Influenza B associated acute necrotising encephalopathy with visual impairment in a child

Billa, Ramya Deepthi; Czech, Theresa; Badheka, Aditya; Chegondi, Madhuradhar

doi:10.1136/bcr-2020-238221

Cited by 2 publications

(2 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The lesion was transient, which suggested that the virus's effect on the brain was reversible (Ventresca et al 2021). Another case was reported for a 4-year-old healthy female child who suffered from influenza-associated encephalopathy (IAE); the visualized symptoms included neurological complications of temporary visual impairment and significant motor deficits (Billa et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus

et al. 2022

View full text Add to dashboard Cite

Influenza viruses not only cause respiratory illness, but also have been reported to elicit neurological manifestations following acute viral infection. The central nervous system (CNS) has a specific defense mechanism against pathogens structured by cerebral microvasculature lined with brain endothelial cells to form the blood–brain barrier (BBB). To investigate the response of human brain microvascular endothelial cells (hBMECs) to the Influenza A virus (IAV), we inoculated the cells with the A/WSN/33 (H1N1) virus. We then conducted an RNAseq experiment to determine the changes in gene expression levels and the activated disease pathways following infection. The analysis revealed an effective activation of the innate immune defense by inducing the pattern recognition receptors (PRRs). Along with the production of proinflammatory cytokines, we detected an upregulation of interferons and interferon-stimulated genes, such as IFN-β/λ, ISG15, CXCL11, CXCL3 and IL-6, etc. Moreover, infected hBMECs exhibited a disruption in the cytoskeletal structure both on the transcriptomic and cytological levels. The RNAseq analysis showed different pathways and candidate genes associated with the neuroactive ligand-receptor interaction, neuroinflammation, and neurodegenerative diseases, together with a predicted activation of the neuroglia. Likewise, some genes linked with the mitochondrial structure and function displayed a significantly altered expression. En masse, this data supports that hBMECs could be infected by the IAV, which induces the innate and inflammatory immune response. The results suggest that the influenza virus infection could potentially induce a subsequent aggravation of neurological disorders.

show abstract

Section: Introductionmentioning

confidence: 99%

Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus

et al. 2022

View full text Add to dashboard Cite

show abstract

“…The lesion was transient, which suggested that the virus's effect on the brain was reversible (Ventresca et al 2021). Another case was reported for a 4-year-old healthy female child who suffered from in uenza-associated encephalopathy (IAE); the visualized symptoms included neurological complications of temporary visual impairment and signi cant motor de cits (Billa et al 2020). However, the mechanism by which the in uenza virus could induce neuroin ammation is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Altered Gene Expression in Human Brain Microvascular Endothelial Cells in Response to the Infection of Influenza H1N1 Virus

Higazy

Lin

Xie

et al. 2021

Preprint

View full text Add to dashboard Cite

Influenza viruses are not only causing respiratory illness, but also neurological manifestations were reported following acute viral infection. The Central nervous system (CNS) has a specific defence mechanism against pathogens structured by cerebral microvasculature lined with brain endothelial cells to form the blood-brain barrier (BBB). To investigate the response of human brain microvascular endothelial cells (hBMECs) to the influenza A virus, we inoculated the cells with the A/WSN/33 (H1N1) virus. We then conducted an RNAseq experiment to determine the changes in gene expression levels and the activated disease pathways following infection. The analysis revealed an effective activation of the innate immune defence by inducing the pattern recognition receptors (PRRs). Along with the production of proinflammatory cytokines, we detected an upregulation of interferons and interferon-stimulated genes, such as IFN-β/λ, ISG15, CXCL11, CXCL3, and IL-6, etc. Moreover, infected hBMECs exhibited a disruption in the cytoskeletal structure both on the transcriptomic and cellular levels. We also noted that pathways of neuroactive ligand-receptor interaction, neuroinflammation, and neurodegenerative diseases were noticeably induced together with a predicted activation of the neuroglia. Likewise, a number of genes linked with the mitochondrial structure and function display a significant differential expression. En masse, this data supports that hBMECs could be infected by the influenza A virus, which induces the innate and inflammatory immune response. The results suggest that the influenza virus infection could potentially induce a subsequent aggravation of neurological disorders.

show abstract

Influenza B associated acute necrotising encephalopathy with visual impairment in a child

Cited by 2 publications

References 18 publications

Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus

Altered gene expression in human brain microvascular endothelial cells in response to the infection of influenza H1N1 virus

Altered Gene Expression in Human Brain Microvascular Endothelial Cells in Response to the Infection of Influenza H1N1 Virus

Contact Info

Product

Resources

About