While much is known about the influenza A viral lifecycle, the precise interactions between the virus and host remain unclear. A recent RNAi screen, performed in the Hacohen Laboratory, identified sixty genes that either dramatically increased or decreased virion production. Amongst this list of genes were five genes that are associated with the Hermansky-Pudlak Syndrome (HPS). As a step towards characterizing the list of sixty genes, we examined the five HPS genes for their role in viral entry. We used siRNA to knockdown candidate genes and then infected A549 human lung epithelial cells with Thai/H5N1, Machupo virus (MACV), Lassa virus (LASV) and Lymphocytic choriomeningitis virus (LCMV) pseudotypes. Our results demonstrate that the HPS genes do not participate in MACV, LASV, and LCMV viral entry. With these results, we are unable to further characterize where these genes play a role in influenza A virus entry. However, these results are consistent with previous work in the lab that Hps1 does not play a role in arenavirus entry, only influenza A virus entry.
"Working at the Broad Institute allows you to surround yourself with the best – the best colleagues and mentors that all want to see you succeed."