Human norovirus (HuNoV) is the leading cause of global infectious acute gastroenteritis, causing ~20% of reported diarrheal episodes. Typically, GII.4 strains cause 50–70% of yearly outbreaks, and pandemic waves of disease approximately every 2–7 years due to rapid evolution. Importantly, GII.4 dominance is occasionally challenged by the sudden emergence of other GII strains, most recently by GII.2 strains which peaked in 2016–2017, dramatically increasing from 1% to 20% of total HuNoV outbreaks. To determine if viral capsid evolution may account for the sudden rise in GII.2 outbreaks, Virus Like Particles (VLPs) of two 2016–2017 GII.2 strains were compared by antigenic and histo blood group antigen (HBGA) binding profiles to the prototypic 1976 GII.2 Snow Mountain Virus (SMV) strain. Despite >50 years of GII.2 strain persistence in human populations, limited sequence diversity and antigenic differences were identified between strains. However, capsid microvariation did affect HBGA binding patterns, with contemporary strains demonstrating decreased avidity for type A saliva. Furthermore, bile salts increased GII.2 VLP avidity for HBGAs, but did not alter antigenicity. These data indicate that large changes in antigenicity or receptor binding are unlikely to explain GII.2 emergence, in contrast to the pandemic GII.4 strains, and indicate that host factors such as waning or remodeling of serum or mucosal immunity likely contributed to the surge in GII.2 prevalence.

中文翻译：

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胆汁促进人类诺如病毒与多种组织血型抗原的相互作用，补偿 2016-2017 年 GII.2 菌株中观察到的衣壳微变异。


人类诺如病毒 (HuNoV) 是全球传染性急性胃肠炎的主要原因，约 20% 的腹泻病例都是由其引起的。通常，GII.4 菌株导致每年 50-70% 的疫情爆发，并且由于快速进化，大约每 2-7 年就会发生一次疾病大流行。重要的是，GII.4 的主导地位偶尔会受到其他 GII 毒株突然出现的挑战，最近一次是受到 GII.2 毒株的挑战，该毒株在 2016 年至 2017 年达到顶峰，占 HuNoV 爆发总数的比例从 1% 急剧增加至 20%。为了确定病毒衣壳进化是否可以解释 GII.2 爆发的突然增加，通过抗原和组织血型抗原 (HBGA) 与原型的结合谱对两种 2016-2017 年 GII.2 毒株的病毒样颗粒 (VLP) 进行了比较1976 GII.2 雪山病毒 (SMV) 株。尽管 GII.2 菌株在人群中持续存在超过 50 年，但菌株之间的序列多样性和抗原差异有限。然而，衣壳微变异确实影响了 HBGA 结合模式，当代菌株表现出对 A 型唾液的亲合力降低。此外，胆汁盐增加了 GII.2 VLP 对 HBGA 的亲和力，但不改变抗原性。这些数据表明，与大流行的 GII.4 菌株相比，抗原性或受体结合的巨大变化不太可能解释 GII.2 的出现，并表明血清或粘膜免疫的减弱或重塑等宿主因素可能导致了激增GII.2 患病率。