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Published on: July 14, 2020
Influenza H7N9 virus disrupts the monolayer human brain microvascular endothelial cells barrier in vitro
Yuxuan Lei1, Ying Sun2, Weihua Wu2
1School of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen, 518107, China.
Abstract:
Influenza H7N9 virus causes human infections with about 40% case fatality rate. The severe cases usually present with pneumonia; however, some present with central nervous system complications. Pneumonia syndrome is attributed to the cytokine storm after infection with H7N9, but the pathogenic mechanism of central nervous system complications has not been clarified. This study used immortalized human brain microvascular endothelial cells hCMEC/D3 to simulate the blood-brain barrier. It demonstrated that H7N9 virus could infect brain microvascular endothelial cells and compromise the blood-brain barrier integrity and permeability by down-regulating the expression of cell junction-related proteins, including claudin-5, occludin, and vascular endothelial (VE)-cadherin. These results suggested that H7N9 could infect the blood-brain barrier in vitro and affect its functions, which could be a potential mechanism for the pathogenesis of H7N9 viral encephalopathy.
Insights
The Influenza H7N9 virus can infect brain cells, damaging the blood-brain barrier. This finding offers a potential explanation for H7N9-related brain damage and neurological complications.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Influenza H7N9 (H7N9) infection has a high fatality rate, often causing pneumonia.
- While pneumonia is linked to cytokine storms, the mechanism of H7N9's central nervous system (CNS) complications remains unclear.
Purpose of the Study:
- To investigate the pathogenic mechanism of H7N9-induced central nervous system complications.
- To determine if the H7N9 virus can compromise blood-brain barrier (BBB) integrity.
Main Methods:
- Utilized immortalized human brain microvascular endothelial cells (hCMEC/D3) to model the BBB.
- Assessed the effect of H7N9 virus infection on BBB integrity and permeability.
- Measured the expression of key cell junction proteins: claudin-5, occludin, and VE-cadherin.
Main Results:
- Demonstrated that the H7N9 virus can infect brain microvascular endothelial cells.
- Showed that H7N9 infection compromises BBB integrity and increases permeability.
- Observed down-regulation of cell junction proteins (claudin-5, occludin, VE-cadherin) following H7N9 infection.
Conclusions:
- H7N9 virus can infect and impair the function of the blood-brain barrier in vitro.
- BBB dysfunction by H7N9 infection is a potential mechanism underlying H7N9 viral encephalopathy.
