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Differential Interaction of Virulent and Attenuated Infuenza Virus Strains with Ferret Alveolar Macrophages: Possible Role in Pathogenicity

Identifieur interne : 002093 ( Main/Exploration ); précédent : 002092; suivant : 002094

Differential Interaction of Virulent and Attenuated Infuenza Virus Strains with Ferret Alveolar Macrophages: Possible Role in Pathogenicity

Auteurs : Bruce L. Riser ; Hunein F. Maassab [États-Unis]

Source :

RBID : ISTEX:41FB6938C4A07656ADD1DF095D4CCCD5FE074056

Descripteurs français

English descriptors

Abstract

The ferret provides a unique model for the study of human influenza. The interaction between alveolar macrophages and virus strains with different levels of virulence was examined in vitro. The greater virulence ofwild-type A strains over type Band C viruses was reflected in the higher production of infectious virus progeny and subsequent cytopathology, even though the expression of viral antigens wasequivalent for all strains tested. These included A/Ann Arbor/6/60 (H2N2) and A/Rochester/1/82 (H3N2), B/Hong Kong/72, and C/Ann Arbor/1/50. The attenuated coldadapted and temperature-sensitive variant of A/Ann Arbor/6/60 behaved like its parent except that a longer period was needed to reach peakviral release. In contrast, the avirulent host-range reassortant CR-43-3 did not productively replicate, though viral antigen expression was comparable to that of the other strains. Type C virus infected few cells and these continued to release low virus levels in the absence of detectable cytopathology. The results suggest that the ability of certain strains to infect and replicate in alveolar macrophages can be correlated to their in vivo virulence and may play a role in determining the course of viral pathogenesis.

Url:
DOI: 10.1093/infdis/161.4.699


Affiliations:


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Le document en format XML

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<div type="abstract">The ferret provides a unique model for the study of human influenza. The interaction between alveolar macrophages and virus strains with different levels of virulence was examined in vitro. The greater virulence ofwild-type A strains over type Band C viruses was reflected in the higher production of infectious virus progeny and subsequent cytopathology, even though the expression of viral antigens wasequivalent for all strains tested. These included A/Ann Arbor/6/60 (H2N2) and A/Rochester/1/82 (H3N2), B/Hong Kong/72, and C/Ann Arbor/1/50. The attenuated coldadapted and temperature-sensitive variant of A/Ann Arbor/6/60 behaved like its parent except that a longer period was needed to reach peakviral release. In contrast, the avirulent host-range reassortant CR-43-3 did not productively replicate, though viral antigen expression was comparable to that of the other strains. Type C virus infected few cells and these continued to release low virus levels in the absence of detectable cytopathology. The results suggest that the ability of certain strains to infect and replicate in alveolar macrophages can be correlated to their in vivo virulence and may play a role in determining the course of viral pathogenesis.</div>
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