Sera from 100 flying foxes collected during 2003-2005 from Queensland, Australia were screened for neutralizing antibodies to CedPV. Virus neutralization test was conducted as described above (antibody tests). All serum samples were tested at a dilution of 1:20.  Host Modulators of H1N1 Cytopathogenicity Influenza A virus infects 5–20% of the population annually, resulting in ∼35,000 deaths and significant morbidity. Current treatments include vaccines and drugs that target viral proteins. However, both of these approaches have limitations, as vaccines require yearly development and the rapid evolution of viral proteins gives rise to drug resistance. In consequence additional intervention strategies, that target host factors required for the viral life cycle, are under investigation. Here we employed arrayed whole-genome siRNA screening strategies to identify cell-autonomous molecular components that are subverted to support H1N1 influenza A virus infection of human bronchial epithelial cells. Integration across relevant public data sets exposed druggable gene products required for epithelial cell infection or required for viral proteins to deflect host cell suicide checkpoint activation. Pharmacological inhibition of representative targets, RGGT and CHEK1, resulted in significant protection against infection of human epithelial cells by the A/WS/33 virus. In addition, chemical inhibition of RGGT partially protected against H5N1 and the 2009 H1N1 pandemic strain. The observations reported here thus contribute to an expanding body of studies directed at decoding vulnerabilities in the command and control networks specified by influenza virulence factors. The Orthomyxoviridae family member influenza A virus is the causal agent of acute respiratory tract infections suffered annually by 5-20% of the human population. There is a significant impact on morbidity, concentrated in people younger than 20 years, with economic consequences running into the billions of dollars during large epidemics [1] . In addition, viral infections are associated with development of chronic asthma and disease exacerbation in both children and adults. In particular, acute influenza infection can amplify airway inflammation in asthmatic patients and induce alterations in epithelial and stromal cell physiology contributing to allergen sensitization, exaggerated bronchoconstriction, and remodeling of airway epithelia [2] . Mortality rates associated with seasonal flu are low, but the aging population is at risk for development of severe congestive pneumonia which kills ,35,000 people each year in the U.S. [1] . Of continual concern is the threat of emergent high virulence strains such as the Spanish flu (H1N1), Asian flu (H2N2) and Hong Kong flu (H3N2) pandemics which claimed millions of lives world-wide. Current treatments are focused on vaccines and drugs that target viral proteins. However, both of these approaches have limitations as vaccines require yearly development and lag detection of new strains, while viral proteins have a stunning capacity to evolve resistance to targeted agents [3] . The genome of the influenza A virus consists of 8 negative single-strand RNA segments that encode 11 functional peptides necessary for viral replication and virulence [1] . Thus the viral-autonomous repertoire of gene products is extremely limited and influenza A replication is dependent upon hijacking host-cell biological systems to facilitate viral entry, replication, assembly, and budding. The recognition that a suit of human host proteins are required for IVA infection and replication presents additional targeting strategies that may be less prone to deflection by the highly plastic viral genome.