National Institute for Communicable Diseases Division, National Health Laboratory Service, Department of Medical Virology, University of Pretoria, Johannesburg, South Africa.
J Infect Dis. 2012 Dec 15;206 Suppl 1:S166-72. doi: 10.1093/infdis/jis539.
The 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) was first detected in June 2009 in South Africa and later resulted in extensive transmission throughout Africa. Established routine surveillance programs and collaboration between private and public sector laboratories allowed for comprehensive molecular epidemiological and antigenic investigation of the first and second waves of 2009-2010 pandemic influenza in South Africa.
We used reverse-transcription polymerase chain reaction to screen for influenza virus in 9792 specimens recovered during 2009 and 6915 specimens recovered during 2010 from inpatients and outpatients with influenza-like illness or severe acute respiratory illness symptoms identified by surveillance programs. Influenza-positive specimens were subjected to genetic and antigenic characterization. Bayesian and maximum likelihood analyses of the hemagglutinin genes of 96 A(H1N1)pdm09 strains were used for molecular epidemiological investigations. Hemagglutination inhibition assays and sequencing of the PB2 and neuraminidase genes were used to investigate pathogenicity and resistance mutations.
The A(H1N1)pdm09 epidemic occurred as a second epidemic peak following seasonal influenza A virus subtype H3N2 cases in 2009 and in 2010. Progressive drift away from the A/California/7/2009 vaccine strain was observed at both the nucleotide and amino acid level, with 2010 strains clustering separate to 2009 strains. A few unique clusters of amino acid changes in severe cases were identified, but most strains were antigenically similar to the vaccine strain, and no resistance or known pathogenicity mutations were detected.
Despite limited drift observed over the 2 seasons in South Africa, circulating A(H1N1)pdm09 strains remained antigenically similar to strains identified in other northern and southern hemisphere countries from 2010 and 2011.
2009 年甲型 H1N1 流感病毒(A[H1N1]pdm09)于 2009 年 6 月在南非首次被发现,随后在非洲广泛传播。已建立的常规监测计划以及私营和公共部门实验室之间的合作,使南非能够对 2009-2010 年大流行流感的第一波和第二波进行全面的分子流行病学和抗原调查。
我们使用逆转录聚合酶链反应,从 2009 年和 2010 年监测计划确定的有流感样症状或严重急性呼吸道疾病症状的住院和门诊患者中采集的 9792 份和 6915 份样本中筛选流感病毒。对流感阳性样本进行遗传和抗原特征分析。对 96 株 A(H1N1)pdm09 株的血凝素基因进行贝叶斯和最大似然分析,进行分子流行病学研究。血凝抑制试验和 PB2 及神经氨酸酶基因测序用于研究致病性和耐药突变。
A(H1N1)pdm09 疫情在 2009 年季节性甲型 H3N2 病毒病例后作为第二波流行高峰出现,2009 年和 2010 年都有发生。在核苷酸和氨基酸水平上均观察到与 A/加利福尼亚/7/2009 疫苗株逐渐分离,2010 年的株系聚类与 2009 年的株系分离。在重症病例中鉴定出一些独特的氨基酸变化簇,但大多数株系与疫苗株具有相似的抗原性,未检测到耐药或已知的致病性突变。
尽管在南非的 2 个季节中观察到有限的漂移,但循环的 A(H1N1)pdm09 株与 2010 年和 2011 年来自北半球和南半球其他国家的株系在抗原上仍相似。