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Illnesses such as upper respiratory tract infections (URTls(coughs and colds) are positioned within medical discourse as 'minor' and 'trivial', and consulting doctors with cough and cold symptoms is morally accountable. In this thesis I explore different methodological approaches to understanding doctor-patient consultations for URTls. I critically review quantitative and qualitative approaches to URTI consultation research, and explore qualitative discursive approaches through analyses of consultation data. Data comprise 33 video-taped consultations and post-consultation interviews with inner London general practitioners and patients with cough and cold symptoms, supplemented with ethnographic data. I draw from a range of discursive methodological approaches including conversation analysis, socio-Iinguistic analysis of institutional talk and discursive psychology. I show how discursive approaches can illuminate the complexity and meaning of doctor-patient interaction, exploring the way that coughing is used by patients as an interactional resource. In a detailed micro-analysis, I show that coughing is associated with interactional problems such as misunderstanding and disagreement, and how it also functions as a resource to assert patients' legitimacy. ,. In another detailed analysis, I show that the 'minor' status of coughs and colds (and consequent 'no problem' diagnosis) is associated with interactional difficulty for both doctors and patients: I show how doctors' and patients'legitimacy and 'face' are at stake in a contest to define the meaning of cough and cold symptoms (as significant and treatable, or alternatively, 'no problem'). I discuss conflicts between doctors' and patients' interests: for example, prescribing antibiotics may legitimise the patient but discredit the doctor. . I discuss the way that discourse analytic approaches can contribute richer understandings of doctor-patient interaction through detailed analysis of social transactions in consultation (such as the negotiation of identity and face). I contend that discursive approaches represent valuable and under-utilised resources for research and practice in primary care.

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Temporomandibular disorders (TIVID) are a group of relatively common chronic disorders that often result in pain affecting the face, specifically the temporomandibular joint and associated muscles. Treatment strategies are varied, with only a minimal evidence base. The psychosocial aspects of TIVID are generally recognised to be important and complex. The aim of this thesis is to understand the philosophies of care that underpin the professional management of TIVID, and to explore the patients ) experiences of their illness and its management. The ultimate purpose is to use this information to target future interventions at specific points in the care pathway. Qualitative studies of professionals' and individuals' experiences of managing and living with TIVID were undertaken. In depth interviews were conducted with eighteen professionals and twenty-nine individuals suffering from TIVID. The data were then analysed and used to develop a map illustrating the patients' journey through care. The results exposed the large variation in clinical practice and considerable professional uncertainty about optimum management. Patients' experiences reflected the professional uncertainty, and some of the psychosocial effects experienced on the journey through care appeared to have an impact on outcome. The uncertainty over diagnosis in primary care led to a lack of legitimisation of the sufferer's complaint, which had concomitant effects on their day-to-day functioning. This, in turn, perpetuated any psychological distress they might already be experiencing. In conclusion, this thesis highlights the experiential basis of TIVID management, and the underlying ideology of, "do no harm". In primary care the sufferers experience a lack of legitimacy in their complaint due, in part, to a lack of a diagnosis. There is a need for a targeted programme of education in primary care in the diagnosis and management of TMD. This might reduce the level of uncertainty and concomitant psychosocial effects that sufferers experience currently.

Human respiratory syncytial viruses (hRSV) are a major cause of lower respiratory tract disease on primary infection of infants and children. There is no effective vaccine against the virus, but high risk infants can be protected by administration of palivizumab (PZ), a humanised anti-fusion glycoprotein. In previous studies, hRSV isolated from the naso-pharyngeal secretions of infected infants were found to be dominated by slow growing variants which were largely refractory to neutralization by PZ. On further passage in tissue culture, the slow growing variants were replaced by fast growing, neutralization susceptible variants. The aim of this study was to investigate the mechanism of neutralization phenotype shift between slow-growing neutralization resistant and fast-growing neutralization susceptible clones. Neutralization resistance was found to be cell-line dependent with cell lines varying in their permissiveness to antibody treated virus. Antibody resistant and susceptible viruses showed no differences in the amount of the membrane expressed F glycoprotein or post-translational processing of the F polypeptide. They were also equally susceptible to inhibition by clathrin endocytosis inhibitors (monodansylcadaverine and chlorpromazine) suggesting that endocytosis was required for entry of both. They were further tested for susceptibility to anti-fusion inhibitors. These included a peptide derived from the F glycoprotein heptad repeat 2 and two small molecular weight compouds BMS-433771 and BTA9881. It was found that all three compounds failed to inhibit slow growing PZ resistant virus clones in parallel with PZ, but efficiently blocked fast growing PZ susceptible virus clones. These studies suggest that differences in antibody susceptibility stem from differences in the mechanism of fusion for the two virus clones. The full genomes of virus clones with resistant and susceptible phenotypes were sequenced to identify mutations which correlate with the difference in antibody susceptibility. The two clones differed at four sites in the SH, G, F and L genes. These mutations were sought in a number of virus clones expressing a range of susceptibility to antibody neutralization. No single mutation was associated with the shift from neutralization resistant to susceptible phenotype in all clones. However, a mutation at nucleotide 6162 in the L gene was associated with the shift from resistance to susceptibility in one virus lineage.

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