一项为期20个月的纵向研究,评估COVID-19疫苗后的体液和细胞免疫

IF 2.5 4区 医学 Q2 PARASITOLOGY
Memorias do Instituto Oswaldo Cruz Pub Date : 2025-07-18 eCollection Date: 2025-01-01 DOI:10.1590/0074-02760240193
Wlademir Braga Salgado Sobrinho, Bárbara Batista Salgado, Aguyda Rayany Cavalcante Barbosa, Vanessa Araújo Passos, Lisvane Paes Vieira, Lhorruama Dias do Nascimento, Jaila Dias Borges Lalwani, Pritesh Jaychand Lalwani, Paulo Afonso Nogueira
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引用次数: 0

摘要

背景:2019冠状病毒病(COVID-19)疫苗的有效性已得到证实;然而,疫苗诱导免疫的长期持久性仍有待充分阐明。目的:本研究纵向比较了两组患者的体液和细胞免疫反应:G1组接受了两剂sinovaco - coronavac, G2组接受了两剂AstraZeneca-Oxford,两组患者随后都接受了辉瑞的增强治疗。方法:在5个时间点评估免疫应答:P1(第二次注射前)、P2(第二次注射后90-180天)、P3(加强前、第二次注射后6 - 8个月)、P4(加强后90-180天)和P5(加强后180-270天)。采用酶联免疫吸附法(ELISA)检测抗穗状病毒冠状病毒2 (SARS-CoV-2) IgG水平,采用酶联免疫吸附斑点法(ELISPOT)检测响应穗状肽产生ifn γ的细胞。在一部分样本中分析IgG亚类。结果:在第一次给药后,sinovacc - coronavac诱导的抗刺突IgG水平低于阿斯利康-牛津,但在第二次给药后水平持平。在辉瑞加强后,抗刺突IgG水平在两组中保持升高长达6个月。两组均以IgG1为主,IgG2和IgG4偶有表达。与阿斯利康-牛津相比,在第二次给药前和第二次给药后6个月,Sinovac-CoronaVac组产生ifn - γ细胞的平均频率较低。然而,辉瑞助推器之后,这两种手段变得可比性。在增强后90-180天,与阿斯利康-牛津+辉瑞组相比,Sinovac-CoronaVac +辉瑞组的ifn γ生成细胞数量有统计学意义的下降。到P5时,超过一半的Sinovac-CoronaVac + Pfizer组患者未表现出可检测到的细胞反应。主要结论:在同种和异种疫苗接种后,高抗体水平可维持长达6个月。然而,在Sinovac-CoronaVac +辉瑞组中,细胞免疫下降更为明显,导致无应答比例更高。这些发现强调了量身定制的增强策略对维持对COVID-19的保护性免疫的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A 20-month longitudinal study to evaluate humoral and cellular immunity after COVID-19 vaccines.

A 20-month longitudinal study to evaluate humoral and cellular immunity after COVID-19 vaccines.

A 20-month longitudinal study to evaluate humoral and cellular immunity after COVID-19 vaccines.

A 20-month longitudinal study to evaluate humoral and cellular immunity after COVID-19 vaccines.

Background: The effectiveness of coronavirus disease 2019 (COVID-19) vaccines is well established; however, the long-term durability of vaccine-induced immunity remains to be fully elucidated.

Objectives: This study longitudinally compared humoral and cellular immune responses in two groups: G1, who received two doses of Sinovac-CoronaVac, and G2, who received two doses of AstraZeneca-Oxford, both subsequently boosted with Pfizer.

Methods: Immune responses were assessed at five time points: P1 (prior to the second dose), P2 (90-180 days after the second dose), P3 (pre-booster, six-eight months post-second dose), P4 (90-180 days post-booster), and P5 (180-270 days post-booster). Anti-Spike severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) IgG levels were measured by enzyme-linked immunosorbent assay (ELISA), while IFNγ-producing cells in response to Spike peptides were quantified using enzyme-linked immune absorbent spot (ELISPOT). IgG subclasses were analysed in a subset of samples.

Results: Following the first dose, Sinovac-CoronaVac induced lower anti-Spike IgG levels than AstraZeneca-Oxford, though levels equalised after the second dose. After the Pfizer booster, anti-Spike IgG levels remained elevated for up to six months in both groups. IgG1 was predominant in both groups, with occasional expression of IgG2 and IgG4. The mean frequency of IFNγ-producing cells was lower in the Sinovac-CoronaVac group before and up to six months after the second dose, compared to AstraZeneca-Oxford. However, post-Pfizer booster, both means became comparable. Between 90-180 days post-booster, the Sinovac-CoronaVac + Pfizer group exhibited a statistically significant decline in IFNγ-producing cells relative to the AstraZeneca-Oxford + Pfizer group. By P5, over half of individuals in the Sinovac-CoronaVac + Pfizer group demonstrated no detectable cellular response.

Main conclusions: High antibody levels were maintained for up to six months following both homologous and heterologous vaccination. However, cellular immunity declined more markedly in the Sinovac-CoronaVac + Pfizer group, resulting in a higher proportion of non-responders. These findings underscore the importance of tailored booster strategies to sustain protective immunity against COVID-19.

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来源期刊
CiteScore
5.00
自引率
3.60%
发文量
91
审稿时长
3-8 weeks
期刊介绍: Memórias do Instituto Oswaldo Cruz is a journal specialized in microbes & their vectors causing human infections. This means that we accept manuscripts covering multidisciplinary approaches and findings in the basic aspects of infectious diseases, e.g. basic in research in prokariotes, eukaryotes, and/or virus. Articles must clearly show what is the main question to be answered, the hypothesis raised, and the contribution given by the study. Priority is given to manuscripts reporting novel mechanisms and general findings concerning the biology of human infectious prokariotes, eukariotes or virus. Papers reporting innovative methods for diagnostics or that advance the basic research with these infectious agents are also welcome. It is important to mention what we do not publish: veterinary infectious agents research, taxonomic analysis and re-description of species, epidemiological studies or surveys or case reports and data re-analysis. Manuscripts that fall in these cases or that are considered of low priority by the journal editorial board, will be returned to the author(s) for submission to another journal.
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