Hervé Pierre-Louis, Lorin Valérie, Jouvion Grégory, Da Costa Bruno, Escriou Nicolas
Institut Pasteur, Unité de Génétique Moléculaire des Virus à ARN, 25-28 rue du Docteur Roux, F-75015 Paris, France; CNRS UMR 3569, 25-28 rue du Docteur Roux, F-75015 Paris, France; Université Paris Diderot, Sorbonne, Paris Cité, EA 302, 25-28 rue du Docteur Roux, Paris, France.
Institut Pasteur, Unité de Génétique Moléculaire des Virus à ARN, 25-28 rue du Docteur Roux, F-75015 Paris, France; CNRS UMR 3569, 25-28 rue du Docteur Roux, F-75015 Paris, France; Université Paris Diderot, Sorbonne, Paris Cité, EA 302, 25-28 rue du Docteur Roux, Paris, France.
Virology. 2015 Dec;486:134-45. doi: 10.1016/j.virol.2015.08.033. Epub 2015 Oct 1.
Highly pathogenic avian influenza A H5N1 viruses remain endemic in poultry in several countries and still constitute a pandemic threat. Since the early 20th century, we experienced four influenza A pandemics. H3N2 and H1N1pdm09 viruses that respectively emerged during 1968 and 2009 pandemics are still responsible for seasonal epidemics. These viruses evolve regularly by substitutions in antigenic sites of the hemagglutinin (HA), which prevent neutralization by antibodies directed against previous strains (antigenic drift). For seasonal H3N2 viruses, an addition of N-glycosylation sites (glycosites) on H3 contributed to this drift. Here, we questioned whether additional glycosites on H5 could induce an escape of H5N1 virus from neutralization, as it was observed for seasonal H3N2 viruses. Seven H5N1 mutants were produced by adding glycosites on H5. The most glycosylated virus escaped from neutralizing antibodies, in vitro and in vivo. Furthermore, a single additional glycosite was responsible for this escape.
高致病性甲型H5N1禽流感病毒在几个国家的家禽中仍然流行,并且仍然构成大流行威胁。自20世纪初以来,我们经历了四次甲型流感大流行。分别在1968年和2009年大流行期间出现的H3N2和H1N1pdm09病毒仍然是季节性流行的原因。这些病毒通过血凝素(HA)抗原位点的替换而定期进化,这阻止了针对先前毒株的抗体的中和作用(抗原漂移)。对于季节性H3N2病毒,H3上N-糖基化位点(糖基化位点)的增加促成了这种漂移。在这里,我们质疑H5上额外的糖基化位点是否会像在季节性H3N2病毒中观察到的那样,导致H5N1病毒逃避中和作用。通过在H5上添加糖基化位点产生了七个H5N1突变体。糖基化程度最高的病毒在体外和体内均能逃避中和抗体。此外,单个额外的糖基化位点导致了这种逃避。