tetano
Editor, Senior Moderator
Sci Adv
. 2025 Mar 28;11(13):eadu3344.
doi: 10.1126/sciadv.adu3344. Epub 2025 Mar 28. Neuraminidase-specific antibodies drive differential cross-protection between contemporary FLUBV lineages
Caroline K Page[SUP] 1 2 3 [/SUP], Justin D Shepard[SUP] 1 2 3 [/SUP], Sean D Ray[SUP] 1 2 3 [/SUP], James A Ferguson[SUP] 4 [/SUP], Alesandra J Rodriguez[SUP] 4 [/SUP], Julianna Han[SUP] 4 [/SUP], Joel C Jacob[SUP] 5 6 [/SUP], Dawne K Rowe-Haas[SUP] 1 2 3 [/SUP], Jasmine Y Akinpelu[SUP] 1 [/SUP], Lilach M Friedman[SUP] 5 6 [/SUP], Tomer Hertz[SUP] 5 6 7 [/SUP], Andrew B Ward[SUP] 4 [/SUP], Stephen M Tompkins[SUP] 1 2 3 [/SUP]
Affiliations
The two influenza B virus (FLUBV) lineages have continuously diverged from each other since the 1980s, with recent (post-2015) viruses exhibiting accelerated evolutionary rates. Emerging data from human studies and epidemiological models suggest that increased divergence in contemporary viruses may drive differential cross-protection, where infection with Yamagata lineage viruses provides limited immunity against Victoria lineage viruses. Here, we developed animal models to investigate the mechanisms behind asymmetric cross-protection between contemporary FLUBV lineages. Our results show that contemporary Victoria immunity provides robust cross-protection against the Yamagata lineage, whereas Yamagata immunity offers limited protection against the Victoria lineage. This differential cross-protection is driven by Victoria-elicited neuraminidase (NA)-specific antibodies, which show cross-lineage reactivity, unlike those from Yamagata infections. These findings identify a phenomenon in contemporary FLUBV that may help explain the recent disappearance of the Yamagata lineage from circulation, highlighting the crucial role of targeting NA in vaccination strategies to enhance cross-lineage FLUBV protection.
. 2025 Mar 28;11(13):eadu3344.
doi: 10.1126/sciadv.adu3344. Epub 2025 Mar 28. Neuraminidase-specific antibodies drive differential cross-protection between contemporary FLUBV lineages
Caroline K Page[SUP] 1 2 3 [/SUP], Justin D Shepard[SUP] 1 2 3 [/SUP], Sean D Ray[SUP] 1 2 3 [/SUP], James A Ferguson[SUP] 4 [/SUP], Alesandra J Rodriguez[SUP] 4 [/SUP], Julianna Han[SUP] 4 [/SUP], Joel C Jacob[SUP] 5 6 [/SUP], Dawne K Rowe-Haas[SUP] 1 2 3 [/SUP], Jasmine Y Akinpelu[SUP] 1 [/SUP], Lilach M Friedman[SUP] 5 6 [/SUP], Tomer Hertz[SUP] 5 6 7 [/SUP], Andrew B Ward[SUP] 4 [/SUP], Stephen M Tompkins[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 40153499
- DOI: 10.1126/sciadv.adu3344
The two influenza B virus (FLUBV) lineages have continuously diverged from each other since the 1980s, with recent (post-2015) viruses exhibiting accelerated evolutionary rates. Emerging data from human studies and epidemiological models suggest that increased divergence in contemporary viruses may drive differential cross-protection, where infection with Yamagata lineage viruses provides limited immunity against Victoria lineage viruses. Here, we developed animal models to investigate the mechanisms behind asymmetric cross-protection between contemporary FLUBV lineages. Our results show that contemporary Victoria immunity provides robust cross-protection against the Yamagata lineage, whereas Yamagata immunity offers limited protection against the Victoria lineage. This differential cross-protection is driven by Victoria-elicited neuraminidase (NA)-specific antibodies, which show cross-lineage reactivity, unlike those from Yamagata infections. These findings identify a phenomenon in contemporary FLUBV that may help explain the recent disappearance of the Yamagata lineage from circulation, highlighting the crucial role of targeting NA in vaccination strategies to enhance cross-lineage FLUBV protection.