tetano
Editor, Senior Moderator
J Med Virol
. 2024 May;96(5):e29671.
doi: 10.1002/jmv.29671. SARS-CoV-2 induces blood-brain barrier and choroid plexus barrier impairments and vascular inflammation in mice
Haowen Qiao[SUP] 1 [/SUP], Xiangxue Deng[SUP] 2 [/SUP], Lingxi Qiu[SUP] 2 [/SUP], Yafei Qu[SUP] 1 [/SUP], Yuanpu Chiu[SUP] 1 [/SUP], Feixiang Chen[SUP] 1 [/SUP], Shangzhou Xia[SUP] 1 3 [/SUP], Cheyene Muenzel[SUP] 1 [/SUP], Tenghuan Ge[SUP] 1 [/SUP], Zixin Zhang[SUP] 1 [/SUP], Pengfei Song[SUP] 4 [/SUP], Alexandre Bonnin[SUP] 1 [/SUP], Zhen Zhao[SUP] 1 3 [/SUP], Weiming Yuan[SUP] 2 [/SUP]
Affiliations
The coronavirus disease of 2019 (COVID-19) pandemic has led to more than 700 million confirmed cases and nearly 7 million deaths. Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus mainly infects the respiratory system, neurological complications are widely reported in both acute infection and long-COVID cases. Despite the success of vaccines and antiviral treatments, neuroinvasiveness of SARS-CoV-2 remains an important question, which is also centered on the mystery of whether the virus is capable of breaching the barriers into the central nervous system. By studying the K18-hACE2 infection model, we observed clear evidence of microvascular damage and breakdown of the blood-brain barrier (BBB). Mechanistically, SARS-CoV-2 infection caused pericyte damage, tight junction loss, endothelial activation and vascular inflammation, which together drive microvascular injury and BBB impairment. In addition, the blood-cerebrospinal fluid barrier at the choroid plexus was also impaired after infection. Therefore, cerebrovascular and choroid plexus dysfunctions are important aspects of COVID-19 and may contribute to neurological complications both acutely and in long COVID.
Keywords: SARS‐CoV‐2; blood‐brain barrier; choroid plexus barrier; mouse modeling; neuroinflammation; severe COVID.
. 2024 May;96(5):e29671.
doi: 10.1002/jmv.29671. SARS-CoV-2 induces blood-brain barrier and choroid plexus barrier impairments and vascular inflammation in mice
Haowen Qiao[SUP] 1 [/SUP], Xiangxue Deng[SUP] 2 [/SUP], Lingxi Qiu[SUP] 2 [/SUP], Yafei Qu[SUP] 1 [/SUP], Yuanpu Chiu[SUP] 1 [/SUP], Feixiang Chen[SUP] 1 [/SUP], Shangzhou Xia[SUP] 1 3 [/SUP], Cheyene Muenzel[SUP] 1 [/SUP], Tenghuan Ge[SUP] 1 [/SUP], Zixin Zhang[SUP] 1 [/SUP], Pengfei Song[SUP] 4 [/SUP], Alexandre Bonnin[SUP] 1 [/SUP], Zhen Zhao[SUP] 1 3 [/SUP], Weiming Yuan[SUP] 2 [/SUP]
Affiliations
- PMID: 38747003
- DOI: 10.1002/jmv.29671
The coronavirus disease of 2019 (COVID-19) pandemic has led to more than 700 million confirmed cases and nearly 7 million deaths. Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus mainly infects the respiratory system, neurological complications are widely reported in both acute infection and long-COVID cases. Despite the success of vaccines and antiviral treatments, neuroinvasiveness of SARS-CoV-2 remains an important question, which is also centered on the mystery of whether the virus is capable of breaching the barriers into the central nervous system. By studying the K18-hACE2 infection model, we observed clear evidence of microvascular damage and breakdown of the blood-brain barrier (BBB). Mechanistically, SARS-CoV-2 infection caused pericyte damage, tight junction loss, endothelial activation and vascular inflammation, which together drive microvascular injury and BBB impairment. In addition, the blood-cerebrospinal fluid barrier at the choroid plexus was also impaired after infection. Therefore, cerebrovascular and choroid plexus dysfunctions are important aspects of COVID-19 and may contribute to neurological complications both acutely and in long COVID.
Keywords: SARS‐CoV‐2; blood‐brain barrier; choroid plexus barrier; mouse modeling; neuroinflammation; severe COVID.