Division of Virology, Department of Infectious Diseases, St Jude Children's Research Hospital, 262 Danny Thomas Place, Mail Stop 330, Memphis, TN 38105, USA.
J Clin Virol. 2011 Jul;51(3):170-4. doi: 10.1016/j.jcv.2011.04.001. Epub 2011 May 11.
In June 2009, the World Health Organization announced the 21st century's first influenza pandemic caused by pandemic influenza H1N1 2009 (H1N1 pdm).
Our goal was to analyze antiviral drug resistance and the phylogenetic relationships among hemagglutinin (HA) and neuraminidase (NA) genes of H1N1 pdm samples in Lebanon.
Nasopharyngeal swabs were collected from 197 patients with influenza-like illness from May 2009 through January 2010. Of the 50 influenza A-positive samples, 30 were analyzed for antiviral drug resistance by using in vitro susceptibility assays and cycling-probe real-time PCR. The HA and NA genes were also analyzed.
The results of hemagglutination-inhibition assays confirmed that all 30 analyzed samples were H1N1 pdm. In July 2009, community transmission of H1N1 pdm was detected in Lebanon, and an outbreak occurred in October 2009. The outbreak cases were caused by a strain with 4 mutations in the NA gene (i.e., V42I, N68T, N248D, and E462K) and 2 mutations in the HA gene: 1 in the Ca1 antigenic site (i.e., S206T) and 1 in the Ca2 antigenic site (i.e., D225E). This strain was closely related to a major H1N1 pdm cluster that was isolated worldwide. All 30 samples were amantadine-resistant, and none were zanamivir-resistant. The 1 oseltamivir-resistant sample appeared to be from a community-transmitted case in an otherwise healthy 2-year-old child.
Continuous monitoring of oseltamivir susceptibility among H1N1 pdm is essential to guide the effective use of this drug.
2009 年 6 月，世界卫生组织宣布 21 世纪首次由大流行性流感 H1N1 2009（H1N1pdm）引发的流感大流行。
我们的目的是分析黎巴嫩大流行性流感 H1N1pdm 样本的血凝素（HA）和神经氨酸酶（NA）基因的抗病毒药物耐药性和系统发育关系。
2009 年 5 月至 2010 年 1 月期间，从 197 例流感样疾病患者中采集鼻咽拭子。对 50 份甲型流感阳性样本中的 30 份进行了抗病毒药物耐药性分析，方法是采用体外药敏试验和循环探针实时 PCR。还分析了 HA 和 NA 基因。
血凝抑制试验的结果证实，分析的 30 个样本均为 H1N1pdm。2009 年 7 月，在黎巴嫩检测到 H1N1pdm 的社区传播，2009 年 10 月发生了疫情。疫情由株具有 4 个 NA 基因突变（即 V42I、N68T、N248D 和 E462K）和 2 个 HA 基因突变的菌株引起：1 个在 Ca1 抗原位点（即 S206T），1 个在 Ca2 抗原位点（即 D225E）。该株与全球分离的主要 H1N1pdm 聚类密切相关。所有 30 个样本均对金刚烷胺耐药，无对扎那米韦耐药。1 个奥司他韦耐药样本似乎来自社区传播的无其他疾病的 2 岁健康儿童。
持续监测大流行性流感 H1N1pdm 的奥司他韦敏感性对于指导该药的有效使用至关重要。
