J Gen Virol Faster Access
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 44 (1979), 505-514; DOI 10.1099/0022-1317-44-2-505
© 1979 Society for General Microbiology

This Article
Right arrow Full Text (PDF)
Right arrow Correction (v45,pNP)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cavanagh, D.
Right arrow Articles by Smith, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cavanagh, D.
Right arrow Articles by Smith, H.
Agricola
Right arrow Articles by Cavanagh, D.
Right arrow Articles by Smith, H.

The Localization of Influenza Virus in the Respiratory Tract of Ferrets: Susceptible Nasal Mucosa Cells Produce and Release More Virus than Susceptible Lung Cells

D. Cavanagh*, F. Mitkis{dagger}, C. Sweet, M. H. Collie and H. Smith{ddagger}

Department of Microbiology, University of Birmingham, Birmingham B15 2TT, U.K.

Infectious virus production by ferret nasal mucosa and lung organ cultures has been monitored in both tissue pieces and medium over 24 h following inoculation with an Asian (H2N2) strain of influenza virus. Freshly prepared cultures of nasal mucosa produced approx. 10-fold more virus per cell than fresh lung cultures. Also the nasal mucosa cells liberated into the medium a greater proportion (mean 31%) of the total virus produced than did fresh lung (mean 6%). Maintenance of lung explants for 24 h prior to inoculation resulted in a 20- to 100-fold increase in the amount of virus released. However, total virus production by fresh and maintained lung was similar. Trypsin did not increase the infectivity of virus released from any of the cultures, indicating that the haemagglutinin in the virus particles was cleaved. Similar results were obtained with a Hong Kong (H3N2) virus strain. Hence, one factor operating in the lower susceptibility of the lung compared with the nasal mucosa in vivo may be a lower capacity of lung cells both to produce and release influenza virus.

* Present address: Department of Microbiology, Houghton Poultry Research Station, Houghton, Huntingdon, Cambs., U.K.

{dagger} Department of Bacteriology, Faculty of Medicine, Cairo University, Cairo, Egypt.

{ddagger} To whom correspondence should be sent.

Received 23 November 1978; accepted 5 February 1979.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1979 by the Society for General Microbiology.