tetano
Editor, Senior Moderator
Vet Pathol
. 2021 Sep 1;3009858211043084.
doi: 10.1177/03009858211043084. Online ahead of print.
Cellular tropism of SARS-CoV-2 in the respiratory tract of Syrian hamsters and B6.Cg-Tg(K18-ACE2)2Prlmn/J transgenic mice
Hui-Ling Yen[SUP] 1 [/SUP], Sophie Valkenburg[SUP] 1 [/SUP], Sin Fun Sia[SUP] 1 [/SUP], Ka Tim Choy[SUP] 1 [/SUP], J S Malik Peiris[SUP] 1 [/SUP], Karen H M Wong[SUP] 1 [/SUP], Nicholas Crossland[SUP] 2 [/SUP], Florian Douam[SUP] 2 [/SUP], John M Nicholls[SUP] 1 [/SUP]
Affiliations
Abstract
Several animal models have been developed to study the pathophysiology of SARS-CoV-2 infection and to evaluate vaccines and therapeutic agents for this emerging disease. Similar to infection with SARS-CoV-1, infection of Syrian hamsters with SARS-CoV-2 results in moderate respiratory disease involving the airways and lung parenchyma but does not lead to increased mortality. Using a combination of immunohistochemistry and transmission electron microscopy, we showed that the epithelium of the conducting airways of hamsters was the primary target for viral infection within the first 5 days of infection, with little evidence of productive infection of pneumocytes. At 6 days postinfection, antigen was cleared but parenchymal damage persisted, and the major pathological changes resolved by day 14. These findings are similar to those previously reported for hamsters with SARS-CoV-1 infection. In contrast, infection of K18-hACE2 transgenic mice resulted in pneumocyte damage, with viral particles and replication complexes in both type I and type II pneumocytes together with the presence of convoluted or cubic membranes; however, there was no evidence of virus replication in the conducting airways. The Syrian hamster is a useful model for the study of SARS-CoV-2 transmission and vaccination strategies, whereas infection of the K18-hCE2 transgenic mouse results in lethal disease with fatal neuroinvasion but with sparing of conducting airways.
Keywords: COVID-19; SARS-CoV-2; coronavirus; immunohistochemistry; pathology; severe acute respiratory syndrome; ultrastructure.
. 2021 Sep 1;3009858211043084.
doi: 10.1177/03009858211043084. Online ahead of print.
Cellular tropism of SARS-CoV-2 in the respiratory tract of Syrian hamsters and B6.Cg-Tg(K18-ACE2)2Prlmn/J transgenic mice
Hui-Ling Yen[SUP] 1 [/SUP], Sophie Valkenburg[SUP] 1 [/SUP], Sin Fun Sia[SUP] 1 [/SUP], Ka Tim Choy[SUP] 1 [/SUP], J S Malik Peiris[SUP] 1 [/SUP], Karen H M Wong[SUP] 1 [/SUP], Nicholas Crossland[SUP] 2 [/SUP], Florian Douam[SUP] 2 [/SUP], John M Nicholls[SUP] 1 [/SUP]
Affiliations
- PMID: 34467820
- DOI: 10.1177/03009858211043084
Abstract
Several animal models have been developed to study the pathophysiology of SARS-CoV-2 infection and to evaluate vaccines and therapeutic agents for this emerging disease. Similar to infection with SARS-CoV-1, infection of Syrian hamsters with SARS-CoV-2 results in moderate respiratory disease involving the airways and lung parenchyma but does not lead to increased mortality. Using a combination of immunohistochemistry and transmission electron microscopy, we showed that the epithelium of the conducting airways of hamsters was the primary target for viral infection within the first 5 days of infection, with little evidence of productive infection of pneumocytes. At 6 days postinfection, antigen was cleared but parenchymal damage persisted, and the major pathological changes resolved by day 14. These findings are similar to those previously reported for hamsters with SARS-CoV-1 infection. In contrast, infection of K18-hACE2 transgenic mice resulted in pneumocyte damage, with viral particles and replication complexes in both type I and type II pneumocytes together with the presence of convoluted or cubic membranes; however, there was no evidence of virus replication in the conducting airways. The Syrian hamster is a useful model for the study of SARS-CoV-2 transmission and vaccination strategies, whereas infection of the K18-hCE2 transgenic mouse results in lethal disease with fatal neuroinvasion but with sparing of conducting airways.
Keywords: COVID-19; SARS-CoV-2; coronavirus; immunohistochemistry; pathology; severe acute respiratory syndrome; ultrastructure.