Multiscale assessment of patterns of avian species richness

The search for a common cause of species richness gradients has spawned more than 100 explanatory hypotheses in just the past two decades. Despite recent conceptual advances, further refinement of the most plausible models has been stifled by the difficulty of compiling high-resolution databases at continental scales. We used a database of the geographic ranges of 2,869 species of birds breeding in South America (nearly a third of the world's living avian species) to explore the influence of climate, quadrat area, ecosystem diversity, and topography on species richness gradients at 10 spatial scales (quadrat area, ≈12,300 to ≈1,225,000 km2). Topography, precipitation, topography × latitude, ecosystem diversity, and cloud cover emerged as the most important predictors of regional variability of species richness in regression models incorporating 16 independent variables, although ranking of variables depended on spatial scale. Direct measures of ambient energy such as mean and maximum temperature were of ancillary importance. Species richness values for 1° × 1° latitude-longitude quadrats in the Andes (peaking at 845 species) were ≈30–250% greater than those recorded at equivalent latitudes in the central Amazon basin. These findings reflect the extraordinary abundance of species associated with humid montane regions at equatorial latitudes and the importance of orography in avian speciation. In a broader context, our data reinforce the hypothesis that terrestrial species richness from the equator to the poles is ultimately governed by a synergism between climate and coarse-scale topographic heterogeneity.

RNA virus error catastrophe: Direct molecular test by using ribavirin

RNA viruses evolve rapidly. One source of this ability to rapidly change is the apparently high mutation frequency in RNA virus populations. A high mutation frequency is a central tenet of the quasispecies theory. A corollary of the quasispecies theory postulates that, given their high mutation frequency, animal RNA viruses may be susceptible to error catastrophe, where they undergo a sharp drop in viability after a modest increase in mutation frequency. We recently showed that the important broad-spectrum antiviral drug ribavirin (currently used to treat hepatitis C virus infections, among others) is an RNA virus mutagen, and we proposed that ribavirin's antiviral effect is by forcing RNA viruses into error catastrophe. However, a direct demonstration of error catastrophe has not been made for ribavirin or any RNA virus mutagen. Here we describe a direct demonstration of error catastrophe by using ribavirin as the mutagen and poliovirus as a model RNA virus. We demonstrate that ribavirin's antiviral activity is exerted directly through lethal mutagenesis of the viral genetic material. A 99.3% loss in viral genome infectivity is observed after a single round of virus infection in ribavirin concentrations sufficient to cause a 9.7-fold increase in mutagenesis. Compiling data on both the mutation levels and the specific infectivities of poliovirus genomes produced in the presence of ribavirin, we have constructed a graph of error catastrophe showing that normal poliovirus indeed exists at the edge of viability. These data suggest that RNA virus mutagens may represent a promising new class of antiviral drugs.