Autism is typically framed as stemming from empathy deficits as well as more general cognitive and sensory issues. In turn it is further associated with other purported harms: ranging from psychological suffering to diminished moral agency. Given such associations, in the philosophical literature, autism is widely taken to hinder the possibility of both thriving and attaining personhood. Indeed, this purported stifling of thriving personhood can be taken as the core harm associated with autism as such. In direct contrast to this dominant view, the key aim of this thesis is to raise reasonable doubt as to the validity of this exclusion, by establishing that there is no decisive reason to accept the notion that autism is inherently harmful. This builds on arguments made by autistic self-advocates who argue in favour of de-medicalising and instead politicising autistic disablement and distress. However, the originality of this thesis lies in three key factors. First: it focuses more specifically on the purported impossibility of thriving autistic personhood, since I take this more fundamental matter to underlie all the other issues relating to these wider debates. Second: I use a negativist methodology. That is, instead of, say, arguing that autistic individuals can be useful to society or have positive attributes, my aim is to raise reasonable doubt regarding the core assumption underlying the dominant framing of autism as a pathology: namely, that autism and thriving personhood are inherently at odds. Third, I draw on methodologies developed by feminist philosophers and critical theorists in order to further our understanding of autism and the ethical issues surrounding it with more nuance than I have found in the existing literature. In sum: after a critical analysis of the concept of autism, and then further analysis of the relationship between autism and the harms it is associated with, I conclude that we have no decisive reason to think that being autistic, in and of itself, is at odds with either thriving or personhood. This chimes with the notion that autism is best framed as a difference, disabled by society rather than medical pathology, raises important problems for both ethical and psychiatric theory, and has significant implications for autism policy and practice.

This thesis argues that the neglected images of the history of science, found in the western alchemical tradition, provide a unique resource for thinking about same-sex union. It provides an opportunity to re-examine the cultural appropriation of these images, used by Jungian psychoanalysis and Evolian traditionalist metaphysics, which deny the validity of same-sex union and homosexuality. By adopting Foucauldian methodologies and using his effective historical, archaeological and genealogical approaches, the thesis argues that there is a silent secondary discourse supported through alchemical imagery that celebrates male same-sex union. The thesis shows how alchemy can be seen as a counter-memory to the dominant regime of sexual-union. By integrating Foucault and the suppressed alchemical images of the Solidonius manuscript with its unique all-male union I argue that this manuscript is a contemporary to Jung's seminal exploration of the Rosarium Philosophorum from which Jung, and Evola, outline the basis of a compulsive heteronormativity in their respective individuation and intiatic techniques. The thesis challenges the existing denial of same-sex union manifesting through identity politics and same-sex marriage. Chapter 1 demonstrates the problem and paradox of the internalized image of the hermaphrodite of Jung and Evola. It outlines a framework of etymological and phenomenological language which is used to critically expose the sui generis claims of the hermaphrodite's role in denying same-sex union. Chapter 2 provides the historical contextualization of the alchemical images, tracing the hermaphrodite trope through four successive phases. These are the philosophical, the alchemical (proper), the hermetic and the psychic. Finally, chapters 3 and 4 combined the alchemical symbols and Foucauldian critical perspectives to develop a reclamation of alchemical same-sex union. Although Foucault dismissed the value of alchemy, this integration offers an original reconceptualization that has the potential to impact directly on the internalized lives of those participating in same-sex identity politics today.

The central aim of this thesis is to examine five of Norma Shearer's pre-Code films - all made between 1930 and 1934 - and to place these films and their accompanying fan magazine rhetoric into a wider context, both within Shearer's career and within Hollywood history. It does this for two reasons. Firstly, it hopes to problematise the now commonly held view of Shearer as a noble, respectable, but ultimately rather dull star by demonstrating the ways in which these films allowed her to become an active advocate for a particular brand of often sexually transgressive modernity, in which she embraced consumer and leisure culture, female employment, companionate marriage and even the sexual single standard. Secondly, the thesis examines the fan magazine rhetoric on the star alongside these films and shows how her successful and happy marriage to MGM Head of Production Irving G. Thalberg served to strengthen, rather than soften, her position as a quintessential modern both on and off screen. After all, the marriage, in which Shearer and Thalberg were professional as well as romantic partners, allowed Shearer to promote a certain kind of companionate marriage, complete with mutual professional satisfaction, successful parenthood, and sexual compatibility. At the height of her fame, Shearer was the star who demonstrated to her female fans that a woman, in the brave new world of the early 20th century, should be able to have it all. Finally, then, the thesis examines how Shearer's ultra-modern reputation came to an end in the mid-1930s, and attributes this development primarily to two influences, one historical and one biographical. Firstly, in July 1934, the Hays Production Code was enforced; particularly targeting female sexual transgression on screen, this censorship text would make it virtually impossible for Shearer to make the types of films she had become most famous for. Secondly, then, in September 1936, Shearer's husband's premature death ensured that the star, who had previously been characterised as a modern wife, now became identified as a tragic, aristocratic, noble widow. Since her films no longer allowed her to develop an alternative persona, this is how Shearer remained known after her retirement, after her death, and to this day.

Hepatitis B virus (HBV) is hyperendemic to southern Africa, the Asia-Pacific region, and the Amazon Basin. HBV causes both acute, and chronic infection of the liver that result in a wide spectrum of liver diseases ranging from acute mild subclinical infection, and an asymptomatic carrier state (ASC) to severe clinical manifestations, including, severe acute and, chronic hepatitis, which can progress to cirrhosis, and the development of hepatocellular carcinoma (HCC). Several viral factors have been implicated in the activation, and inhibition of apoptosis. The development, and progression of this wide spectrum of liver diseases are associated with an unregulated increase or decrease in hepatocyte apoptosis as well as a loss of balance between cell proliferation, and apoptosis. In southern Africa, genotype A of HBV is the predominant genotype, with subgenotype A1 prevailing. Individuals infected with subgenotype A1 have several unique characteristics, including relatively lower levels of HBV DNA, and early seroconversion of hepatitis B e antigen (HBeAg) to antibodies against HBeAg during the course of HBV infection. Infection with this subgenotype is associated with rapid disease progression, and high frequency of HCC development. Moreover, patients infected with subgenotype A1 had increased levels of apoptosis when compared to the other subgenotypes. The G1862T mutation occurs most frequently in subgenotype A1. In the clinical setting, South African HCC patients infected with G1862T subgenotype A1 strains had higher levels of apoptosis while ASCs patients infected with G1862T subgenotype A1 strains had lower levels of apoptosis, when compared to those infected with wild-type. To date, G1862T has been functionally characterized in subgenotype A2, genotype B and in a genotype D HBV genome containing a subgenotype A1 precore (PreC) region. The objectives of our study were to construct 1.28 mer replication competent clones containing an endogenous HBV promoter for wild-type subgenotypes A1, A2, and D3 as well as mutant G1862T subgenotype A1, and to functionally characterize these strains in tissue culture. Transfection of Huh7 cells was used to follow the viral replication, expression of HBeAg, activation of the unfolded protein response (UPR), and subsequent apoptosis. The strategy used for the generation of these replication competent clones had several advantages. Very few PCR errors were introduced, and carry-over of enzymes, nonspecific products, and reaction reagents downstream was prevented. The clones contained endogenous HBV promoters, and enhancers, and were generated from a single complete genome of HBV. These replication competent clones may be used in future studies for the establishment of stable cell lines that constitutively express HBV proteins without the need for further manipulation. This strategy can be used for the generation of replication competent clones belonging to genotypes A to D, and G, and with a few minor modifications, for genotypes E, F, and H. Using the newly generated clones, their replication competence was demonstrated using transfection of Huh7 cells. Even in the absence of an exogenous promoter, these clones were able to support the expression of intracellular, and extracellular HBV DNA at levels of 108 to 109 genome copies/ml. HBcAg, HBeAg, and HBsAg were expressed for a period of five days, and the order of expression was similar to that seen during acute HBV infection. Comparison of transfection with a replication competent clone containing an exogenous HBV promoter demonstrated higher expression of HBV DNA, and proteins, as well as an earlier expression, and accumulation of HBeAg in the endoplasmic reticulum (ER) relative to the clone containing an endogenous HBV promoter. This initial increased accumulation of HBeAg in the ER did not affect the level of activation of the UPR, but led to an increased level of total cell death as a consequence of necrosis. When comparing the different subgenotypes following transfection into Huh7 cells, subgenotype D3 replicated at a lower level, as measured by HBsAg, and HBV DNA levels, with HBeAg passing through the secretory pathway earlier, when compared to cells transfected with genotype A. There was no difference in the intracellular, and extracellular HBsAg between cells transfected with either subgenotype A1 or A2. However, cells transfected with subgenotype A1 had higher levels of intracellular replicative intermediates, HBeAg, and HBcAg, and lower extracellular expression of HBeAg from days 1 to 3, when compared to cells transfected with subgenotype A2. The intracellular retention of the PreC/ core (C) precursor protein in cells transfected with subgenotype A1 was clearly demonstrated by its lower expression in the secretory pathway, and its higher co-localization in the nucleus, using indirect immunofluorescence. This intracellular retention led to greater ER stress, and an earlier, and prolonged activation of the UPR. This correlated well with the higher PERK, ATF6, and IRE1/XBP1 activity seen on days 3 than on day 5. These findings suggest that the prolonged activation of the UPR in cells transfected with subgenotype A1 led to increased apoptosis, and subsequent induction of liver damage, and may therefore, be a contributing factor to the higher hepatocarcinogenic potential of subgenotype A1. Our study demonstrated that G1862T reduced replication, and led to the initial temporal retardation of intracellular core-particle-associated HBV DNA. Although, G1862T did not affect HBsAg expression, it led to a decreased expression of HBcAg, and HBeAg. The decreased expression of extracellular HBeAg was probably as a result of decreased cleavage efficiency by the signal peptide, which consequently led to the retardation of the PreC/C precursor protein in the ER, and ER-Golgi intermediate compartment (ERGIC), and its decreased expression in the nucleus. This retardation, and accumulation led to the earlier activation of all three UPR pathways, but not to increased apoptosis. Therefore, it is evident that G1862T does not completely abolish HBeAg expression, but affects the rate of HBeAg maturation, and its expression through the secretory pathway. These findings suggest that in response to the accumulation of HBeAg in the ER, the UPR was activated resulting in the alteration of the capacity to overcome this stress, consequently leading to a new homeostasis of the ER being reached. The capacity of the ER is increased, with no further activation of the UPR and apoptosis, which facilitates maturation of HBeAg. In conclusion, our study for the first time demonstrated that there are a number of factors that influence the expression of proteins in HBV transfection studies including the type of transcriptional promoter, the different genotypes/subgenotypes of HBV, the use of protein expressing as opposed to replication competent clones, and the presence, and absence of mutations, such as the G1862T. Therefore, when comparing the outcomes of various experiments these factors should be taken into consideration, and the results interpreted with caution, because experiments may not be strictly speaking comparable. Importantly, replication competent clones were generated from strains circulating in southern Africa. The generation of these clones is an important step in further functional characterization of African strains of HBV, and their comparison to strains circulating other geographical regions of the world. These strains, in particular, subgenotype A1 can develop unique mutations, such as the G1862T, which we demonstrated can influence the expression of HBeAg, in a way that it can possibly account for the higher hepatocarcinogenic potential of subgenotype A1.

In the last part of Ethics Spinoza introduces the doctrine of the intellectual love of God: God loves himself with an infinite intellectual love. This doctrine has raised one of the most discussed puzzles in Spinoza scholarship: How can God have intellectual love if, as Spinoza says, God is Nature itself? After examining existing.approaches to the puzzle and revealing their failures, I will propose a Neo- Confucian approach to the puzzle. I will compare Spinoza's philosophy with Neo-Confucian (especially Wan Yang-Ming's) philosophy and argue that we can develop a new approach to the puzzle by appealing to the comparison. I conclude that the intellectual love of God can be properly understood from different perspectives. From God's perspective it is understood as the creative power of God. From an individual's perspective it is understood as the essence of this very individual. Moreover, once we combine these two perspectives we can reach what I consider to be the correct interpretation of Spinoza' s view: Given that intuitive knowledge and action are one and the same the intellectual love of God should be comprehended not only as man's final fulfillment of freedom through intuitive knowledge, but also as man's self-cultivation in practice. I maintain that a free man, as Spinoza endeavors to become, is equivalent to a Neo-Confucian sage.

This thesis will survey several prominent approaches to analysing causation, discuss their differences and similarities, and look at a number of problems which are common to all of them. I will be arguing for the following claims about how we should approach the process of analysing causation. Firstly, I will be arguing that a reductive analysis is desirable, since if we can reductively analyse causation in terms of something empirically accessible, we can explain how it is possible to know anything about causation. I will argue that to reductively analyse causation is to find out what kind of facts ground causal facts. Secondly, I will argue, following Hall and Strevens, that there are two kinds of causation, causal difference making and causal influence. This two-tiered approach explains the cases where we are tempted to ascribe conflicting characteristics to our concept of causation. Thirdly, I will argue that causal influence grounds causal difference making and that it does so necessarily. That the grounding relation holds necessarily is important for defending the two-tiered approach against the objection that it would yield a disjunctive account.

In my thesis, I challenge existing philosophical and scientific accounts of pain to explain certain constitutional, functional and empirical problems. Though difficult, some of these problems will be familiar. Unlike perceptual experiences, pains are strikingly affective and when we are in pain we are primarily concerned with the experience itself rather than mind-independent objects. The obvious explanation, that pain is not a perceptual experience, would be appealing if it were not for the fact that pains vary in quality, intensity and location. These seem to be features of paradigmatic perceptual experiences. The magnitude of another problem, the weakness of the correlation between pain and the stimulus, has been under-played. It is widely observed that those with chronic conditions experience pain in the absence of the stimulus and in circumstances like sport and war severe injuries occur in the absence of pain. I argue that the variable relationship between pain and the stimulus is normal; it is not confined to abnormal cases or circumstances. As no existing account proves explanatorily adequate, I develop a novel position called ‘near-motivationalism’ from a revisionary approach to the conceptual models of pain science. This has the power to solve the problems I set.

Thesis (MPH)--University of Limpopo, 2009. / BACKGROUND AND AIM: Hepatitis B virus (HBV) is the major cause of hepatitis in South Africa (SA), with an estimated 4 million carriers. It is transmitted by infected blood and other body fluids, placing health care workers (HCWs) at high risk of infection. The SA Department of Health strongly recommends that all HCWs be vaccinated against HBV, but studies have shown that uptake of the vaccine is sub-optimal. This study aimed to estimate HB vaccination coverage levels among nurses, and describe the demographics and characteristics of the HB vaccination policies associated with different levels of coverage, at private and public hospitals in Tshwane. METHODS: This was a questionnaire-based cross-sectional study on 300 randomly selected nurses and 12 chief infection control officers (CICOs) from 13 hospitals (6 public and 7 private) in Tshwane performing high risk procedures. CICOs were asked questions about HB vaccination policies and coverage, while nurses were asked about demographics, HB vaccination status, and the HB vaccination policies of their institutions. RESULTS: The response rate was 84.3% (253/300) for nurses, and 75% (9/12) for CICOs. Of the nurses, 68.0% (172/253) were vaccinated, and logistic regression analysis found that those statistically significantly most likely to be vaccinated were: 30 years and younger (odds ratio [OR]=2.9; 95% CI: 1.11–7.59); employed in private hospitals (OR=3.0; 95% CI: 1.24–7.32); and graduated after 1990 (OR=2.6; 95% CI: 1.10–6.19). Also, logistic regression analysis found two statistically significant policy-related predictor for vaccination uptake, which was the presence of HB vaccination program (OR=4.6; 95% CI: 2.11-10.06); and compulsory HB vaccination (OR=2.8; 95% CI: 1.37-5.70. CONCLUSION: There is a need for a national policy on HB vaccination of HCWs which should include compulsory vaccination, to increase the vaccination coverage level amongst nurses.

Thesis (MSc. (Medical Virology))-- University of Limpopo, 2011. / Introduction: Sub-Saharan Africa is a region with hepatitis B virus (HBV) hyperendemicity with more than 8% HBsAg prevalence. An estimate of two billion people has been reported to carry HBV markers. HBV was associated with about 25% of annual deaths in Africa. HBV possesses a DNA polymerase which lacks proofreading mechanism. This results in highly variability and genetic diversity which poses a challenge for the diagnosis and therapeutic management of HBV infection. High mutation rate of HBV also has great implications on the development of drug resistant mutations. Moreover, HBV diversity represents a challenge for the sensitivity of immunological and molecular diagnostic assays. A number of studies on HBV full length genome have been conducted particularly in developed countries. Limited studies are available in Africa and South Africa. In South Africa, few studies have been done analysing the complete genome of HBV isolates from patients with asymptomatic carriers and fulminant hepatitis B (Owideru et ai, 2001 a; Owideru et ai, 2001 b; Kimbi et ai, 2004; Kramvis et ai, 2002).This study was aimed at characterising the full-length genome of HBV isolates at Dr George Mukhari Hospital, Pretoria, South Africa, with a view of developing a PCR-based technology for amplification and characterisation of HBV strains with different serological profiles. The technology, if successfully developed, will contribute in understanding the molecular mechanisms resulting in various HBV variants or isolates. Methods: The study design was exploratory. Four stored serum samples collected from HBV infected patients at Dr George Mukhari hospital, Pretoria, were used to develop the molecular technology and test the hypothesis. HBV serology was previously performed targeting 5 HBV serological markers; HBsAg, anti-HBs, anti-HBc, HBeAg and anti-HBe using Elecsys version; HBV DNA quantification was done using Cobas Amplicor HBV DNA monitor assay, HBV DNA was extracted and subjected to nested PCR assay targeting HBV full length genome as two overlapping fragments: fragment A (1670 bp) and fragment B (1868 bp). The generated PCR products for both fragments were cloned into the pGEM T easy vector and 2 clones were selected from each sample. The plasm ids were purified using Invisorb@ Spin Plasmid Mini Two and the clones were recovered by PCR assay. The sample PCR products and the clone PCR products were purified and sequenced using SpectruMedix SCE2410 genetic analysis system. HBV genotyping was performed using the NCBI web-based genotyping tool. Phylogenetic analysis was done using MEGA 4 software to confirm HBV genotypes. Results: Serology results were as follows: All samples were HBsAg positive, Anti-HBs negative, anti-HBc positive and anti-HBe negative. Sample B1121 and sample 6 were HBeAg positive while samples B452 and 5 were HBeAg negative. A total of 12 PCR products were sequenced (4 study samples and 8 clones [2 clones each sample]). In total, 7 HBV full length genome sequences were deduced from this study, with 3 sequences belonging to genotype A, 2 to genotype C and 2 to genotype D. 3 HBV genotypes were detected from this study; genotype A, C and D with subgenotype A2, C1 and D1 respectively. Mutations were observed throughout the genome. In the pre-S/S open reading frame (ORF), the most significant findings were the detection of mutations within the "a" determinant site and major hydrophilic region (MHR). These mutations included Y161F,E164G observed in sample B1121 and B1121C1 belonging to subtype A1; 2 amino acid insertion at aa 161-162 in sample 5 belonging to subtype C1. Drug resistance associated mutations were identified in the polymerase gene, these included M204T and L217R which are associated with adefovir resistance, M204T also resulted in a change from tryptophan (W) to arginine (R) at aa 196 on the overlapping surface gene on sample B452 C1. Basal core promoter (BCP) and pre core/core mutations were detected in study isolates; specifically the BCP double mutation (1762/1764) was seen in 8 isolates which belonged to subtype C1 (5) and D1 (3) and the pre-core stop codon mutations (G1896A) in 4 isolates. (2 belonging to subtype C1 and the other 2 to D1). Other changes observed included a 48 nucleotides deletion in the pre-core gene, 6 nucleotides insertion in the HBx gene of all subtype D1 isolates and a 3 nucleotides deletion in subtype C1 clone. Conclusion: This study successfully optimised a PCR-based technology for the amplification and characterisation of HBV full length genome. 3 HBV genotypes were detected with subtypes A2, C1 and D1. However, the detected subtypes are rarely detected in South Africa. The detection of subtype A2 may confirm its Southern African origin. Drug resistance associated mutations were observed in this study. These included the adefovir resistance mutation which the current study confirmed it is a naturally occurring mutation as it was detected in adefovir therapy na'ive patient. The BCP and pre-core/core mutations were detected in genotype C and D isolates; however, their association with serological profile and clinical outcomes could not be deduced. Unique or novel mutations were seen in the study isolates, these included 48 nucleotides deletion in the pre core gene, 3 amino acids insertion in the RNase H and 8 amino acids deletion in the RT domain of polymerase gene. To our knowledge, these mutations have not been identified or reported in the literature. The detection of 6 nucleotide insertion in the HBx gene was reported for the first time in South African isolates. Further analysis is required to ascertain the biological significance of the unique mutations detected in this study.

Thesis ( M Med ( Virology ) )-- University of Limpopo (Medunsa Campus), 2013. / Introduction: The hepatitis B virus (HBV) causes a serious type of liver disease referred to as hepatitis B, which is associated with various fatal sequelae following the onset of chronic infection. As a result of the global burden of chronic HBV infection, HBV-related mortality is currently estimated at 620 000 annual deaths worldwide (Hwang and Cheung, 2011). The World Health Assembly (WHA) recommended in 1992 that the hepatitis B vaccine be incorporated into national immunization programmes universally, especially in the hyperendemic regions of the world, in order to curb the global burden of hepatitis B (WHO, 1992). Accordingly, South Africa introduced the hepatitis B vaccine into the national Expanded Programme on Immunization (EPI-SA) in April 1995. Almost 17 years later, South Africa has not conducted any nationwide serosurveys to monitor the population impact of the hepatitis B vaccine. Instead, a number of field and laboratory studies have been conducted only in vaccinated children within the first 5 years of life and as such reports on the short¬term impact made by the hepatitis B vaccine in the country have largely relied on these studies (Tsebe et al., 2001; Schoub et al., 2002; Simani et al., 2008). The aim of the current study therefore was to assess the population impact made by the hepatitis B vaccine post its introduction into EPI-SA using an age stratified, cross-sectional study. The objectives were to compare the prevalence of HBV exposure between the post- and pre-vaccination populations of South Africa, determine the influence of HIV infection on the prevalence of HBV exposure between the post- and pre-vaccination populations of South Africa by performing a subset analyses, and lastly, to perform molecular characterization of hepatitis B surface and polymerase genes in HBV DNA positive individuals. Materials and Methods: This was an explorative and descriptive retrospective, cross¬ sectional study based on recently tested and stored blood samples from the NHLS fi Diagnostic Laboratory in the Department of Virology. For the purpose of this study, these samples were obtained after Ethics approval, and two target populations identified based on the year (Le. 1995) the hepatitis B vaccine was introduced into EPI-SA; a post-vaccination population consisting of 605 blood samples from individuals aged 1-15 years and a pre¬vaccination population consisting of 601 blood samples from individuals aged 16-25 years. The post-vaccination population was further stratified by age as follows; 1-5,6-10 and 11-15 years, in order to assess immunity and chronic carriage of HBV across the different age groups. All samples were tested for the following primary serological markers; HBsAg, anti¬HBc and anti-HBs, to determine the prevalence of HBV chronic carriage, past HBV exposure and immunity to HBV infection respectively. Samples were further assessed for the vi incidence of acute HBV infection by testing for IgM anti-HBc. All serological testing was performed using the Elecsys@ 2010 Immunoassay System. Samples with serological evidence of infection or exposure to HBV were selected and screened for HBV DNA using a real time PCR assay to determine the prevalence of active HBV infection within this group. Study subjects with records of their HIV status, either positive or negative, were also pooled for subset analyses in order to determine the influence of HIV infection on immunity and chronic carriage of HBV. Finally, samples positive for HBV DNA were subjected to molecular characterization of the hepatitis B surface (S) and polymerase (pol) genes. Results: Following serological screening, immunity to HBV infection was found to be significantly (p<0.001) higher (56.7%) in the post-vaccination population than in the pre-vaccination population (15.5%). Within the post-vaccination population alone, immunity was found to wane with increasing age from 76.1 % in those 1-5 years of age to 50.0% in those 6-10 years and 44.2% in those 11-15 years of age. Chronic carriage on the other hand was significantly (p=0.008) reduced in the post-vaccination population with 1.5% HBsAg prevalence as compared to 4.0% in the pre-vaccination population. Within the different age strata, chronic carriage increased with increasing age (0.5% in 1-5 years; 1.3% in 6-10 years; 2.5% in 11-15 years). Overall, no acute HBV infection was detected within the post-vaccination population, while a 14.6% prevalence rate of acute HBV infection was found for the pre-vaccination population. From the subset analyses, immunity was found to be significantly (p<0.001) higher in the HIV uninfected population as compared to the HIV infected population; 82.5% versus 22.0% in the post-vaccination population and 26.7% versus 0% in the pre-vaccination population, while chronic carriage was found to be higher in the HIV infected population than in the HIV uninfected population. Following molecular characterization of the HBV S gene, it was revealed that the majority of the viral isolates were genotype A, with only 1 genotype D isolate found. A number of notable amino acid i$ variations were also detected within the antigenic region of the HBsAg of viral isolates, inCluding the K122R, N131T, T143S, and E164D mutations. Conclusion: Introduction of the hepatitis B vaccine into EPI-SA has shown remarkable success in children under the age of 5 years. Overall, immunity and chronic carriage of HBV within the post-vaccination population has been greatly impacted by hepatitis B immunization. Within the HIV infected population, susceptibility to HBV infection remains a cause for concern. Finally, although amino acid variations within the viral HBsAg are present, vaccine escape-related mutants appear to be rare or even absent within the South African population. vii