Showing papers by "George M. Happ published in 2008"
TL;DR: It is proposed that AIV in wild birds forms transient “genome constellations,” continually reshuffled by reassortment, in contrast to the spread of a limited number of stable genome constellation that characterizes the evolution of mammalian-adapted influenza A viruses.
Abstract: We surveyed the genetic diversity among avian influenza virus (AIV) in wild birds, comprising 167 complete viral genomes from 14 bird species sampled in four locations across the United States. These isolates represented 29 type A influenza virus hemagglutinin (HA) and neuraminidase (NA) subtype combinations, with up to 26% of isolates showing evidence of mixed subtype infection. Through a phylogenetic analysis of the largest data set of AIV genomes compiled to date, we were able to document a remarkably high rate of genome reassortment, with no clear pattern of gene segment association and occasional inter-hemisphere gene segment migration and reassortment. From this, we propose that AIV in wild birds forms transient “genome constellations,” continually reshuffled by reassortment, in contrast to the spread of a limited number of stable genome constellations that characterizes the evolution of mammalian-adapted influenza A viruses.
388 citations
TL;DR: A novel method for molecular subtyping of avian influenza A virus hemagglutinin genes using degenerate primers designed to amplify all known hemag GLUTinin subtypes is reported, which demonstrates the complex ecobiology of avan influenza A viruses in wild birds.
55 citations
TL;DR: It is shown that F. novicida invades hemocyte-like cells of the Sua1B cell line derived from Anopheles gambiae and replicates vigorously within these cells, showing that bacterial growth within these insect cells is dependent on virulence factors encoded in a bacterial pathogenicity island that has been linked to replication in mammalian macrophages.
Abstract: Francisella tularensis, a potential bioterrorism agent, is transmitted by arthropod vectors and causes tularemia in many mammals, including humans. Francisella novicida causes disease with similar pathology in mice. We show that F. novicida invades hemocyte-like cells of the SualB cell line derived from Anopheles gambiae and replicates vigorously within these cells. We used transposon knockouts of single genes of F. novicida to show that bacterial growth within these insect cells is dependent on virulence factors encoded in a bacterial pathogenicity island that has been linked to replication in mammalian macrophages. The virulence factors MglA, IglA, IglB, IglC, and IglD as well as PdpA and PdpB were necessary for efficient growth in insect cells, but PdpC and PdpD were not required. The SualB cell line presents a valuable model to study the interactions between this important pathogen and insect vectors.
43 citations