Submitted to: International Symposium on Avian Influenza
Publication Type: Abstract Only
Publication Acceptance Date: 4/13/2000
Publication Date: 5/22/2000
Citation: N/A Interpretive Summary:
Technical Abstract: The cellular factors involved in influenza virus pathogenesis are not well understood. Our studies showed that the highly pathogenic avian influenza virus strain A/Turkey/Ontario/7732/66 increased transforming growth factor-beta (TGF-beta) activity in vitro and in vivo. TGF-beta is a multifunctional growth regulatory protein that plays a crucial role in the immune response. To better understand the importance of TGF-beta in viral pathogenesis, we examined the activation of TGF-beta in vitro and in vivo by different high and low pathogenic avian strains of influenza virus, and select human viruses. Our results show that all high and low path avian strains tested activate TGF-beta, except the Hong Kong strains. One possible reason for this could be the deletion in the stalk domain of many of the Hong Kong isolates. To evaluate this, N2 viruses with deletions or full-length neuraminidase stalk regions were tested for activation of TGF-beta. Methods: Confluent monolayers MDCK or chicken embryo fibroblasts were infected with different strains of influenza N2 viruses and culture supernatants were tested for TGF-beta activity. Additionally, chickens were infected with the same strains and sera were collected at days 1 and 3 post-infection. Results suggest that TGF-beta activation is dependent on neuraminidase activity.