In 2010, the government of British Columbia (B.C.) dedicated $48 million to stop the spread of HIV. The STOP HIV/AIDS pilot project promotes the uptake of HIV testing in the general population, and the use of antiretroviral therapy amongst those living with HIV/AIDS. This project operates with the rationale of ‘treatment as prevention’ (TasP), meaning that antiretroviral therapy is beneficial for the person living with HIV/AIDS, and has the secondary benefit of reducing the spread of HIV in the general population. Public health discourses are constructed via particular worldviews and involve the creation and delineation of societal problems. Undertaking a discourse analysis, I identify eight dominant discourses of TasP and STOP HIV/AIDS that include: provincial and international support for TasP and lack of federal leadership in HIV/AIDS; TasP, a ‘paradigm shift’ and a ‘game changer;’ TasP as beneficial to the individual and society; human rights and harm reduction; proof and certainty; failure of current prevention efforts; risk discourses; and, finally, universal treatment. I also identify five alternative discourses: holistic understanding/social determinants of health; stigma and discrimination; rights discourse: GIPA, informed consent and self-determination; coercion/criminalization and alternative risk discourse. Through a lens of governmentality, I explicate two overarching and simultaneous discursive strategies in realizing the objective of decreasing the spread of HIV in B.C. The first strategy acts on individuals living with HIV/AIDS, encouraging individuals to take up antiretroviral therapy. The second strategy acts on the general population, informing the population that HIV is a problem, and that treating people living with HIV/AIDS is the best way to protect society as a whole. There are various techniques within these two strategies. These discursive events have immense consequences for the uptake of health policies and programs by the public. The dominant and alternative discourses of TasP impact HIV policy and practice and specifically the individuals living with HIV and AIDS who are the subjects and targets of these initiatives. / Graduate

<p>The aim of this study was to assess the factors associated with HIV risk behaviours in women in Livingstone, Zambia. A cross-sectional analytical survey using a structured questionnaire was carried out in two sites in Livingstone, which were selected on the basis of differences in socio-economic status. Married women and women in the urban community are at high risk of contracting HIV and every effort should be made to ensure that HIV/AIDS programmes help to reduce their vulnerability to HIV infection.</p>

The human immunodeficiency virus type 1 (HIV-1) uses a mechanism of genetic recoding known as programmed ribosomal frameshifting to translate the proteins encoded by the pol gene. The pol gene overlaps the preceding gag gene in the -1 reading frame relative to gag. It contains neither a start codon nor an internal ribosome entry site (IRES) to initiate translation of its proteins. Rather the host ribosomes are forced to pause due to tension placed on the mRNA when they encounter a specific secondary structural element in the mRNA. This tension is relieved by disruption of the contacts between the mRNA codons and tRNA anticodons at a �slippery� sequence within the ribosomal decoding centre. Re-pairing of the tRNAs occurs in the new -1 frame after movement of the mRNA backwards by one nucleotide, allowing the ribosome to translate the pol gene as a Gag-Pol polyprotein. A change in ratio of Gag to Gag-Pol proteins affects viral assembly, and most significantly dramatically reduces viral infectivity. The prevailing model for the mechanism of -1 frameshifting has focussed on a pre-translocational event, where slippage occurs when the slippery sequence is within the ribosomal A and P sites. This model precludes a contribution from the codon immediately downstream of the slippery sequence leading into the secondary structural element. I have termed this the �intercodon�. Often at frameshifting sites it is a termination codon, whereas in HIV-1 it is a glycine codon, GGG. When the intercodon within the frameshift element was changed from the wild-type GGG to a termination codon UGA, the efficiency of frameshifting decreased 3-4-fold in an in vivo assay in cultured human cells. This result mimicked previous data in the group within bacterial cells and cultured monkey COS-7 cells. Changing the first nucleotide of the intercodon to each of the three other bases altered frameshifting to varying degrees, but not following expected patterns for base stacking effects. Such a result would support a post-translocational model for -1 frameshifting. It suggested that the intercodon might be within the ribosomal A site before frameshifting, and that the slippery sequence was therefore within the P and E sites. This was investigated by modulating the expression of decoding factors for the intercodon - the release factor eRF1 and cognate suppressor tRNAs when it was either of the UGA or UAG termination codons, and tRNA[Gly] for the native GGG glycine codon. These were predicted to affect frameshifting only if slippage were occurring when the ribosomal elongation cycle was in the post-translocational state. Overexpression of tRNA[Gly] gave inconsistent effects on frameshifting in vivo, implying that its concentration may not be limiting within the cell. When eRF1 was overexpressed or depleted by RNAi, significant functional effects of decreased or increased stop codon readthrough respectively were documented. Expression of suppressor tRNAs increased readthrough markedly in a stop codon-specific manner. These altered levels of eRF1 expression were able to modulate the +1 frameshifting efficiency of the human antizyme gene. Overexpression of eRF1 caused significant reduction of frameshifting of the HIV-1 element with the UAG or UGA intercodon. Depletion of the protein by contrast had unexplained global effects on HIV-1 frameshifting. Suppressor tRNAs increased frameshifting efficiency at the UAG or UGA specifically in a cognate manner. These results strongly indicate that a post-translocational mechanism of frameshifting is used to translate the HIV-1 Gag-Pol protein. A new model (�almost� post-translocational) has been proposed with -1 frameshifting occurring for 1 in 10 or 20 ribosomal passages during the end stages of translocation, because of opposing forces generated by translocation and by resistance to unwinding of the secondary structural element. With translocation still incomplete the slippery sequence is partially within the E and P sites, and the intercodon partially within the A site. The nature of the intercodon influences frameshifting efficiency because of how effectively the particular decoding factor is able to bind to the partially translocated intercodon and maintain the normal reading frame.

Thesis (PhD)--University of South Australia, 2001.

Thesis (MMedSc)--University of Stellenbosch, 2005. / Bibliography. Also available via the Internet.

Thesis (Ph. D.)--Georgia State University, 2006. / Title from file title page. Lisa Armistead, committee chair; Gregory Jurkovic, Sarah Cook, Marci Culley, committee members. Electronic text (67 p. : col. ill.) : digital, PDF file. Description based on contents viewed Jan. 9, 2008. Includes bibliographical references (p. 59-67).

Thesis (MSc)--University of Stellenbosch, 2007. / Bibliography. Also available via the Inernet.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 6 uppsatser.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.