Abstract
Materials and methods
A549 cells were infected with Dengue virus or pandemic influenza A virus. Virus replication was measured by plaque assay and immune fluorescence. Apoptosis was measured by multiple assays including TUNEL, Annexin V expression, and Casapse 3 expression. Ferrets were challenged with Dengue for 24 hours prior to influenza challenge. Clinical disease was monitored for 10 days post Dengue challenge. Nasal aspirates were collected and tissues harvested for virology, immunology, and histology studies through the 10-day in life period. Clinical chemistry and hematology were also measured on infected ferrets.
Results
In A549, co-infection enhances influenza virus replication and reduces dengue virus replication compared to singly infected A549. Influenza-specific inhibition of dengue replication was dependant on multiplicity of infection (moi) and timing of influenza infection
A549 cells were infected with Dengue virus or pandemic influenza A virus. Virus replication was measured by plaque assay and immune fluorescence. Apoptosis was measured by multiple assays including TUNEL, Annexin V expression, and Casapse 3 expression. Ferrets were challenged with Dengue for 24 hours prior to influenza challenge. Clinical disease was monitored for 10 days post Dengue challenge. Nasal aspirates were collected and tissues harvested for virology, immunology, and histology studies through the 10-day in life period. Clinical chemistry and hematology were also measured on infected ferrets.
Results
In A549, co-infection enhances influenza virus replication and reduces dengue virus replication compared to singly infected A549. Influenza-specific inhibition of dengue replication was dependant on multiplicity of infection (moi) and timing of influenza infection
| Original language | English (US) |
|---|---|
| Journal | Retrovirology |
| DOIs | |
| State | Published - Dec 1 2012 |