The tragedy of the commons in evolutionary biology

Garrett Hardin's tragedy of the commons is an analogy that shows how individuals driven by self-interest can end up destroying the resource upon which they all depend. The proposed solutions for humans rely on highly advanced skills such as negotiation, which raises the question of how non-human organisms manage to resolve similar tragedies. In recent years, this question has promoted evolutionary biologists to apply the tragedy of the commons to a wide range of biological systems. Here, we provide tools to categorize different types of tragedy and review different mechanisms, including kinship, policing and diminishing returns that can resolve conflicts that could otherwise end in tragedy. A central open question, however, is how often biological systems are able to resolve these scenarios rather than drive themselves extinct through individual-level selection favouring self-interested behaviours.

Soft and hard tissue histologic dimensions around dental implants in the canine restored with smaller-diameter abutments: a paradigm shift in peri-implant biology

PURPOSE To evaluate the biologic width dimensions around implants with nonmatching implant-abutment diameters. MATERIALS AND METHODS Five canines had their mandibular premolars and first molars removed bilaterally and replaced with 12 implants that had nonmatching implant-abutment diameters. On one side, six implants were placed in a submerged surgical approach, and the other side utilized a nonsubmerged approach. Two of the implants on each side were placed either 1 mm above, even with, or 1 mm below the alveolar crest. Two months later, gold crowns were attached, and the dogs were sacrificed 6 months postloading. Block sections were processed for histologic and histomorphometric analyses. RESULTS The bone level, connective tissue length, epithelial dimension, and biologic width were not significantly different when the implants were initially placed in a submerged or nonsubmerged surgical approach. The bone level was significantly different around implants placed 1 mm above the crest compared to implants placed even with or 1 mm below the alveolar crest. The connective tissue dimension was not different for any implant level placement. The epithelial dimension and biologic width were significantly greater for implants placed 1 mm below the alveolar crest compared to implants placed even with or 1 mm above the alveolar crest. For five of six implant placements, connective tissue covered the implant/abutment interface. CONCLUSIONS This study reveals a fundamental change in the biologic response to implants with nonmatching implant-abutment diameters. Unlike implants with matching implant-abutment diameters, the connective tissue extended coronally past the interface (microgap). This morphologic tissue alteration represents a significant change in the biologic reaction to implant-abutment interfaces and suggests that marginal inflammation is eliminated or greatly reduced in these implant designs.

Bovine viral diarrhea (BVD): from biology to control

Bovine viral diarrhea virus (BVDV) is endemic worldwide. Together with classical swine fever and border disease viruses, it belongs to the genus Pestivirus of the family Flaviviridae. Most infections with BVDV take a transient, acute, course. Only rarely BVDV persists in its hosts. Due to the early time point of infection in utero, persistently infected (PI) animals are immunotolerant to the infecting non-cytopathic BVDV. In such animals the virus may mutate to a cytopathic biotype, causing lethal mucosal disease. In BVD-endemic regions, approximately 1% of the animals are PI. Removal of all PI animals leads to extinction of BVD. This approach to BVD eradication has been vindicated in Scandinavia. Following the same principles, regional and country-wide eradication programs are run in different parts of the world. These programs differ in the way PI animals are detected and in the role of vaccines. The Scandinavian two-step method of detecting PI animals is based on (i) the high level of seroprevalence in herds where PI animals are present and (ii) on testing all animals for virus in such herds. However, the high average herd seroprevalence in Switzerland made it impossible to define a reasonable threshold for virus testing. Therefore, all animals were directly tested for virus in the year 2008 and all newborn calves until the end of 2012, when the PI prevalence had dropped to 0.02%. Vaccination remains prohibited. Since 2013, surveillance for BVD is accomplished by serology. As a unique consequence of eradication, over 7500 viral strains are available to us for genetic studies.

Revealing the elusive molecular biology of the vault RNA

Recently several novel and previously reported non-protein-coding RNAs (ncRNAs) have been identified to be upregulated upon Epstein-Barr virus (EBV) infection in human B-lymphocytes. A group of these significantly upregulated ncRNAs are called vault RNAs (vtRNAs). ,b Only about 5% of the total cellular vtRNAs are connected to the vault particle, the largest known ribonucleoprotein particle (RNP) in eukaryotic cells. However the function of this ncRNA family and moreover of the vault particle remains still rather unclear. Our previous findings suggest a link between EBV infection and vtRNA expression. Consequently we are interested which part of the viral genome is responsible for the upregulation and moreover which function the vtRNAs might possess during virus propagation. To address this question we have separately overexpressed specific EBV-encoded, latently expressed proteins in BL2-cells to determine the influence on the vault RNA levels. Thereby we identified one EBV-encoded protein, called Latent Membrane Protein 1 (LMP1), which significantly contributes to the vtRNA upregulation. We used LMP1 mutants to characterize the region of the protein and the responsible pathway for triggering the elevated vtRNA expression. Our results suggest that the NFkB- pathway might be involved in this process. To investigate a possible functional connection between the vtRNA and EBV infection, we have overexpressed vtRNA1-1 in BL41, a cell line usually not expressing this vault RNA. We show that overexpression of vtRNA1-1 leads to a better viral establishment and markedly protects cells from undergoing apoptosis. Knock-down of the major vault protein, the main component of the vault particle, had no effect on EBV infection and apoptosis resistance. Thus these results support the view that the observed phenotype is caused by the vtRNA rather than the vault particle.