tetano
Editor, Senior Moderator
Sci Rep
. 2023 Feb 27;13(1):3303.
doi: 10.1038/s41598-023-29909-x.
Delta (B1.617.2) variant of SARS-CoV-2 induces severe neurotropic patterns in K18-hACE2 mice
Ju-Hee Yang[SUP] #[/SUP][SUP] 1 [/SUP], Myeon-Sik Yang[SUP] #[/SUP][SUP] 2 [/SUP], Dae-Min Kim[SUP] 1 [/SUP], Bumseok Kim[SUP] 2 [/SUP], Dongseob Tark[SUP] 3 [/SUP], Sang-Min Kang[SUP] 4 [/SUP], Gun-Hee Lee[SUP] 5 [/SUP]
Affiliations
Abstract
A highly contagious virus, severe acute respiratory syndrome coronavirus 2, caused the coronavirus disease 19 (COVID-19) pandemic (SARS-CoV-2). SARS-CoV-2 genetic variants have been reported to circulate throughout the COVID-19 pandemic. COVID-19 symptoms include respiratory symptoms, fever, muscle pain, and breathing difficulty. In addition, up to 30% of COVID-19 patients experience neurological complications such as headaches, nausea, stroke, and anosmia. However, the neurotropism of SARS-CoV-2 infection remains largely unknown. This study investigated the neurotropic patterns between the B1.617.2 (Delta) and Hu-1 variants (Wuhan, early strain) in K18-hACE2 mice. Despite both the variants inducing similar pathogenic patterns in various organs, B1.617.2-infected K18-hACE2 mice demonstrated a higher range of disease phenotypes such as weight loss, lethality, and conjunctivitis when compared to those in Hu-1-infected mice. In addition, histopathological analysis revealed that B1.617.2 infects the brain of K18-hACE2 mice more rapidly and effectively than Hu-1. Finally, we discovered that, in B1.617.2-infected mice, the early activation of various signature genes involved innate cytokines and that the necrosis-related response was most pronounced than that in Hu-1-infected mice. The present findings indicate the neuroinvasive properties of SARS-CoV-2 variants in K18-hACE2 mice and link them to fatal neuro-dissemination during the disease onset.
. 2023 Feb 27;13(1):3303.
doi: 10.1038/s41598-023-29909-x.
Delta (B1.617.2) variant of SARS-CoV-2 induces severe neurotropic patterns in K18-hACE2 mice
Ju-Hee Yang[SUP] #[/SUP][SUP] 1 [/SUP], Myeon-Sik Yang[SUP] #[/SUP][SUP] 2 [/SUP], Dae-Min Kim[SUP] 1 [/SUP], Bumseok Kim[SUP] 2 [/SUP], Dongseob Tark[SUP] 3 [/SUP], Sang-Min Kang[SUP] 4 [/SUP], Gun-Hee Lee[SUP] 5 [/SUP]
Affiliations
- PMID: 36849513
- DOI: 10.1038/s41598-023-29909-x
Abstract
A highly contagious virus, severe acute respiratory syndrome coronavirus 2, caused the coronavirus disease 19 (COVID-19) pandemic (SARS-CoV-2). SARS-CoV-2 genetic variants have been reported to circulate throughout the COVID-19 pandemic. COVID-19 symptoms include respiratory symptoms, fever, muscle pain, and breathing difficulty. In addition, up to 30% of COVID-19 patients experience neurological complications such as headaches, nausea, stroke, and anosmia. However, the neurotropism of SARS-CoV-2 infection remains largely unknown. This study investigated the neurotropic patterns between the B1.617.2 (Delta) and Hu-1 variants (Wuhan, early strain) in K18-hACE2 mice. Despite both the variants inducing similar pathogenic patterns in various organs, B1.617.2-infected K18-hACE2 mice demonstrated a higher range of disease phenotypes such as weight loss, lethality, and conjunctivitis when compared to those in Hu-1-infected mice. In addition, histopathological analysis revealed that B1.617.2 infects the brain of K18-hACE2 mice more rapidly and effectively than Hu-1. Finally, we discovered that, in B1.617.2-infected mice, the early activation of various signature genes involved innate cytokines and that the necrosis-related response was most pronounced than that in Hu-1-infected mice. The present findings indicate the neuroinvasive properties of SARS-CoV-2 variants in K18-hACE2 mice and link them to fatal neuro-dissemination during the disease onset.