tetano
Editor, Senior Moderator
NPJ Vaccines
. 2025 Feb 27;10(1):40.
doi: 10.1038/s41541-025-01095-z. SARS-CoV-2 infection primes cross-protective respiratory IgA in a MyD88- and MAVS-dependent manner
Moe Kobayashi[SUP] 1 [/SUP], Nene Kobayashi[SUP] 1 [/SUP], Kyoka Deguchi[SUP] 1 [/SUP], Seira Omori[SUP] 1 [/SUP], Takeshi Ichinohe[SUP] 2 [/SUP]
Affiliations
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is constantly evolving mutations in the Spike protein to evade humoral immunity. Respiratory tract antiviral IgA antibodies are superior to circulating IgG antibodies in preventing SARS-CoV-2 infection. However, the role of innate immune signals required for the induction of mucosal IgA against SARS-CoV-2 infection is unknown. Here we show that hamsters recovered from ancestral SARS-CoV-2 infection are cross-protected against heterologous SARS-CoV-2 alpha, gamma, delta, and omicron BA.1 variants. Intranasal vaccination with an inactivated whole virus vaccine completely protects hamsters against heterologous SARS-CoV-2 infection. In addition, we show that intranasal boost vaccination of mice recovered from SARS-CoV-2 infection with unadjuvanted Spike protein induces robust levels of respiratory anti-Spike IgA and protects the mice from a heterologous SARS-CoV-2 infection. Furthermore, our findings suggest that MyD88 and MAVS play a role in the induction of the memory IgA response following an intranasal booster with unadjuvanted Spike protein in mice recovered from the SARS-CoV-2 infection. These findings provide a useful basis for the development of cross-protective mucosal vaccines against heterologous SARS-CoV-2 infection.
. 2025 Feb 27;10(1):40.
doi: 10.1038/s41541-025-01095-z. SARS-CoV-2 infection primes cross-protective respiratory IgA in a MyD88- and MAVS-dependent manner
Moe Kobayashi[SUP] 1 [/SUP], Nene Kobayashi[SUP] 1 [/SUP], Kyoka Deguchi[SUP] 1 [/SUP], Seira Omori[SUP] 1 [/SUP], Takeshi Ichinohe[SUP] 2 [/SUP]
Affiliations
- PMID: 40016252
- DOI: 10.1038/s41541-025-01095-z
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is constantly evolving mutations in the Spike protein to evade humoral immunity. Respiratory tract antiviral IgA antibodies are superior to circulating IgG antibodies in preventing SARS-CoV-2 infection. However, the role of innate immune signals required for the induction of mucosal IgA against SARS-CoV-2 infection is unknown. Here we show that hamsters recovered from ancestral SARS-CoV-2 infection are cross-protected against heterologous SARS-CoV-2 alpha, gamma, delta, and omicron BA.1 variants. Intranasal vaccination with an inactivated whole virus vaccine completely protects hamsters against heterologous SARS-CoV-2 infection. In addition, we show that intranasal boost vaccination of mice recovered from SARS-CoV-2 infection with unadjuvanted Spike protein induces robust levels of respiratory anti-Spike IgA and protects the mice from a heterologous SARS-CoV-2 infection. Furthermore, our findings suggest that MyD88 and MAVS play a role in the induction of the memory IgA response following an intranasal booster with unadjuvanted Spike protein in mice recovered from the SARS-CoV-2 infection. These findings provide a useful basis for the development of cross-protective mucosal vaccines against heterologous SARS-CoV-2 infection.