Sironi Manuela, Cagliani Rachele, Pontremoli Chiara, Rossi Marianna, Migliorino Guglielmo, Clerici Mario, Gori Andrea
Scientific Institute IRCCS E, MEDEA, Bioinformatics, 23842 Bosisio Parini, Italy.
BMC Res Notes. 2014 Aug 7;7:504. doi: 10.1186/1756-0500-7-504.
Host genetic factors are thought to modulated the severity of disease caused by infection with the 2009 H1N1 pandemic influenza virus (H1N1pdm09). The human CCR5 gene encodes a cytokine receptor important for cell-mediated immune response against H1N1pdm09. A 32-bp polymorphic deletion in the coding sequence of CCR5, the so-called CCR5Δ32 allele, segregates in populations of European ancestry with a frequency of 8-15%. A high proportion of CCR5Δ32 heterozygotes was reported in a sample of white Canadian critically-ill H1N1pdm09 infected subjects, suggesting an association with disease severity.
We recruited 29 H1N1pdm09 infected subjects from Southern Europe (mostly Italians) with a wide clinical spectrum of disease symptoms; the sample included 7 subjects who developed acute respiratory distress syndrome requiring extracorporeal membrane oxygenation. The CCR5Δ32 variant was genotyped in all subjects.
The CCR5Δ32 allele was found in one single subject, who developed a very mild form and was not hospitalized.
The CCR5Δ32 allele was not found to be associated with the risk of H1N1pdm09 infection or with a severe disease course.
宿主遗传因素被认为可调节由2009年甲型H1N1流感大流行病毒(H1N1pdm09)感染所致疾病的严重程度。人类CCR5基因编码一种对针对H1N1pdm09的细胞介导免疫反应很重要的细胞因子受体。CCR5编码序列中的一个32bp多态性缺失,即所谓的CCR5Δ32等位基因,在欧洲血统人群中的分离频率为8%-15%。在一组加拿大白人重症H1N1pdm09感染受试者样本中,报告了高比例的CCR5Δ32杂合子,提示其与疾病严重程度有关。
我们招募了29名来自南欧(主要是意大利人)、具有广泛疾病症状临床谱的H1N1pdm09感染受试者;样本包括7名发生急性呼吸窘迫综合征需要体外膜肺氧合的受试者。对所有受试者进行CCR5Δ32变异基因分型。
在一名仅出现非常轻微症状且未住院的受试者中发现了CCR5Δ32等位基因。
未发现CCR5Δ32等位基因与H1N1pdm09感染风险或严重病程有关。