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The research explores the experience that students with Dyslexia, on law degrees, have of academic assessment, and the environmental factors that influence their experience and perceptions. The research is situated in one HEI (the Research Institution), which has a student population of 18,800, of which 634 had declared a Specific Learning Difficulty (SpLD) (including Dyslexia) during the academic year 2014/15. Previous research has shown that students with Dyslexia are disadvantaged by traditional forms of academic assessment. Whilst little research has been carried out on Dyslexia and law degrees, the predominance of traditional approaches to assessment is commonly believed to disadvantage students with Dyslexia. This potential disadvantage is explored within the Research Institution (RI). In light of their obligation under the Equality Act 2010 to take reasonable steps to alleviate such disadvantages, specific consideration is given to the RI’s response to potential disadvantages faced by such students. In order to facilitate this objective a multiple-methods approach has been utilised for gathering data. Data has been collected through questionnaires, focus groups and interviews, with law students with and without Dyslexia, with lecturers inside and outside the law school, and with student support staff and other professionals. The range of data was then analysed, utilising an inductive approach. Five main themes emerged, and were explored using a social model of Dyslexia and from an emancipatory perspective. The themes are: 1) diagnosis and categorisation of Dyslexia; 2) the students’ experience of academic assessment; 3) the students’ experience of adjustments to academic assessment; 4) the impact of the law school environment on the experience of students with Dyslexia, and 5) the effect of the wider institutional environment and institutional policy and practice on the experiences and perceptions of how students with Dyslexia, and how they are responded to. The data collected pointed to the fact that students with Dyslexia struggled with traditional academic assessment, to a more significant degree than students without Dyslexia. While reasonable adjustments were provided by the institution to help students with Dyslexia overcome such difficulties, and whilst these were helpful to some extent, their overall effectiveness was shown to be limited. The main reasons for the student experiences that emerged from the research were related to the fact that, due to their Dyslexia, the forms of assessment used by their department presented a direct difficulty for students. Traditional forms of assessment utilised on law degrees are therefore considered to be a ‘disabling barrier’, as they inhibit students with Dyslexia from fully demonstrating their academic ability. The thesis then presents pointers to how law degree providers can respond to this issue. It is argued that this can be achieved by adjusting assessment methods in a way that removes, or at least reduces, the ‘disabling barriers’ faced by law students with Dyslexia. The research suggests that this is made possible by utilising a broader range of assessment methods beyond those traditionally utilised in law degrees. It also details how the individualistic nature of Dyslexia means that the most effective means of improving inclusivity for all students is to provide them with elements of choice as to the form of assessment adopted. The research concludes with proposals for alleviating the disadvantage experienced by law students with Dyslexia in respect of their experience of the academic assessment process and academic assessment outcomes. It is argued that to enhance the quality of their learning opportunities, and in order to be inclusive, academic assessment policy and practice should be informed by/premised upon a social interpretation of Dyslexia.

A major feature of the biology of herpes simplex virus type 1 (HSV-1) is it's capacity to establish a latent infection in peripheral nervous system ganglionic neurons and to periodically reactivate to produce recrudescent disease. Until recently the extent and the nature of any expression from latent HSV genomes was unknown. In 1987, latency associated transcripts (LATs) were detected in murine ganglia which were latently infected with HSV-1. The LATs map to the long repeat region and are transcribed in the opposite direction to and partially overlap with IE-1 mRNA. Subsequent work has refined our knowledge of the HSV-1 LATs and shown that transcripts associated with latency are also encoded by a number of other herpesviruses including pseudorabies virus in swine and bovine herpes virus in rabbits. It is now known that the HSV-1 LATs comprise at least 3 overlapping non-polyadenylated RNAs which share common 5' and 3' ends, but differ in size through differential splicing. These LAT species are thought to be stable introns or stable processing products of a less stable 8.3 kb (m-LAT) polyadenylated primary transcript. Since LAT appears to be the only actively transcribed gene during latency, the control of LAT gene expression must differ considerably from that of any of the lytic cycle genes. A great deal of attention has thus been focussed on the LAT promoter in order to identify cis-acting sequences responsible for this unique pattern of transcription. In this study, in order to determine the location of the LAT promoter, various sequences upstream from the 2 kb LATs were cloned and examined for their ability to drive expression of an adjoining reporter gene in transient expression assays in a plasmid expression vector. The response of these sequences to the presence of HSV-1 trans- acting factors was also examined by infecting cells transfected with the various LAT promoter/CAT fusion constructs. Both the promoter and HSV-1 responsive elements mapped to a 137 bp region 800 bp upstream from the 5' end of the 2kb LATs. Sequence analysis of this region demonstrated that it contained several homologies to recognised promoter elememts including a TATA box, a CAAT box and two putative Sp1 binding sites. Comparison of this region to the corresponding region of the HSV-2 genome revealed that while the 2kb LAT transcription unit itself is completely unconserved, the putative LAT promoter region bears several interesting conserved loci, possibly indicative of the presence of enhancer like elements responsible for tissue-specific expression of the LAT gene. Several of the LAT promoter/CAT fusion constructs were examined in the context of the virus genome by use of a virus vector whereby DNA sequences of interest are introduced into the viral genome by direct ligation. To facilitate this analysis, the parental vector was modified by deletion of the endogenous LAT sequences, thereby preventing possible rearrangments of the viral genome by homologous recombination between the endogenous and introduced LAT promoter sequences. These recombinant viruses were subsequently used for analysis of the LAT promoter during infection of tissue culture cell lines. The most significant result to come from these studies was the finding that sequences upstream from the core LAT promoter, while not having any effect on LAT promoter strength in BHK cells, considerably enhanced LAT promoter strength in C1300 neuroblastoma cells, thereby suggesting that these sequences harbour neuronal specific enhancer elements. In addition to studying the LAT promoter, it was considered interesting to examine the behaviour of an endogenous neuronal specific promoter when introduced into the virus genome. To this end, the 5' flanking region of the human neurofilament-light chain gene was obtained, and two constructs, extending from -296 to +84 and -896 to +84 of the HNF-L promoter fused to the CAT reporter gene were made. Transient transfection assays showed that these constructs performed at least as well as the HSV-1 gD promoter, and were similarly strongly trans-activated upon infection of transfected cells with HSV-1. Introduction of the HNF-L/CAT fusions into the HSV-1 genome, and subsequent examination of these constructs during infection of tissue culture cell lines revealed that sequences upstream from -296, while only moderately enhancing promoter activity in BHK cells, had a greater effect in C1300 neuroblastoma cells, thereby suggesting that these sequences perhaps also containied neuronal specific enhancer elements. The original aim of these studies was to examine promoter/reporter gene activity of the various recombinant viruses in animal latency systems. However, due to lack of time and the necessity of replacing the CAT with the lacZ reporter gene for reasons of sensitivity, these studies were unable to be carried out. One virus which was available, (vFJ12) containing the HSV-2 IE-4/5 promoter fused to the lad reporter gene was used in animal latency studies. In situ analysis showed that the parental virus vector expressed LAT in latently infected murine sensory ganglia, thereby demonstrating that this virus could establish latency in this system.