A case of unusually high severity of influenza pneumonia leading to acute respiratory distress syndrome and death was investigated. This was a previously a healthy 28-year-old man with no underlying conditions, admitted to a hospital during the first wave of influenza pandemic in Thailand in July 2009. He had experienced high fever and influenza-like illness for 5 days before coming to the hospital. He developed acute respiratory distress syndrome and expired on day 7 after admission. In comparison to three other cases of influenza pneumonia in the same outbreak with known risk factors for severe influenza, such as pregnancy and diabetes mellitus, a much higher viral load was detected in the lungs of this patient despite antiviral treatment. In agreement with the high viral load, the lung specimens from this patient, but not the other three patients, showed a high expression of α-2,6-linked sialic acid by lectin staining. The gene responsible for the synthesis of this sialic acid was also found to be upregulated. The data indicated overexpression of the viral receptor as a potential mechanism for severe disease in some patients.
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http://dx.doi.org/10.1002/jmv.23201 | DOI Listing |
Alzheimers Dement
December 2024
Department of Medicine (Biomedical Genetics), Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Several viruses have been linked to Alzheimer disease (AD) by independent lines of evidence.
Method: Whole genome and whole exome sequences (WGS/WES) derived from brain (3,404 AD cases, 894 controls) and blood (15,612 AD cases, 24,544 controls) obtained from European ancestry (EU), African American (AA), Mexican (HMX), South Asian Indian (IND), and Caribbean Hispanic (CH) participants of the Alzheimer's Disease Sequencing Project (ADSP) and 276 AD cases 3,584 controls (all EU) from the Framingham Heart Study (FHS) that did not align to the human reference genome were aligned to viral reference genomes. A genome-wide association study (GWAS) for viral DNA load was conducted using PLINK software and regression models with covariates for sex, age, ancestry principal components, and tissue source.
Alzheimers Dement
December 2024
Amsterdam UMC, Amsterdam, Netherlands.
Background: The TMEM106B protein is critical for proper functioning of the endolysomal system, which is utilised by all cells to traffic and degrade molecular cargo. Genome-wide association studies identified a haplotype in the TMEM106B gene that is associated with increased risk for Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration with TAR DNA binding protein inclusions (FTLD-TDP). However, the causal variant that drives the association has thus far remained elusive.
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December 2024
University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Background: The infectious hypothesis of Alzheimer's disease (AD) suggests that microbes may play a role in pathogenesis by triggering the pathologic cascade or contributing to disease progression. Herpesviruses, such as Epstein-Barr virus (EBV), have been of high interest in AD and related neurodegenerative diseases, in part due to their ability to establish lifelong latent infection and potentially reactivate. However, further research is needed to fully understand the role of herpesviruses in these diseases.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: SARS-CoV-2 causes a variety of neurological sequelae in COVID-19 survivors, including fatigue and cognitive dysfunction. Endothelial dysfunction is the unifying and central mechanism of COVID-19 illness and a major risk factor for vascular dementia (VaD). Endothelial dysfunction stems, in part, from an imbalance between nitric oxide (NO) generated by the endothelial nitric oxide synthase (eNOS) and reactive oxidant species produced by uncoupled-eNOS.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: Increasing evidence suggests that SARS-CoV-2 infection may lead to early onset and aggravation of pre-existing vascular dementia and Alzheimer's disease. Methylene tetrahydrofolate reductase (Mthfr) is a critical enzyme in folate metabolism, also required for optimal brain function. Mthfr deficient mice display cognitive impairments and neurovascular deficits and polymorphisms in MTHFR increases dementia risk.
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