When sinks become sources: Adaptive colonization in asexuals.

The establishment of a population into a new empty habitat outside of its initial niche is a phenomenon akin to evolutionary rescue in the presence of immigration. It underlies a wide range of processes, such as biological invasions by alien organisms, host shifts in pathogens, or the emergence of resistance to pesticides or antibiotics from untreated areas. We derive an analytically tractable framework to describe the evolutionary and demographic dynamics of asexual populations in a source-sink system. We analyze the influence of several factors on the establishment success in the sink, and on the time until establishment. To this aim, we use a classic phenotype-fitness landscape (Fisher's geometrical model in n dimensions) where the source and sink habitats have different phenotypic optima. In case of successful establishment, the mean fitness in the sink follows a typical four-phases trajectory. The waiting time to establishment is independent of the immigration rate and has a "U-shaped" dependence on the mutation rate, until some threshold where lethal mutagenesis impedes establishment and the sink population remains so. We use these results to get some insight into possible effects of several management strategies.

In vivo and in vitro effect of acyclovir on pseudorabies virus, infectious bovine rhinotracheitis virus and pigeon herpesvirus.

The effect of various concentrations of acyclovir on the mean plaque size of pseudorabies virus (SHV), infectious bovine rhinotracheitis virus (IBR virus) and pigeon herpesvirus (PHV) has been studied. Acyclovir significantly reduced the mean plaque size of SHV and PHV, whereas IBR virus was less affected and did only show a reduction of the mean plaque size at the highest concentration of acyclovir used (1000 microM). In vivo effect of acyclovir was tested using pigeons and budgerigars experimentally infected with PHV and rabbits experimentally infected with a very low dose of SHV. Intramuscular injections of acyclovir (100 mg/kg/day; three injections/day) did not prevent the appearance of clinical disease in infected pigeons nor did reduce the level of viral excretion. The same treatment applied, as for the pigeons, before infection protected most of the budgerigars as long as they were treated, but most of them died soon after the end of the treatment. Only one rabbit was protected by the treatment. SHV was recovered in the lung of only one of the treated animals, whereas it was isolated in the lungs of each control animal.