甲型H1N1流感pdm09病毒感染可诱导持久的血清保护:来自Ha Nam队列的结果

Le Nguyen Minh Hoa, Sheena G Sullivan, Le Quynh Mai, Arseniy Khvorov, Hoang Vu Mai Phuong, Nguyen Le Khanh Hang, Pham Quang Thai, Le Thi Thanh, Louise Carolan, Dang Duc Anh, Tran Nhu Duong, Juliet E Bryant, H Rogier van Doorn, Heiman F L Wertheim, Peter Horby, Annette Fox
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引用次数: 8

摘要

背景:流感复发在多大程度上取决于先前感染的免疫力下降尚不明确。我们使用Ha-Nam队列参与者的抗体滴度来估计保护曲线和衰减轨迹。方法:270户家庭参与流感样疾病(ILI)监测,并在实验室确认的病毒传播期间间隔提供血液。用血凝抑制试验检测血清。感染被定义为流感病毒阳性的ILI和/或血清转化。使用比例逻辑回归来估计中位保护滴度,以模拟该季节感染状况的传播前滴度,限制了对感染家庭的分析。使用混合效应线性回归对感染后的月滴度进行建模,以估计衰减和滴度低于保护阈值时的滴度。结果:2008年12月至2012年12月,分别有295名和314名参与者感染了h1n1pdm09样病毒和A/Perth/16/09样(H3N2Pe09)病毒。与H3N2Pe09相比,H1N1pdm09的保护比例随着滴度的增加而急剧上升,估计50%的保护滴度分别为19.6和37.3。H3N2Pe09的感染后滴度开始较高,但比H1N1pdm09的感染后滴度下降得更快。估计对H1N1pdm09的血清保护作用持续,但对H3N2Pe09的血清保护作用减弱8个月。结论:估计表明,感染诱导对H1N1pdm09的持久血清保护,而不是H3N2Pe09,这可能部分解释了A(H1N1)比A(H3N2)病例更年轻的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Influenza A(H1N1)pdm09 But Not A(H3N2) Virus Infection Induces Durable Seroprotection: Results From the Ha Nam Cohort.

Influenza A(H1N1)pdm09 But Not A(H3N2) Virus Infection Induces Durable Seroprotection: Results From the Ha Nam Cohort.

Influenza A(H1N1)pdm09 But Not A(H3N2) Virus Infection Induces Durable Seroprotection: Results From the Ha Nam Cohort.

Influenza A(H1N1)pdm09 But Not A(H3N2) Virus Infection Induces Durable Seroprotection: Results From the Ha Nam Cohort.

Background: The extent to which influenza recurrence depends upon waning immunity from prior infection is undefined. We used antibody titers of Ha-Nam cohort participants to estimate protection curves and decay trajectories.

Methods: Households (270) participated in influenza-like-illness (ILI) surveillance and provided blood at intervals spanning laboratory-confirmed virus transmission. Sera were tested in hemagglutination inhibition assay. Infection was defined as influenza virus-positive ILI and/or seroconversion. Median protective titers were estimated using scaled-logistic regression to model pretransmission titer against infection status in that season, limiting analysis to households with infection(s). Titers were modelled against month since infection using mixed-effects linear regression to estimate decay and when titers fell below protection thresholds.

Results: From December 2008-2012, 295 and 314 participants were infected with H1N1pdm09-like and A/Perth/16/09-like (H3N2Pe09) viruses, respectively. The proportion protected rose more steeply with titer for H1N1pdm09 than for H3N2Pe09, and estimated 50% protection titers were 19.6 and 37.3, respectively. Postinfection titers started higher against H3N2Pe09 but decayed more steeply than against H1N1pdm09. Seroprotection was estimated to be sustained against H1N1pdm09 but to wane by 8-months for H3N2Pe09.

Conclusions: Estimates indicate that infection induces durable seroprotection against H1N1pdm09 but not H3N2Pe09, which could in part account for the younger age of A(H1N1) versus A(H3N2) cases.

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