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Small mammals, namely those species larger than microfauna like rats and murids but smaller than medium, sheep-size fauna, are generally one of the less studied areas of zooarchaeology. While this may be partly influenced by modern cultural biases, it is more often because finding small, rabbit-sized, mammal remains in archaeological deposits presents a problem in accurately differentiating between those arising from natural, biological and anthropogenic agencies. This thesis tackles this subject using a synthesis of different methods, examining the exploitation and role of small, non-ungulate mammals in early Western European prehistory by combining existing ethnographic knowledge and archaeological research with actualistic experiments and bone assemblage analysis. It first presents a detailed summary of the various taphonomic effects on bone from natural, biological and human action, with particular reference to those of small mammals, using empirical evidence to describe the processes and likely resultant effects. Small mammal utilisation is then contextualised using archaeological and ethnographic evidence to examine past and present practices in Europe and other areas of the world. Different acquisition methods, such as hunting and trapping, are described, and using small mammals for dietary and non-dietary purposes is outlined, along with the rationale for such utilisation given their size. Also considered are other, more abstract ideological and symbolic roles they fulfilled within different cultures, whether physically using parts of the animal, or conceptually. To extend the existing methods available to zooarchaeologists, and improve identifying human exploitation of these species, the ‘chaîne opératoire’ of small game use is examined from an osteological perspective, starting with acquisition, through processing, cooking and consumption to discard, using a series of experiments and microscopic analysis to explore potential bone modification signatures and fracture patterns arising from such activities. Finally, it places these results into broader context by comparing the fracture patterns with bones from British and North American archaeological sites, to demonstrate that similar changes can be seen.

Outbreaks of highly pathogenic avian influenza virus (HPAIV) may result in the infection of millions of poultry, causing devastating disease and up to 100% mortality. Avian influenza outbreaks and laboratory experiments have shown that HPAIV can emerge from low pathogenicity avian influenza virus (LPAIV) precursors. The multi-basic cleavage site (MBCS) in the haemagglutinin protein is described as the main pathogenic determinant of HPAIV infection in poultry. Identifying a precursor LPAIV is important for understanding the molecular changes involved in the emergence of HPAIV. In 2008, H7N7 HPAIV was confirmed in Oxfordshire, UK. The presence of a LPAIV precursor with a rare di-basic cleavage site (DBCS) was identified. The DBCS contains an additional basic amino acid compared to common circulating LPAIVs that harbour a single basic amino acid at the cleavage site (SBCS). Using reverse genetics, isogenic viruses based on A/chicken/England/11406/2008 H7N7 HPAIV, from the outbreak, were rescued with the MBCS replaced with either a DBCS (H7N7DB) as seen in the putative LPAIV precursor or a SBCS representative of common H7 LPAIVs (H7N7SB). Intravenous pathogenicity index testing of the recombinant viruses confirmed that only the MBCS conferred the highly pathogenic phenotype. Following passage in ovo, H7N7DB showed evidence of spontaneous evolution to a HPAIV genotype and phenotype as demonstrated by the acquisition of a MBCS, and by influenza virus-specific immunohistochemistry staining in embryo vascular endothelial cells. In contrast, deep sequencing of tissues from embryos in which H7N7SB was serially passaged up to three times showed retention of the LPAIV genotype. Thus, in chicken embryos, an H7N7 virus containing a DBCS displays an unstable nature allowing for rapid evolution to HPAIV. In ovo passage presents a novel approach to assess the likelihood of a LPAIV to evolve into HPAIV, and allows a laboratory-based dissection of molecular mechanisms behind the emergence of HPAIV.