tetano
Editor, Senior Moderator
Viruses
. 2020 Oct 12;12(10):E1155.
doi: 10.3390/v12101155.
Evaluation of the Pathogenicity and the Escape from Vaccine Protection of a New Antigenic Variant Derived from the European Human-Like Reassortant Swine H1N2 Influenza Virus
C?line Deblanc[SUP] 1 [/SUP], St?phane Qu?guiner[SUP] 1 [/SUP], St?phane Gorin[SUP] 1 [/SUP], Am?lie Chastagner[SUP] 1 [/SUP], S?verine Herv?[SUP] 1 [/SUP], Fr?d?ric Paboeuf[SUP] 2 [/SUP], Ga?lle Simon[SUP] 1 [/SUP]
Affiliations
Abstract
The surveillance of swine influenza A viruses in France revealed the emergence of an antigenic variant following deletions and mutations that are fixed in the HA-encoding gene of the European human-like reassortant swine H1N2 lineage. In this study, we compared the outcomes of the parental (H1[SUB]hu[/SUB]N2) and variant (H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB]) virus infections in experimentally-inoculated piglets. Moreover, we assessed and compared the protection that was conferred by an inactivated vaccine currently licensed in Europe. Three groups of five unvaccinated or vaccinated piglets were inoculated with H1[SUB]hu[/SUB]N2 or H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB] or mock-inoculated, respectively. In unvaccinated piglets, the variant strain induced greater clinical signs than the parental virus, in relation to a higher inflammatory response that involves TNF-α production and a huge afflux of granulocytes into the lung. However, both infections led to similar levels of virus excretion and adaptive (humoral and cellular) immune responses in blood. The vaccinated animals were clinically protected from both infectious challenges and did not exhibit any inflammatory responses, regardless the inoculated virus. However, whereas vaccination prevented virus shedding in H1[SUB]hu[/SUB]N2-infected animals, it did not completely inhibit the multiplication of the variant strain, since live virus particles were detected in nasal secretions that were taken from H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB]-inoculated vaccinated piglets. This difference in the level of vaccine protection was probably related to the poorer ability of the post-vaccine antibodies to neutralize the variant virus than the parental virus, even though post-vaccine cellular immunity appeared to be equally effective against both viruses. These results suggest that vaccine antigens would potentially need to be updated if this variant becomes established in Europe.
Keywords: H1N2; pathogenesis; post-infectious immune response; swine influenza virus; vaccine; variant.
. 2020 Oct 12;12(10):E1155.
doi: 10.3390/v12101155.
Evaluation of the Pathogenicity and the Escape from Vaccine Protection of a New Antigenic Variant Derived from the European Human-Like Reassortant Swine H1N2 Influenza Virus
C?line Deblanc[SUP] 1 [/SUP], St?phane Qu?guiner[SUP] 1 [/SUP], St?phane Gorin[SUP] 1 [/SUP], Am?lie Chastagner[SUP] 1 [/SUP], S?verine Herv?[SUP] 1 [/SUP], Fr?d?ric Paboeuf[SUP] 2 [/SUP], Ga?lle Simon[SUP] 1 [/SUP]
Affiliations
- PMID: 33053905
- DOI: 10.3390/v12101155
Abstract
The surveillance of swine influenza A viruses in France revealed the emergence of an antigenic variant following deletions and mutations that are fixed in the HA-encoding gene of the European human-like reassortant swine H1N2 lineage. In this study, we compared the outcomes of the parental (H1[SUB]hu[/SUB]N2) and variant (H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB]) virus infections in experimentally-inoculated piglets. Moreover, we assessed and compared the protection that was conferred by an inactivated vaccine currently licensed in Europe. Three groups of five unvaccinated or vaccinated piglets were inoculated with H1[SUB]hu[/SUB]N2 or H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB] or mock-inoculated, respectively. In unvaccinated piglets, the variant strain induced greater clinical signs than the parental virus, in relation to a higher inflammatory response that involves TNF-α production and a huge afflux of granulocytes into the lung. However, both infections led to similar levels of virus excretion and adaptive (humoral and cellular) immune responses in blood. The vaccinated animals were clinically protected from both infectious challenges and did not exhibit any inflammatory responses, regardless the inoculated virus. However, whereas vaccination prevented virus shedding in H1[SUB]hu[/SUB]N2-infected animals, it did not completely inhibit the multiplication of the variant strain, since live virus particles were detected in nasal secretions that were taken from H1[SUB]hu[/SUB]N2[SUB]Δ146-147[/SUB]-inoculated vaccinated piglets. This difference in the level of vaccine protection was probably related to the poorer ability of the post-vaccine antibodies to neutralize the variant virus than the parental virus, even though post-vaccine cellular immunity appeared to be equally effective against both viruses. These results suggest that vaccine antigens would potentially need to be updated if this variant becomes established in Europe.
Keywords: H1N2; pathogenesis; post-infectious immune response; swine influenza virus; vaccine; variant.