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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Experimental researches in infections with associated myxoviruses in the mouse
M Petica1, A Petrescu, F Bârnaure
1The Stefan S. Nicolau Institute of Virology, Bucharest, Romania.
Abstract:
Infections with influenza virus, A/Beijing 353/89 (H3N2) strain, to which there were associated parainfluenza virus type 3, 739-2D strain, adenovirus type 3, and respiratory syncytial virus Long strain, were experimentally induced in white mice. The experimental models were set up so as to permit the obtaining of an associated infection with three viruses, in which the influenza virus should be inoculated the first, the participation of the others being variable, according to their presence by alternation. The infections were detected by means of the presence of homologous serum antibodies, of positive immunofluorescence reactions in the pulmonary tissue, of the histological, histochemical and histoenzymatic lesions at the level of the respiratory system, as well as of pathomorphological changes in other organs. The severity of lesions varied from one to another infection produced by a viral association. At the level of the pulmonary parenchyma, the inflammatory lesion had a frequency of 100%. The severest pathomorphological picture characterized the diffuse interstitial lymphohistio-macrophagocytic bronchopneumonia. The bronchopulmonary block was marked by cytoinfiltrative processes, with a prevalence of lymphocytes in the infection with influenza virus + adenovirus + respiratory syncytial virus, but with a proportionality between lymphocytes and histiocytes in the other infections. The lesion of the highest incidence was the thickening of interalveolar septa, as a consequence of stasis hyperemia, oedema and lymphohistio-macrophagocytic cytoinfiltrate, sometimes associated with hyalinosis of tunica media of the blood vessels and of the Reisseisen's muscle. In other organs, particularly in the liver and kidney, vascular lesions, stasis hyperemia, inflammatory and dystrophico-inflammatory lesions were present; in the spleen, megakaryocyte hyperplasia was recorded at a significant rate in associated infections in which the adenovirus was present.
Insights
This study investigated how co-infections with influenza virus and other respiratory viruses impact mice. Viral co-infections caused severe lung inflammation and varied pathological changes in other organs.
Area of Science:
- Virology
- Pathology
- Immunology
Background:
- Influenza virus infections can be complicated by co-infections with other respiratory viruses.
- Understanding the synergistic or antagonistic effects of viral co-infections is crucial for disease management.
Purpose of the Study:
- To experimentally induce and characterize co-infections with influenza virus (H3N2) and other respiratory viruses (parainfluenza, adenovirus, RSV) in a mouse model.
- To assess the pathological consequences of these viral associations in the respiratory system and other organs.
Main Methods:
- Experimental induction of viral co-infections in white mice, with influenza virus inoculated first.
- Detection of infections via serum antibodies, immunofluorescence, and histological, histochemical, and histoenzymatic analyses.
- Pathomorphological examination of respiratory tissues and other organs (liver, kidney, spleen).
Main Results:
- All viral co-infections induced 100% inflammatory lesions in the pulmonary parenchyma.
- The most severe pathology was diffuse interstitial lymphohistiocytic-macrophagic bronchopneumonia.
- Specific patterns of cellular infiltration (lymphocytes, histiocytes) were observed depending on the viral combination.
- Vascular and dystrophic lesions were noted in the liver and kidneys; splenic megakaryocyte hyperplasia occurred with adenovirus co-infection.
Conclusions:
- Viral co-infections significantly exacerbate lung pathology compared to single infections.
- The specific combination of viruses influences the severity and type of pathological changes observed.
- These findings highlight the complex interplay of respiratory viruses in disease pathogenesis.
