tetano
Editor, Senior Moderator
Nat Immunol
. 2024 Jun 20.
doi: 10.1038/s41590-024-01868-z. Online ahead of print. Vaccination reduces central nervous system IL-1β and memory deficits after COVID-19 in mice
Abigail Vanderheiden[SUP] 1 2 [/SUP], Jeremy D Hill[SUP] 1 2 [/SUP], Xiaoping Jiang[SUP] 1 2 [/SUP], Ben Deppen[SUP] 1 2 [/SUP], Gayan Bamunuarachchi[SUP] 2 [/SUP], Nadia Soudani[SUP] 2 [/SUP], Astha Joshi[SUP] 2 [/SUP], Matthew D Cain[SUP] 2 [/SUP], Adrianus C M Boon[SUP] 2 3 [/SUP], Robyn S Klein[SUP] 4 5 [/SUP]
Affiliations
Up to 25% of individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exhibit postacute cognitive sequelae. Although millions of cases of coronavirus disease 2019 (COVID-19)-mediated memory dysfunction are accumulating worldwide, the underlying mechanisms and how vaccination lowers risk are unknown. Interleukin-1 (IL-1), a key component of innate immune defense against SARS-CoV-2 infection, is elevated in the hippocampi of individuals with COVID-19. Here we show that intranasal infection of C57BL/6J mice with SARS-CoV-2 Beta variant leads to central nervous system infiltration of Ly6C[SUP]hi[/SUP] monocytes and microglial activation. Accordingly, SARS-CoV-2, but not H1N1 influenza virus, increases levels of brain IL-1β and induces persistent IL-1R1-mediated loss of hippocampal neurogenesis, which promotes postacute cognitive deficits. Vaccination with a low dose of adenoviral-vectored spike protein prevents hippocampal production of IL-1β during breakthrough SARS-CoV-2 infection, loss of neurogenesis and subsequent memory deficits. Our study identifies IL-1β as one potential mechanism driving SARS-CoV-2-induced cognitive impairment in a new mouse model that is prevented by vaccination.
. 2024 Jun 20.
doi: 10.1038/s41590-024-01868-z. Online ahead of print. Vaccination reduces central nervous system IL-1β and memory deficits after COVID-19 in mice
Abigail Vanderheiden[SUP] 1 2 [/SUP], Jeremy D Hill[SUP] 1 2 [/SUP], Xiaoping Jiang[SUP] 1 2 [/SUP], Ben Deppen[SUP] 1 2 [/SUP], Gayan Bamunuarachchi[SUP] 2 [/SUP], Nadia Soudani[SUP] 2 [/SUP], Astha Joshi[SUP] 2 [/SUP], Matthew D Cain[SUP] 2 [/SUP], Adrianus C M Boon[SUP] 2 3 [/SUP], Robyn S Klein[SUP] 4 5 [/SUP]
Affiliations
- PMID: 38902519
- DOI: 10.1038/s41590-024-01868-z
Up to 25% of individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exhibit postacute cognitive sequelae. Although millions of cases of coronavirus disease 2019 (COVID-19)-mediated memory dysfunction are accumulating worldwide, the underlying mechanisms and how vaccination lowers risk are unknown. Interleukin-1 (IL-1), a key component of innate immune defense against SARS-CoV-2 infection, is elevated in the hippocampi of individuals with COVID-19. Here we show that intranasal infection of C57BL/6J mice with SARS-CoV-2 Beta variant leads to central nervous system infiltration of Ly6C[SUP]hi[/SUP] monocytes and microglial activation. Accordingly, SARS-CoV-2, but not H1N1 influenza virus, increases levels of brain IL-1β and induces persistent IL-1R1-mediated loss of hippocampal neurogenesis, which promotes postacute cognitive deficits. Vaccination with a low dose of adenoviral-vectored spike protein prevents hippocampal production of IL-1β during breakthrough SARS-CoV-2 infection, loss of neurogenesis and subsequent memory deficits. Our study identifies IL-1β as one potential mechanism driving SARS-CoV-2-induced cognitive impairment in a new mouse model that is prevented by vaccination.