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J Neurovirol. 2018 Jul 9. doi: 10.1007/s13365-018-0659-8. [Epub ahead of print]
Avian influenza A H7N9 virus infects human astrocytes and neuronal cells and induces inflammatory immune responses.
Ng YP1, Yip TF2, Peiris JSM2, Ip NY1, Lee SMY3.
Author information
Abstract
Seasonal, pandemic, and avian influenza virus infections may be associated with central nervous system pathology, albeit with varying frequency and different mechanisms. Here, we demonstrate that differentiated human astrocytic (T98G) and neuronal (SH-SY5Y) cells can be infected by avian H7N9 and pandemic H1N1 viruses. However, infectious progeny viruses can only be detected in H7N9 virus infected human neuronal cells. Neither of these viral strains can generate infectious progeny virus in human astrocytes despite replication of viral genome was observed. Furthermore, H7N9 virus triggered high pro-inflammatory cytokine expression, while pandemic H1N1 virus induced only low cytokine expression in either brain cell type. The experimental finding here is the first data to demonstrate that avian H7N9 virus can infect, transcribe, and replicate its viral genome; induce cytokine upregulation; and cause cytopathic effects in human brain cells, which may potentially lead to profound central nervous system injury. Observation for neurological problems due to H7N9 virus infection deserves further attention when managing these patients.
KEYWORDS:
Cytokines; Encephalitis; Encephalopathy; Neurodegenerative diseases; Neuroinflammation; Neurological complications
PMID: 29987581 DOI: 10.1007/s13365-018-0659-8
Avian influenza A H7N9 virus infects human astrocytes and neuronal cells and induces inflammatory immune responses.
Ng YP1, Yip TF2, Peiris JSM2, Ip NY1, Lee SMY3.
Author information
Abstract
Seasonal, pandemic, and avian influenza virus infections may be associated with central nervous system pathology, albeit with varying frequency and different mechanisms. Here, we demonstrate that differentiated human astrocytic (T98G) and neuronal (SH-SY5Y) cells can be infected by avian H7N9 and pandemic H1N1 viruses. However, infectious progeny viruses can only be detected in H7N9 virus infected human neuronal cells. Neither of these viral strains can generate infectious progeny virus in human astrocytes despite replication of viral genome was observed. Furthermore, H7N9 virus triggered high pro-inflammatory cytokine expression, while pandemic H1N1 virus induced only low cytokine expression in either brain cell type. The experimental finding here is the first data to demonstrate that avian H7N9 virus can infect, transcribe, and replicate its viral genome; induce cytokine upregulation; and cause cytopathic effects in human brain cells, which may potentially lead to profound central nervous system injury. Observation for neurological problems due to H7N9 virus infection deserves further attention when managing these patients.
KEYWORDS:
Cytokines; Encephalitis; Encephalopathy; Neurodegenerative diseases; Neuroinflammation; Neurological complications
PMID: 29987581 DOI: 10.1007/s13365-018-0659-8