Influenza virus infection of tracheal gland cells in culture

Abstract

Influenza virus-induced tracheobronchitis causes limited epithelial deciliation but markedly decreased mucociliary transport. This suggests that virus-induced alterations in airway mucus play a role in decreased mucociliary transport. Airway submucosal glands are a primary source of mucus. Therefore, we examined virus-gland cell interactions by exposing primary cultures of isolated feline tracheal gland cells to influenza A/Scotland/840/74 H3N2 virus for 1 h at a multiplicity of infection of 0.1. Virus production and release into the culture medium first occurred between 8 and 12 h postinfection and eventually reached a steady state that continued for at least 8 days. Virus which was produced and released by infected cells infected other monolayers, resulting in viral production similar to that after infection with stock virus. Hemadsorption assays conducted 24 h after infection demonstrated that most of the cells in a monolayer became infected. The infection was nonlytic according to cell morphology, trypan blue dye exclusion, and release of lactate dehydrogenase. Because lysis of a cell subpopulation could have been masked by subsequent cell division, we compared the uptake of [3H]thymidine by infected and control monolayers. There was no increase in uptake by infected monolayers. These results demonstrate that feline tracheal gland cells in primary culture undergo productive and nonlytic infection with influenza A virus. This model provides a unique system for the study of virus-gland interactions isolated from the influence of other tissues.