Humans and Ferrets with Prior H1N1 Influenza Virus Infections Do Not Exhibit Evidence of Original Antigenic Sin after Infection or Vaccination with the 2009 Pandemic H1N1 Influenza Virus

Humans and Ferrets with Prior H1N1 Influenza Virus Infections Do Not Exhibit Evidence of Original Antigenic Sin after Infection or Vaccination with the 2009 Pandemic H1N1 Influenza Virus
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DOI:
10.1128/cvi.00790-13
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发表时间:
2014-05-01
影响因子:
--
通讯作者:
Subbarao,Kanta
Subbarao,Kanta
中科院分区:
生物3区
文献类型:
--
作者:
O'Donnell,Christopher D.;Wright,Amber;Subbarao,Kanta

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原始抗原罪假说(OAS)认为,个体首次感染流感病毒所建立的印记决定了此后的抗体反应。随后的流感病毒感染导致针对原始感染病毒的抗体应答和针对新流感病毒的受损免疫应答。我们的研究的目的是寻求OAS感染或接种2009年大流行H1N1(2009 pH1N1)病毒后,在雪貂和人类先前感染H1N1病毒与各种抗原距离从2009 pH1N1病毒,包括从1935年到1999年的病毒。在雪貂中,季节性H1N1引发没有减少对感染或接种2009 pH1N1病毒的抗体应答,也没有减少T细胞应答,表明季节性H1N1病毒引发的雪貂中没有OAS。对2009年pH1N1单价灭活疫苗接种前后采集的人血清配对样本进行分析,结果显示,与每名受试者童年时期流行的H1N1病毒相比,2009年pH1N1病毒抗体滴度显著升高了1倍。因此,H1N1病毒的既往经验并未导致针对2009年pH1N1疫苗的抗体应答受损。我们从雪貂和人类身上获得的数据表明,先前接触H1N1病毒并没有损害对2009年pH1N1病毒的免疫反应。
The hypothesis of original antigenic sin (OAS) states that the imprint established by an individual's first influenza virus infection governs the antibody response thereafter. Subsequent influenza virus infection results in an antibody response against the original infecting virus and an impaired immune response against the newer influenza virus. The purpose of our study was to seek evidence of OAS after infection or vaccination with the 2009 pandemic H1N1 (2009 pH1N1) virus in ferrets and humans previously infected with H1N1 viruses with various antigenic distances from the 2009 pH1N1 virus, including viruses from 1935 through 1999. In ferrets, seasonal H1N1 priming did not diminish the antibody response to infection or vaccination with the 2009 pH1N1 virus, nor did it diminish the T-cell response, indicating the absence of OAS in seasonal H1N1 virus-primed ferrets. Analysis of paired samples of human serum taken before and after vaccination with a monovalent inactivated 2009 pH1N1 vaccine showed a significantly greater-fold rise in the titer of antibody against the 2009 pH1N1 virus than against H1N1 viruses that circulated during the childhood of each subject. Thus, prior experience with H1N1 viruses did not result in an impairment of the antibody response against the 2009 pH1N1 vaccine. Our data from ferrets and humans suggest that prior exposure to H1N1 viruses did not impair the immune response against the 2009 pH1N1 virus.