Landivar Michael, Tohma Kentaro, Pilewski Kelsey A, Ford-Siltz Lauren A, Kendra Joseph, Gao Yamei, Parra Gabriel I
Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, USA.
J Virol. 2025 Jul 22;99(7):e0065225. doi: 10.1128/jvi.00652-25. Epub 2025 May 30.
GII.4 norovirus is responsible for most cases of viral gastroenteritis worldwide. The complex epidemiology and extreme GII.4 antigenic diversity could challenge the development of a vaccine. Most antibody responses to GII.4 norovirus target five antigenic sites mapping to the major viral capsid, whose variability has been associated with the emergence of antigenically distinct variants. Bioinformatics analyses of amino acid sequences from these antigenic sites demonstrated that antigenic site A is the most variable and relevant site for antigenic diversification. Despite this complex diversity, cross-blocking was demonstrated in the profiling of site A-mapping mouse monoclonal antibodies generated against two antigenically distinct GII.4 variants. Using a novel immunoassay, we determined the contribution of specific epitopes to blockade function in polyclonal sera and observed extensive cross-blocking in which 36% was attributed to antibodies mapping to antigenic site A. However, cross-reactivity was virus-dependent, with the greatest breadth exhibited by contemporary variants that emerged after 2006. Notably, cross-blocking titers associated with antibodies mapping to antigenic site A are differentially affected by an increasing number of mutations on the capsid. Since the elicitation of blocking antibodies to conserved regions of the GII.4 norovirus capsid is infrequent, a better understanding of how to elicit cross-protective responses to immunodominant variable antigenic sites could guide norovirus vaccine development.IMPORTANCEGII.4 noroviruses exhibit an accumulation of mutations on their capsid protein, leading to the continuous emergence and turnover of new variants that can escape herd immunity. Despite the fact that most antibodies mapping to the variable antigenic sites of GII.4 norovirus show exquisite specificity, cross-neutralizing antibodies mapping to these variable sites have also been described. In this study, we systematically evaluate the antigenicity of a panel of different GII.4 antigens to demonstrate that cross-reactive responses are elicited in a virus-dependent manner in naïve mice. Notably, one wild-type virus demonstrated multiple instances of potent cross-blocking responses, providing new hopes for the development of cross-protective vaccines against human norovirus.
GII.4 诺如病毒是全球大多数病毒性肠胃炎病例的致病原。其复杂的流行病学特征和极高的GII.4抗原多样性可能对疫苗研发构成挑战。大多数针对GII.4诺如病毒的抗体反应靶向映射到主要病毒衣壳的五个抗原位点,这些位点的变异性与抗原性不同的变体的出现有关。对来自这些抗原位点的氨基酸序列进行生物信息学分析表明,抗原位点A是抗原多样化中最具变异性且最相关的位点。尽管存在这种复杂的多样性,但在针对两种抗原性不同的GII.4变体产生的映射到位点A的小鼠单克隆抗体的分析中显示出交叉阻断现象。使用一种新型免疫测定法,我们确定了特定表位在多克隆血清中对阻断功能的贡献,并观察到广泛的交叉阻断,其中36%归因于映射到抗原位点A的抗体。然而,交叉反应性取决于病毒,2006年后出现的当代变体表现出最大的交叉反应广度。值得注意的是,与映射到抗原位点A的抗体相关的交叉阻断效价受到衣壳上越来越多突变的不同影响。由于诱导针对GII.4诺如病毒衣壳保守区域的阻断抗体并不常见,更好地理解如何诱导针对免疫显性可变抗原位点的交叉保护反应可能会指导诺如病毒疫苗的研发。重要性GII.4诺如病毒在其衣壳蛋白上积累突变,导致能够逃避群体免疫的新变体不断出现和更替。尽管大多数映射到GII.4诺如病毒可变抗原位点的抗体表现出极高的特异性,但也有针对这些可变位点的交叉中和抗体的报道。在本研究中,我们系统地评估了一组不同GII.4抗原的抗原性,以证明在未接触过病毒的小鼠中以病毒依赖的方式引发了交叉反应性应答。值得注意的是,一种野生型病毒表现出多次有效的交叉阻断反应实例,为开发针对人类诺如病毒的交叉保护疫苗带来了新希望。