立HA基因进化树, BioEdit比对核苷酸和氨基酸序列在抗原决定簇及潜在糖基化位点变异情况, 对2019—2020年流行3C.2a1b+T135K和3C.2a1b+T131K亚组同源建模, 分析突变位点构象差异。结果河北省甲型H3N2流感病毒经历1和5簇(2010—2011), 自2012年春季步入3C簇, 3C-2012/13、3C.3和3C.3a分支在2013—2014年迭代流行, 2014—2017年3C.3a分支均有覆盖, 2015—2016流行年度的3C.2a1分化出2017—2020年优势流行株3C.2a1b+T131K和3C.2a1b+T135K。病毒HA蛋白抗原决定簇A、B、C、D和E均有氨基酸突变, 突变类型包括稳定保留、多样突变和特征突变, 通过建模分析比较3C.2a1b+T135K和3C.2a1b+T131K两个亚组HA蛋白抗原表位空间构象, 50、128、131、135、138和193位点空间结构差异可能导致病毒抗...     

广东新型甲型H1N1病毒血凝素基因分子进化与变异

目的 揭示广东地区2009-2011年新型H1N1病毒血凝素基因(HA)进化特征及抗原表位变异特征.方法 采用时空抽样方法抽样,检测2009-2011年广东分离的24株新型H1N1病毒HA基因核苷酸序列,与GenBank中44株国外相应序列比较;比对HA基因核苷酸序列,分析基因分子变异,构建分子遗传动力学MCMC进化树;同时分析2009-2011年广东毒株HA基因的抗原表位变异情况.结果 68株HA基因进化树显示,广东毒株进化树主干至少分为6大分支;其中2011年毒株聚类为2个(Ⅴ和Ⅵ)主要分支,各具基因特征.变异频率较高的位点包括391、467、202和214位,正向选择位点包括8、145和391;广东毒株抗原表位区发生S145L/P、L208I、Q240R、S160G和G187R位点变异.2009年广东毒株HA基因分支Ⅰ毒株可能于2010年传播到亚洲、欧洲和澳洲地区.结论 广东新型H1N1病毒HA基因变异具有传播特征(Ⅰ)和地区特征(Ⅵ),位于抗原表位Ca、Sa和Sb的氨基酸发生变异,其中位点145等变异频率较高,承受着正向选择压力.     

Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015-2016 season and comparison of HA mutations detected in Turkey since 2009

Influenza A(H1N1)pdm09 pandemic virus causing the 2009 global outbreak moved into the post-pandemic period, but its variants continued to be the prevailing subtype in the 2015-2016 influenza season in Europe and Asia. To determine the molecular characteristics of influenza A(H1N1)pdm09 isolates circulating during the 2015-2016 season in Turkey, we identified mutations in the hemagglutinin (HA) genes and investigated the presence of H275Y alteration in the neuraminidase genes in the randomly selected isolates. The comparison of the HA nucleotide sequences revealed a very high homology (>99.5%) among the studied influenza A(H1N1)pdm09 isolates, while a relatively low homology (96.6%-97.2%), was observed between Turkish isolates and the A/California/07/2009 vaccine virus. Overall 14 common mutations were detected in HA sequences of all 2015-2016 influenza A(H1N1)pdm09 isolates with respect to the A/California/07/2009 virus, four of which located in three different antigenic sites. Eleven rare mutations in 12 HA sequences were also detected. Phylogenetic analysis revealed that all characterized influenza A(H1N1)pdm09 isolates formed a single genetic cluster, belonging to the genetic subclade 6B.1, defined by HA amino acid substitutions S84N, S162N, and I216T. Furthermore, all isolates showed an oseltamivir-sensitive genotype, suggesting that Tamiflu (Oseltamivir) could still be the drug of choice in Turkey.     

Epidemiology and full genome sequence analysis of H1N1pdm09 from Northeast China

Pandemic influenza A (H1N1) 2009 virus (H1N1pdm09) was a novel tri-assortment virus that emerged in Mexico and North America in 2009 and caused the first influenza pandemic in the 21st century. This study investigated the prevalence pattern and molecular characteristics of H1N1pdm09 in three continuous years from April 2009 to March 2012 in populations of Tianjin, Northeast China. Totally, 3,068 influenza viruses (25.4 %) were detected from 12,089 respiratory specimens. Among them, 41.4 % (1,269/3,068) were H1N1pdm09 positive. 15.1 % (192/1,269) severe respiratory infection cases were H1N1pdm09 positive. H1N1pdm09 was the predominant prevalence subtype in October 2009–March 2010 (69.1 %, 930/1,346) and October 2010–March 2011 (42.1 %, 220/523). Eight isolated H1N1pdm09 viruses from severe infection/death cases in three different years were selected to sequence the whole genome through splicing the sequences following 46 PCRs. HA sequences of seven H1N1pdm09 isolates from mild infection cases were detected. Phylogenetic analysis showed that HA, NA, M, NP and NS genes of H1N1pdm09 viruses gathered together with swine influenza A (H1N1), whereas PB2 and PA genes originated from avian influenza virus, and PB1 gene originated from human seasonal influenza virus. Identity analysis indicated that all the genes were highly conserved. Compared with vaccine strain A/California/07/2009(H1N1), the maximal mutation gene was HA (0.7–2.6 %), then NA (0.6–1.7 %), last one was M (mutation rate 0–0.6 %). More site substitutions were observed in 2011 isolates than in 2009 and 2010 isolates of HA (p = 0.002), NA (p = 0.003) and PA (p = 0.001) proteins. The amino acid substitution rates were varied among eight gene segments, ranging from 7.39 × 10^?4 for PB2 to 7.40 × 10^?3 for NA. The higher d _N / d _S rates were observed in HA, PA and NS segments in H1N1pdm09 in Tianjin. Three HA amino acid site substitutions occurred at the HA receptor-binding sites and antigenic determinant, including S179N and K180T (located at antigenic site Sa) in A/Tianjinhedong/SWL44/2011(H1) and A/Tianjinjinnan/SWL41/2011(H1), and D239N (located at antigenic site Ca) in A/Tianjinninghe/SWL49/2009(H1). Antigenic drift may have occurred in H1N1pdm09 with time. No oseltamivir-resistance site substitution was observed at 275 and 295 sites. Amino acid residue site at 31 in M2 protein was N in all 8 isolates, which suggested that H1N1pdm09 was resistant to amantadine.     

Genetic characterization of influenza viruses from influenza-related hospital admissions in the St. Petersburg and Valencia sites of the Global Influenza Hospital Surveillance Network during the 2013/14 influenza season

BackgroundContinuous surveillance for genetic changes in circulating influenza viruses is needed to guide influenza prevention and control.ObjectivesTo compare intra-seasonal influenza genetic diversity of hemagglutinin in influenza A strains isolated from influenza hospital admissions collected at two distinct sites during the same season.Study designComparative phylogenetic analysis of full-length hemagglutinin genes from 77 isolated influenza A viruses from the St. Petersburg, Russian Federation and Valencia, Spain sites of the Global Influenza Hospital Surveillance Network (GIHSN) during the 2013/14 season.ResultsWe found significant variability in A(H3N2) and A(H1N1)pdm09 viruses between the two sites, with nucleotide variation at antigenic positions much lower for A(H1N1)pdm09 than for A(H3N2) viruses. For A(H1N1)pdm09, antigenic sites differed by three to four amino acids from the vaccine strain, two of them common to all tested isolates. For A(H3N2) viruses, antigenic sites differed by six to nine amino acids from the vaccine strain, four of them common to all tested isolates. A fifth amino acid substitution in the antigenic sites of A(H3N2) defined a new clade, 3C.2. For both influenza A subtypes, pairwise amino acid distances between circulating viruses and vaccine strains were significantly higher at antigenic than at non-antigenic sites. Whereas A(H1N1)pdm09 viruses clustered with clade 6B and 94% of A(H3N2) with clade 3C.3, at both study sites A(H3N2) clade 3C.2 viruses emerged towards the end of the season, showing greater pairwise amino acid distances from the vaccine strain compared to the predominant clade 3C.3.ConclusionsInfluenza A antigenic variants differed between St. Petersburg and Valencia, and A(H3N2) clade 3C.2 viruses were characterized by more amino acid differences from the vaccine strain, especially at the antigenic sites.     

Molecular evolution of the hemagglutinin and neuraminidase genes of pandemic (H1N1) 2009 influenza viruses in Sendai, Japan, during 2009–2011

Analyzing the evolutionary pattern of the influenza A(H1N1)pdm09 strain in different regions is important for understanding its diversification. We therefore conducted this study to elucidate the genetic variability and molecular evolution of the influenza A(H1N1)pdm09 strains that circulated during the 2009–2010 and 2010–2011 influenza seasons in Sendai, Japan. Nasopharyngeal swab specimens were collected from patients with influenza-like illnesses who visited outpatient clinics in Sendai City, Japan, from September 2009 to April 2011. A total of 75 isolates were selected from September 2009 to April 2011 to analyze the genetic changes in the entire hemagglutinin 1 (HA1) segment of the HA gene and the neuraminidase (NA) gene based on sequence analysis. Bayesian coalescent Markov chain Monte Carlo analyses of HA1 and NA gene sequences were performed for further analysis. High sequence identities were observed for HA1 and NA in influenza A(H1N1)pdm09, displaying 99.06 and 99.33 % nucleotide identities, respectively, with the A(H1N1)pdm09 vaccine strain A/California/07/2009. The substitution rates of nucleotides for HA1 in the 2009–2010 and 2010–2011 were 1.5 × 10^?3 and 1.6 × 10^?3 substitutions per site per year, respectively. Phylogenetic tree analysis demonstrated that Sendai isolates were clustered into global clade 7, which is characterized by an S203T mutation in the HA1 gene. Moreover, two distinct circulation clusters were present in the 2010–2011 season. Mutations were present in antigenic or receptor-binding domains of the HA1 segment, including A141V, S143G, S183P, S185T, and S203T. The Bayesian skyline plot model illustrated a steady rate for the maintenance of genetic diversity, followed by a slight increase in the later part of the 2010–2011 season. Selection analysis revealed that the HA1 (position 197) and NA (position 46) sites were under positive selection; however, no known mutation conferring resistance to NA inhibitors such as H275Y was observed. The effect on control of the influenza A(H1N1)pdm09 virus, including vaccine strain selection, requires continuous monitoring of the strain by genetic surveillance.     

IgM,IgG, and IgA Antibody Responses to Influenza A(H1N1)pdm09 Hemagglutinin in Infected Persons during the First Wave of the 2009 Pandemic in the United States

The novel influenza A(H1N1)pdm09 virus caused an influenza pandemic in 2009. IgM, IgG, and IgA antibody responses to A(H1N1)pdm09 hemagglutinin (HA) following A(H1N1)pdm09 virus infection were analyzed to understand antibody isotype responses. Age-matched control sera collected from U.S. residents in 2007 and 2008 were used to establish baseline levels of cross-reactive antibodies. IgM responses often used as indicators of primary virus infection were mainly detected in young patient groups (≤5 years and 6 to 15 years old), not in older age groups, despite the genetic and antigenic differences between the HA of A(H1N1)pdm09 virus and pre-2009 seasonal H1N1 viruses. IgG and IgA responses to A(H1N1)pdm09 HA were detected in all age groups of infected persons. In persons 17 to 80 years old, paired acute- and convalescent-phase serum samples demonstrated ≥4-fold increases in the IgG and IgA responses to A(H1N1)pdm09 HA in 80% and 67% of A(H1N1)pdm09 virus-infected persons, respectively. The IgG antibody response to A(H1N1)pdm09 HA was cross-reactive with HAs from H1, H3, H5, and H13 subtypes, suggesting that infections with subtypes other than A(H1N1)pdm09 might result in false positives by enzyme-linked immunosorbent assay (ELISA). Lower sensitivity compared to hemagglutination inhibition and microneutralization assays and the detection of cross-reactive antibodies against homologous and heterologous subtype are major drawbacks for the application of ELISA in influenza serologic studies.     

Phylogenetic analysis of pandemic 2009 influenza A virus circulating in the South American region: genetic relationships and vaccine strain match

The first influenza pandemic of this century was declared in April of 2009, with the emergence of a novel H1N1 influenza A virus strain (H1N1pdm). Understanding the evolution of H1N1pdm strains within the South American region is essential for studying global diversification, emergence and resistance, as well as determining vaccine efficacy. In order to gain insight into these matters, phylogenetic analysis was performed using 29 hemagglutinin (HA) gene sequences from H1N1pdm strains isolated in South America. The results of these studies revealed that clade 7 was the dominant H1N1pdm lineage in South America. None of the strains isolated in South America clustered together with the 2010 H1 vaccine strain. Amino acid substitutions P100S, S220T and I338V were found in almost all HAs of South American H1N1pdm strains.     

Genetic diversity of HA1 domain of hemagglutinin gene of pandemic influenza H1N1pdm09 viruses in New Delhi, India

Genetic analysis of pandemic 2009 influenza A (H1N1; H1N1pdm09) virus was undertaken to understand virus evolution during 2009 and 2010 in India. Surveillance of influenza viruses from July 2009 to December 2010 revealed major peaks of circulating H1N1pdm09 viruses in August–September and December–January 2009 and then in August–September 2010. To understand the diversity of the H1N1pdm09 virus, selected specimens (n = 23) from 2009 or 2010 were characterized by nucleotide sequence determination of the HA1 subunit of the HA gene. Phylogenetic analysis revealed that 22 clustered with clade 7 viruses characterized by S203T mutations, whereas one virus from 2010 fell within clade 6. None of the viruses from either 2009 or 2010 formed a monophyletic group, suggesting a continuum of independent introduction of circulating viral strains. Amino acid analysis revealed minor amino acid changes in the antigenic or receptor‐binding domains. Importantly, we observed mutations that were also present in 1918 pandemic virus, which includes S183P in 4 and S185T mutation in 3 of 13 viruses analyzed from 2010, while none of the 2009 viruses carried these mutations. Whether antibody‐mediated pressure is imposing such changes remains to be determined. Continued genetic surveillance is warranted to monitor pathogenicity as the virus evolves to acquire new features. J. Med. Virol. 84:386–393, 2012. © 2011 Wiley Periodicals, Inc.     

Antigenic variation of H1N1, H1N2 and H3N2 swine influenza viruses in Japan and Vietnam

The antigenicity of the influenza A virus hemagglutinin is responsible for vaccine efficacy in protecting pigs against swine influenza virus (SIV) infection. However, the antigenicity of SIV strains currently circulating in Japan and Vietnam has not been well characterized. We examined the antigenicity of classical H1 SIVs, pandemic A(H1N1)2009 (A(H1N1)pdm09) viruses, and seasonal human-lineage SIVs isolated in Japan and Vietnam. A hemagglutination inhibition (HI) assay was used to determine antigenic differences that differentiate the recent Japanese H1N2 and H3N2 SIVs from the H1N1 and H3N2 domestic vaccine strains. Minor antigenic variation between pig A(H1N1)pdm09 viruses was evident by HI assay using 13 mAbs raised against homologous virus. A Vietnamese H1N2 SIV, whose H1 gene originated from a human strain in the mid-2000s, reacted poorly with post-infection ferret serum against human vaccine strains from 2000-2010. These results provide useful information for selection of optimal strains for SIV vaccine production.