<p>Respiratory long COVID symptoms, including dyspnea and breathing pattern disorders, are frequently reported in convalescent COVID-19 patients. Yet the mechanisms driving these persistent respiratory manifestations remain poorly elucidated. In this study, we characterized persistent upper respiratory tract pathology in SARS-CoV-2-infected hamsters. Strikingly, we observed persistent expression of SARS-CoV-2 nucleocapsid (N) protein and subgenomic RNA (sgRNA) gene, which resulted in sustained tissue pathologies, dysregulation of pro-inflammatory markers, pro-apoptotic genes, as well as the altered expression of viral entry receptors, in the nasal turbinate of infected hamsters up to 120 days post-infection. These findings indicate that residual viral components may contribute to dysregulation of tissue repair and remodeling, chronic tissue pathology, and potentially enhanced susceptibility to secondary respiratory infections upon SARS-CoV-2 infection even upon recovery of acute infection. Collectively, our study provides insights into potential drivers of post-acute COVID-19 sequelae in the upper respiratory tract.</p>

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Prolonged dysregulation and pathological changes in the upper respiratory tract of SARS-CoV-2 infected hamsters

  • Feifei Liu,
  • Yao Xia,
  • Andrew Chak-Yiu Lee,
  • Yanxia Chen,
  • Zhe Chen,
  • Yixin He,
  • Celia Hoi-Ching Chan,
  • Jianpiao Cai,
  • Terrence Tsz-Tai Yuen,
  • Zi-Wei Ye,
  • Jinxia Zhang,
  • Zhaohui Qian,
  • Kwok-Yung Yuen,
  • Jasper Fuk-Woo Chan,
  • Hin Chu

摘要

Respiratory long COVID symptoms, including dyspnea and breathing pattern disorders, are frequently reported in convalescent COVID-19 patients. Yet the mechanisms driving these persistent respiratory manifestations remain poorly elucidated. In this study, we characterized persistent upper respiratory tract pathology in SARS-CoV-2-infected hamsters. Strikingly, we observed persistent expression of SARS-CoV-2 nucleocapsid (N) protein and subgenomic RNA (sgRNA) gene, which resulted in sustained tissue pathologies, dysregulation of pro-inflammatory markers, pro-apoptotic genes, as well as the altered expression of viral entry receptors, in the nasal turbinate of infected hamsters up to 120 days post-infection. These findings indicate that residual viral components may contribute to dysregulation of tissue repair and remodeling, chronic tissue pathology, and potentially enhanced susceptibility to secondary respiratory infections upon SARS-CoV-2 infection even upon recovery of acute infection. Collectively, our study provides insights into potential drivers of post-acute COVID-19 sequelae in the upper respiratory tract.