Bacteriology and Histopathology of the Respiratory Tract and Lungs in Fatal Asian Influenza

Hers, J.; Masurel, N.; Mulder, J.

doi:10.1016/s0140-6736(58)92404-8

Cited by 179 publications

(139 citation statements)

References 9 publications

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“…This strain has differences from some circulating human influenza strains and may only be representative of severe or pandemic influenza infections. Consistent with this, it was shown that both adults 32,33 and children 34 recovering from severe influenza outbreaks experienced necrotizing bronchiolitis, alveolitis, intimal thickening, and fibrosis. Highly pathogenic influenza (H5N1) was shown to cause lung fibrosis in patients 30 days after infection.…”

Section: Discussionsupporting

confidence: 63%

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Pociask

Robinson

Chen

et al. 2017

The American Journal of Pathology

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Seasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild-to-moderate disease phenotypes and recover within a few weeks. Influenza is known to cause persistent alveolitis in animal models; however, little is known about the molecular pathways involved in this phenotype. We challenged C57BL/6 mice with influenza A/PR/8/34 and examined lung pathologic processes and inflammation, as well as transcriptomic and epigenetic changes at 21 to 60 days after infection. Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and epithelial endoplasmic reticulum stress that were evident after the clearance of virus and resolution of morbidity. Influenza infection induced robust changes in the lung transcriptome, including a significant impact on inflammatory and extracellular matrix protein expression. Despite the robust changes in lung gene expression, preceding influenza (21 days) did not exacerbate secondary Staphylococcus aureus infection. Finally, we examined the impact of influenza on miRNA expression in the lung and found an increase in miR-155. miR-155 knockout mice recovered from influenza infection faster than controls and had decreased lung inflammation and endoplasmic reticulum stress. These data illuminate the dynamic molecular changes in the lung in the weeks after influenza infection and characterize the repair process, identifying a novel role for miR-155. (Am J Pathol 2017, 187: 851e863; http://dx

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Section: Discussionsupporting

confidence: 63%

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Pociask

Robinson

Chen

et al. 2017

The American Journal of Pathology

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“…92 In later pandemics, this percentage declined in favor of deaths from primary influenza viral pneumonia, possibly because of the widespread administration of antibiotics. 49 Although human influenza virus primarily infects and causes disease in the respiratory tract, it is associated with disease in extrarespiratory organs, albeit to a lesser extent, including influenza-associated acute encephalopathy, 135 myocarditis, 114 and myopathy. 1 In general, there two explanations for the pathogenesis of these extrarespiratory complications.…”

Section: Human Influenza Virusesmentioning

confidence: 99%

Comparative Pathology of Select Agent Influenza A Virus Infections

et al. 2010

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Influenza A virus infections may spread rapidly in human populations and cause variable mortality. Two of these influenza viruses have been designated as select agents: 1918 H1N1 virus and highly pathogenic avian influenza (HPAI) virus. Knowledge of the pathology of these virus infections in humans, other naturally infected species, and experimental animals is important to understand the pathogenesis of influenza, to design appropriate models for evaluation of medical countermeasures, and to make correct diagnoses. The most important complication of influenza in humans is viral pneumonia, which often occurs with or is followed by bacterial pneumonia. Viremia and extrarespiratory disease are uncommon. HPAI viruses, including HPAI H5N1 virus, cause severe systemic disease in galliform species as well as in anseriform species and bird species of other orders. HPAI H5N1 virus infection also causes severe disease in humans and several species of carnivores. Experimental animals are used to model different aspects of influenza in humans, including uncomplicated influenza, pneumonia, and virus transmission. The most commonly used experimental animal species are laboratory mouse, domestic ferret, and cynomolgus macaque. Experimental influenza virus infections are performed in various other species, including domestic pig, guinea pig, and domestic cat. Each of these species has advantages and disadvantages that need to be assessed before choosing the most appropriate model to reach a particular goal. Such animal models may be applied for the development of more effective antiviral drugs and vaccines to protect humans from the threat of these virus infections.

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“…In one single fulminating case in which autopsy study was permitted a fully sensitive staphylococcus was recovered. In the seven cases reported by Hers (1955) and quoted above, strains of fully sensitive staphylococci were recovered from six. This finding was confirmed by Robertson, Caley and Moor, (1958), who recovered sensitive staphylococci from I2 of I4 patients with fulminating influenzal staphylococcal pneumonia dying within seven days of onset.…”

Section: Gastroduodenal Hmemorrhagementioning

confidence: 90%

Influenza in Hospital 1960-1961

Hearn

1963

Postgraduate Medical Journal

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Bacteriology and Histopathology of the Respiratory Tract and Lungs in Fatal Asian Influenza

Cited by 179 publications

References 9 publications

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection

Comparative Pathology of Select Agent Influenza A Virus Infections

Influenza in Hospital 1960-1961

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