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Nelson, Patrick William. "Mathematical models of HIV pathogenesis and immunology /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6783.
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De, la Harpe Alana. "A comparative analysis of mathematical models for HIV epidemiology." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/96983.
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Thesis (MSc)--Stellenbosch University, 2015.ENGLISH ABSTRACT: HIV infection is one of the world’s biggest health problems, with millions of people infected worldwide. HIV infects cells in the immune system, where it primarily targets CD4+ T helper cells and without treatment, the disease leads to the collapse of the host immune system and ultimately death. Mathematical models have been used extensively to study the epidemiology of HIV/AIDS. They have proven to be effective tools in studying the transmission dynamics of HIV. These models provide predictions that can help better our understanding of the epidemiological patterns of HIV, especially the mechanism associated with the spread of the disease. In this thesis we made a functional comparison between existing epidemiological models for HIV, with the focus of the comparison on the force of infection (FOI). The spread of infection is a crucial part of any infectious disease, as the dynamics of the disease depends greatly on the rate of transmission from an infectious individual to a susceptible individual. First, a review was done to see what deterministic epidemiological models exist. We found that many manuscripts do not provide the necessary information to recreate the authors’ results and only a small amount of the models could be simulated. The reason for this is mainly due to a lack of information or due to mistakes in the article. The models were divided into four categories for the analysis. On the basis of the FOI, we distinguished between frequency- or density-dependent transmission, and as a second criterion we distinguished models on the sexual activity of the AIDS group. Subsequently, the models were compared in terms of their FOI, within and between these classes. We showed that for larger populations, frequency-dependent transmission should be used. This is the case for HIV, where the disease is mainly spread through sexual contact. Inclusion of AIDS patients in the group of infectious individuals is important for the accuracy of transmission dynamics. More than half of the studies that were selected in the review assumed that AIDS patients are too sick to engage in risky sexual behaviour. We see that including AIDS patients in the infectious individuals class has a significant effect on the FOI when the value for the probability of transmission for an individual with AIDS is bigger than that of the other classes. The analysis shows that the FOI can vary depending on the parameter values and the assumptions made. Many models compress various parameter values into one, most often the transmission probability. Not showing the parameter values separately makes it difficult to understand how the FOI works, since there are unknown factors that have an influence. Improving the accuracy of the FOI can help us to better understand what factors influence it, and also produce more realistic results. Writing the probability of transmission as a function of the viral load can help to make the FOI more accurate and also help in the understanding of the effects that viral dynamics have on the population transmission dynamics.
AFRIKAANSE OPSOMMING: MIV-infeksie is een van die wêreld se grootste gesondheidsprobleme, met miljoene mense wat wêreldwyd geïnfekteer is. MIV infekteer selle in die immuunstelsel, waar dit hoofsaaklik CD4+ T-helperselle teiken. Sonder behandeling lei die siekte tot die ineenstorting van die gasheer se immuunstelsel en uiteindelik sy dood. Wiskundige modelle word breedvoerig gebruik om die epidemiologie van MIV/vigs te bestudeer. Die modelle is doeltreffende instrumente in die studie van die oordrag-dinamika van MIV. Hulle lewer voorspellings wat kan help om ons begrip van epidemiologiese patrone van MIV, veral die meganisme wat verband hou met die verspreiding van die siekte, te verbeter. In hierdie tesis het ons ‘n funksionele vergelyking tussen bestaande epidemiologiese modelle vir MIV gedoen, met die fokus van die vergelyking op die tempo van infeksie (TVI). Die verspreiding van infeksie is ‘n belangrike deel van enige aansteeklike siekte, aangesien die dinamika van die siekte grootliks afhang van die tempo van oordrag van ‘n aansteeklike persoon na ‘n vatbare persoon. ‘n Oorsig is gedoen om te sien watter kompartementele epidemiologiese modelle alreeds bestaan. Ons het gevind dat baie van die manuskripte nie die nodige inligting voorsien wat nodig is om die resultate van die skrywers te repliseer nie, en slegs ‘n klein hoeveelheid van die modelle kon gesimuleer word. Die rede hiervoor is hoofsaaklik as gevolg van ‘n gebrek aan inligting of van foute in die artikel. Die modelle is in vier kategorieë vir die analise verdeel. Op grond van die TVI het ons tussen frekwensie- of digtheidsafhanklike oordrag onderskei, en as ‘n tweede kriterium het ons die modelle op die seksuele aktiwiteit van die vigs-groep onderskei. Daarna is die modelle binne en tussen die klasse vergelyk in terme van hul TVIs. Daar is gewys dat frekwensie-afhanklike oordrag gebruik moet word vir groter bevolkings. Dit is die geval van MIV, waar die siekte hoofsaaklik versprei word deur seksuele kontak. Die insluiting van die vigs-pasiënte in die groep van aansteeklike individue is belangrik vir die akkuraatheid van die oordrag-dinamika van MIV. Meer as helfte van die uitgesoekte studies aanvaar dat vigs-pasiënte te siek is om betrokke te raak by riskante seksuele gedrag. Ons sien dat die insluiting van vigs-pasiënte in die groep van aansteeklike individue ‘n beduidende uitwerking op die TVI het wanneer die waarde van die waarskynlikheid van oordrag van ‘n individu met vigs groter is as dié van die ander klasse. Die analise toon dat die TVI kan wissel afhangende van die parameter waardes en die aannames wat gemaak is. Baie modelle voeg verskeie parameter waardes bymekaar vir die waarskynlikheid van oordrag. Wanneer die parameter waardes nie apart gewys word nie, is dit moeilik om die werking van die TVI te verstaan, want daar is onbekende faktore wat ‘n invloed op die TVI het. Die verbetering van die akkuraatheid van die TVI kan ons help om die faktore wat dit beïnvloed beter te verstaan, en dit kan ook help om meer realistiese resultate te produseer. Om die waarskynlikheid van oordrag as ‘n funksie van die viruslading te skryf kan help om die TVI meer akkuraat te maak en dit kan ook help om die effek wat virale dinamika op die bevolkingsoordrag-dinamika het, beter te verstaan.
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Wodarz, Dominik. "Mathematical models of virus immune system interactions." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268104.
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Mishra, Sharmistha. "Using mathematical models to characterize HIV epidemics for the design of HIV prevention strategies." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24913.
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Since 2000, we have been trying to characterize and classify HIV epidemics to guide the strategic design of HIV prevention policies and focus HIV programmes and resource allocation by a regions' epidemic type. We have used arbitrary thresholds of HIV prevalence across different risk-groups in a given population, 'static' mathematical models and classical epidemiological measures of the population attributable fraction that do not account for chains of transmission. As a result, these traditional approaches could be missing the underlying transmission dynamics and the role of key populations - such as female sex workers and their clients - on HIV spread. In this thesis, I build on a growing paradigm shift on how we should re-classify HIV epidemics based on the epidemiological features that lead to HIV emergence and persistence (i.e. the 'epidemic drivers' that influence the basic reproductive ratio, R0). I examine the extent to which our traditional approaches have been underestimating the contribution of sex work to HIV spread and likely misclassifying epidemic type by developing dynamic mathematical models of HIV transmission and simulating a large number of plausible 'synthetic' HIV epidemics. I then develop - as proof-of-concept - a novel algorithm to diagnose epidemic type using these synthetic epidemics and glean the key epidemiological data that would be most useful to help distinguish between 'epidemic drivers', and therefore would be most useful to collect as part of HIV surveillance and future empirical research.
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Akinlotan, Deborah Morenikeji. "Modelling the dynamics of HIV related malignancies." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86573.
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Thesis (MSc)--Stellenbosch University, 2014.ENGLISH ABSTRACT: In recent years, HIV-associated cancers have proven to be the bane of our time, since HIV is decimating humanity across the globe, even in the twilight of the last century. Cancer rates continue to rise in developing countries, where 95% of the world’s HIV-infected population lives, yet less than 1% have access to antiretroviral therapy. HIV-infected individuals have a higher proclivity to develop cancers, mainly from immunosuppression. An understanding of the immunopathogenesis of HIV-related cancers (HRC) is therefore a major prerequisite for rationally developing and/or improving therapeutic strategies, developing immunotherapeutics and proplylatic vaccines. In this study, we explore the pathology of HIV-related cancer malignancies, taking into account the pathogenic mechanisms and their potential for improving the treatment of management of these malignancies especially in developing countries. We mathematically model the dynamics of malignant tumors in an HIV-free environment, investigate the impact of cancer malignancies on HIV-positive patients and explore the benefits of various therapeutic intervention strategies in the management of HIV-related cancers. We present two deterministic models of infectious diseases to implement these, and they were analysed. We use HIV-related lymphomas in the Western Cape of South Africa as a case study. We validated the proposed models using lymphoma incidence data from the Tygerberg Lymphoma Study Group (TLSG), Tygerberg Hospital, Western Cape, South Africa. We show that the increasing prevalence of HIV increases lymphoma cases, and thus, other HIV-related cancers. Our models also suggests that an increase in the roll-out of the HAART program can reduce the number of lymphoma cases in the nearest future, while it averts many deaths. Furthermore, the results indicate that a highly crucial factor to consider in the prognosis of the incidence of lymphoma (and other cancer types) in HIV-infected patients is their CD4 cell count, irrespective of whether the patient has developed an HRC or not.
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Lutambi, Angelina Mageni. "Basic properties of models for the spread of HIV/AIDS." Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/19641.
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Thesis (MSc)--University of Stellenbosch, 2007.ENGLISH ABSTRACT: While research and population surveys in HIV/AIDS are well established in developed countries, Sub-Saharan Africa is still experiencing scarce HIV/AIDS information. Hence it depends on results obtained from models. Due to this dependence, it is important to understand the strengths and limitations of these models very well. In this study, a simple mathematical model is formulated and then extended to incorporate various features such as stages of HIV development, time delay in AIDS death occurrence, and risk groups. The analysis is neither purely mathematical nor does it concentrate on data but it is rather an exploratory approach, in which both mathematical methods and numerical simulations are used. It was found that the presence of stages leads to higher prevalence levels in a short term with an implication that the primary stage is the driver of the disease. Furthermore, it was found that time delay changed the mortality curves considerably, but it had less effect on the proportion of infectives. It was also shown that the characteristic behaviour of curves valid for most epidemics, namely that there is an initial increase, then a peak, and then a decrease occurs as a function of time, is possible in HIV only if low risk groups are present. It is concluded that reasonable or quality predictions from mathematical models are expected to require the inclusion of stages, risk groups, time delay, and other related properties with reasonable parameter values.
AFRIKAANSE OPSOMMING: Terwyl navorsing en bevolkingsopnames oor MIV/VIGS in ontwikkelde lande goed gevestig is, is daar in Afrika suid van die Sahara slegs beperkte inligting oor MIV/VIGS beskikbaar. Derhalwe moet daar van modelle gebruik gemaak word. Dit is weens hierdie feit noodsaaklik om die moontlikhede en beperkings van modelle goed te verstaan. In hierdie werk word ´n eenvoudige model voorgelˆe en dit word dan uitgebrei deur insluiting van aspekte soos stadiums van MIV outwikkeling, tydvertraging by VIGS-sterftes en risikogroepe in bevolkings. Die analise is beklemtoon nie die wiskundage vorme nie en ook nie die data nie. Dit is eerder ´n verkennende studie waarin beide wiskundige metodes en numeriese simula˙sie behandel word. Daar is bevind dat insluiting van stadiums op korttermyn tot ho¨er voorkoms vlakke aanleiding gee. Die gevolgtrekking is dat die primˆere stadium die siekte dryf. Verder is gevind dat die insluiting van tydvestraging wel die kurwe van sterfbegevalle sterk be¨ınvloed, maar dit het min invloed op die verhouding van aangestekte persone. Daar word getoon dat die kenmerkende gedrag van die meeste epidemi¨e, naamlik `n aanvanklike styging, `n piek en dan `n afname, in die geval van VIGS slegs voorkom as die bevolking dele bevat met lae risiko. Die algehele gevolgtrekking word gemaak dat vir goeie vooruitskattings met sinvolle parameters, op grond van wiskundige modelle, die insluiting van stadiums, risikogroepe en vertragings benodig word.
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Mäkitalo, Barbro. "HIV and SIV specific cellular immunity in macaque models /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-751-7/.
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Dasgupta, Abhijit. "Parametric identifiability and related problems /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9602.
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Baxley, Dana Ali. "A MATHEMATICAL STUDY OF TWO RETROVIRUSES, HIV AND HTLV-I." Master's thesis, University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/2369.
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In this thesis, we examine epidemiological models of two different retroviruses, which infect the human body. The two viruses under study are HIV or the human immunodefiency virus and HTLV-I, which is the human T lymphotropic virus type I. A retrovirus is a virus, which injects its RNA into the host, rather than it's DNA. We will study each of the different mathematical models for each of the viruses separately. Then we use MATLAB-SIMULINK to analyze the models by studying the reproductive numbers in each case and the disease progression by examining the graphs. In Chapter 1, we mention basic ideas associated with HIV and HTLV-I. In Chapter 2 some of the basic mathematical model of epidemiology is presented. Chapter 3 is devoted to a model describing the intra-host dynamics of HIV. Here, we take into account how HIV infects and replicates in the CD4+ T cells. The model studied in this thesis examines the difference between cells, which are susceptible to the virus, and cells, which are not susceptible. Through the graphs associated with this model, we are able to see how this difference affects disease progression. In Chapter 4, we examine the effect of HTLV-I virus on human body. The HTLV-I virus causes a chronic infection in humans and may eventually lead to other diseases. In particular, the development of Adult T-cell Leukemia or ATL is studied in this thesis. The T-cell dynamics and progression to ATL is described using a mathematical model with coupled differential equations. Using mathematical analysis and SIMULINK, we obtain results on stability, asymptotic stability and the manner of progression of the disease. In Chapter 5 and appendices, we mention our inference and the MATLAB-SIMULINK codes used in this thesis, so that a reader can verify the details of the work carried out in this thesis.M.S.
Department of Mathematics
Sciences
Mathematical Science MS
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Liang, Yanfeng. "Modelling the effect of stochasticity in epidemic and HIV models." Thesis, University of Strathclyde, 2016. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=27380.
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An epidemic of an infectious disease can be modelled by using either a deterministic model or a stochastic model. In this thesis, we consider the effect that different types of noise has on the dynamical behaviour of deterministic SIS models and SIR/SIRS models as well as an HIV model. We start off with a literature review giving previous work and the mathematical background to the area. Next, we introduce demographic stochasticity into the well-established deterministic SIS model with births and deaths and derive a stochastic differential equation (SDE). We assume that an infected individual or a susceptible individual who dies is immediately replaced by a susceptible individual and thus the population size is kept constant. In order for our model to make sense, we then prove that the SDE has a strong unique nonnegative solution which is bounded above and establish the conditions needed for the disease to become extinct. Based on the idea of the Feller test, we also calculate the respective probabilities of the solution first hitting zero or the upper limit. Numerical simulations are then produced using the Milstein method with both theoretical and realistic parameter values to confirm our theoretical results. Motivated by the model discussed in the first topic, we then continue our study on the effect of demographic stochasticity on the deterministic SIS model by now assuming that the births and deaths of individuals are independent of each other and thus the population size can vary with respect to time. In this case, the per capita disease contact rate may be dependent on the population size and we have shown that this model allows us to consider the cases when the population size tends to a large number and when the population size tends to a small number. First we look at the SDE model for the total population size and show that there exists a strong unique nonnegative solution. Then we look at the two-dimensional SDE SIS model and show that there also exists a strong unique nonnegative solution which is bounded above given the total population size. We then obtain the conditions needed in order for the disease to become extinct in finite time almost surely. Numerical simulations with both theoretical and realistic parameter values are also produced to confirm our theoretical results. Next we look at a different type of noise, namely the telegraph noise, which is an example of an environmental noise. Telegraph noise could be modelled as changing between two or more regimes of environment which differ by factors such as rainfalls or nutrition. This form of switching can be modelled using a finite-state Markov Chain. We incorporate the telegraph noise into the SIRS epidemic model. First we start with a two-state Markov Chain and show that there exists a unique nonnegative solution and establish the conditions for extinction and persistence for the stochastic SIRS model. We then explain how the results can be generalised to a finite-state Markov Chain. Furthermore we also show that the results for the SIR model with Markov switching are a special case of the SIRS model. Numerical simulations are produced using theoretical and realistic parameter values to confirm our theoretical results. Lastly we look at the modified Kaplan HIV model amongst injecting drug users. We introduce environmental stochasticity into the deterministic HIV model by the well-known standard technique of parameter perturbation. We then prove that the resulting SDE has a unique global nonnegative solution. As well as constructing the conditions required for extinction and persistence we also show that there exists a stationary distribution for the persistence case. Simulations using the Euler-Maruyama method with realistic parameter values are then constructed to illustrate and support our theoretical results. A brief discussion and summary section is given at the end to conclude the thesis.
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Ribeiro, Ruy Miguel. "Models of viral diversity and disease development in HIV infection." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302403.
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Vieira, Israel Teixeira. "Small world network models of the dynamics of HIV infection." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433933.
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Powell, Megan Olivia. "Mathematical Models of the Activated Immune System During HIV Infection." University of Toledo / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1301415627.
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Beaton, James. "Investigation of Gold(III) Complexes with HIV-NCp7 and Models." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5679.
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The medicinal uses of gold date as far back as 2500 B.C. in China. In modern times, gold has been used in the treatment of a number of different human diseases including rheumatoid arthritis, cancer, and viral infections. This dissertation will focus on the development of gold complexes for the purpose of selective inhibition of HIV NCp7, a 55 amino acid zinc finger protein with two Cys3His zinc binding domains.
NCp7 is involved in a number of viral life cycle processes including activation of reverse transcription, integration, DNA recognition, RNA packaging, and formation of the viral envelope. The diversity in the roles of NCp7 across the viral life cycle make it a highly attractive target for chemical intervention. Ejection of the tetrahedrally coordinated zinc atoms, modification or deletion of the zinc coordinating amino acids, or modification or deletion of the “essential” tryptophan residue can result in the loss of viral infectivity. This is due to the inability of NCp7 to recognize its “natural” substrate – polynucleic acids. Previous studies have investigated the differences in the manner in which platinum(II), gold(I), and gold(III) complexes interact with NCp7. The platinum(II) complex [Pt(dien)(9-EtGua)]2+ interacts with the C-terminal zinc finger of NCp7 in a non-covalent manner, through a π-π stacking interaction between the platinated 9-EtGua and the “essential” tryptophan residue. The isostructural and isoelectronic complex [Au(dien)(9-EtGua)]3+ ejects the tetrahedrally coordinated zinc atom and replaces it with a gold atom, forming “gold fingers”. This result is consistent with the interactions of the gold(I) complex [(PPh3)Au(9-EtGua)]+.
In order to complete the series of isoelectronic and isostructural platinum(II), palladium(II), and gold(III) complexes with N-heterocyclic ligands and diethylenetriamine chelates, the complexes [Au(dien)(1-MeCyt)]3+ and [Au(N-Medien)(1-MeCyt)]3+ were synthesized. These complexes were found to dimerize the C-terminal zinc finger once the central zinc atom is ejected. This is likely the result of a charge transfer from the 1-methylcytosine ligand to the tryptophan residue, and is a product that was not seen as a result of interaction with the previously published 4-dimethylaminopyridine and 9-ethylguanine analogs. The 1-methylcytosine complexes also stabilize the gold(III) oxidation state and associate with N-acetyltryptophan in a manner consistent with the previously studied gold(III) analogs. Finally, in order to address concerns arising from the inner filter effect, a proof of concept study using 1H-NMR spectroscopy was utilized to show that the complex [Au(dien)(1-MeCyt)]3+ likely has a lower association constant with N-acetyltryptophan than the value determined by fluorescence quenching.
The impact of the incorporation of additional steric hindrance on the gold(III) chelate was studied using the di-(2-picolyl)amine ligand. The gold(III) chlorides incorporating this ligand and the centrally methylated analog were found to eject zinc from the C-terminal zinc finger of NCp7, and the electronegativity differences between the gold(III) and platinum(II) metal centers were highlighted. The attempts to incorporate an N-heterocyclic ligand into these complexes were unsuccessful due to the steric and electronic demands of the chelate.
The use of an organometallic chelating ligand led to the investigation of the ability of gold(III) complexes to catalyze the arylation of zinc-coordinating cysteine residues. The complex [AuCl2(dampa)], which had been formerly investigated as a chemotherapeutic agent due to its structural similarities to cisplatin, was found to arylate N-acetylcysteine, glutathione, and NCp7. The arylation was not found to be dependent on the cis- chloride ligand, as blocking that site with the ligand triphenylphosphine did not prevent the arylation of NCp7. The X-Ray crystal structure of the complex [AuCl(dampa)(PPh3)](PF6) was also solved. Using the advancement of the knowledge of how the electronic and structural properties of gold(III) complexes described herein impact interactions with NCp7, it is possible that a coordination complex that is a selective inhibitor of NCp7 may eventually be developed.
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Chen, Jinyan, and 陈锦艳. "Residual risks estimating models of transmission of HBV, HIV and HCV with different assays : lesson for screening strategies for Chinese blood banks." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193767.
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Blood safety is an issue of public health concern. Sensitive screening assays for excluding infectious donations have been widely adopted to reduce the risk of transfusion-transmitted infections, especially for hepatitis B virus (HBV), hepatitis C virus (HCV) and (human immunodeficiency virus) HIV infections. Even with sensitive screening assays, residual risk of undetectable infectious donations remains because donations may be made in the “window period” when the infection is present but difficult to detect with serological tests. Currently, serological screening tests are mainly used in China, rather than the more expensive and sensitive DNA based tests. From a public health perspective, choice of the screening test depends on overall cost-effectiveness, including assessment of the residual risk. To facilitate a full cost-effectiveness analysis, this review identifies the best residual risk estimating model in a Chinese setting. The search was conducted using databases including PubMed and ISI Web of Knowledge filtered by publication date, English language and accessibility of full text. Both exclusion and inclusion criteria were used for articles identification. Five papers on residual model estimation were retrieved. The blood donor profile in China was used to understand how these models differ and how these differences would affect their use and interpretation. This study identified the Michael P. Busch model as the optimal residual risk estimating model for Chinese blood banks’ to facilitate the cost-effectiveness assessment of a screening strategy in terms of achieving a balance of blood safety and cost.published_or_final_version
Public Health
Master
Master of Public Health
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Medlock, Jan P. "The effect of stochastic migration on an SIR model for the transmission of HIV." Thesis, Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/30547.
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Hussaini, Nafiu. "Mathematical modelling and analysis of HIV transmission dynamics." Thesis, Brunel University, 2010. http://bura.brunel.ac.uk/handle/2438/5672.
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This thesis firstly presents a nonlinear extended deterministic Susceptible-Infected (SI) model for assessing the impact of public health education campaign on curtailing the spread of the HIV pandemic in a population. Rigorous qualitative analysis of the model reveals that, in contrast to the model without education, the full model with education exhibits the phenomenon of backward bifurcation (BB), where a stable disease-free equilibrium coexists with a stable endemic equilibrium when a certain threshold quantity, known as the effective reproduction number (Reff ), is less than unity. Furthermore, an explicit threshold value is derived above which such an education campaign could lead to detrimental outcome (increase disease burden), and below which it would have positive population-level impact (reduce disease burden in the community). It is shown that the BB phenomenon is caused by imperfect efficacy of the public health education program. The model is used to assess the potential impact of some targeted public health education campaigns using data from numerous countries. The second problem considered is a Susceptible-Infected-Removed (SIR) model with two types of nonlinear treatment rates: (i) piecewise linear treatment rate with saturation effect, (ii) piecewise constant treatment rate with a jump (Heaviside function). For Case (i), we construct travelling front solutions whose profiles are heteroclinic orbits which connect either the disease-free state to an infected state or two endemic states with each other. For Case (ii), it is shown that the profile has the following properties: the number of susceptible individuals is monotone increasing and the number of infectives approaches zero, while their product converges to a constant. Numerical simulations are shown which confirm these analytical results. Abnormal behavior like travelling waves with non-monotone profile or oscillations are observed.
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Quintana, Marcel de Souza Borges. "Análise longitudinal de coinfecções por HPV em pacientes HIV-positivas." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/45/45133/tde-04042013-141055/.
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Avaliamos a incidência e o clareamento para o vírus do papiloma humano (HPV) dos tipos oncogênicos e não-oncogênicos em uma coorte aberta com 202 mulheres portadoras do vírus da imunodeficiência humana (HIV), e identificamos alguns fatores de risco e proteção associados a cada desfecho utilizando modelos de fragilidade Gama. No modelo de incidência, foram estudados os tempos até incidência de HPV oncogênicos e não-oncogênicos para cada mulher; no modelo de clareamento, foram estudados os correspondentes tempos até clareamento. Comparamos os erros-padrões estimados pela matriz de informação observada com os erros-padrões bootstrap para ambos os modelos e verificamos que a proposta de Verweij & Houwelingen (1994) para a matriz de variâncias e covariâncias dos parâmetros é a mais apropriada. Para a incidência de HPV oncogênicos, identificamos como fator de risco o uso de drogas em que a taxa de incidência para as pacientes que usam drogas é 1.88 (IC 90%, 1.01; 3.5) vezes aquela correspondente a mulheres que não usam e como fator de proteção a renda em que a taxa de incidência de pacientes com renda igual ou superior a 3 salários mínimos é 0.62 (IC 90%, 0.38; 1.00) vezes a taxa referente àquelas com renda menor que 3 salários mínimos. Para a incidência de HPV não-oncogênicos identificamos como fatores de risco a escolaridade e o total de gestações, em que, para a última, a taxa de incidência para as mulheres que tiveram mais do que uma gestação é 1.76 (IC 90%, 1.09; 2.86) vezes a taxa referente àquelas que tiveram uma ou nenhuma. Para o clareamento de HPV oncogênicos identificamos como fatores que indicam um clareamento mais rápido a renda, a idade e o tratamento antirretroviral (ARV), em que, para a última, supondo mulheres com fragilidades iguais, a taxa de clareamento para as pacientes que eram tratadas com o esquema inibidor de protease (IP) é 1.79 (IC 90%, 1.1; 2.9) vezes aquela correspondente a mulheres que não foram tratadas com nenhum tratamento ARV e como fator que indicam um clareamento mais lento o número de parceiros sexuais no último ano, em que, as pacientes com mais de um parceiro tiveram taxa de clareamento 0.39 (IC 90%, 0.16; 0.98) vezes a taxa de clareamento referente à uma mulher que teve um parceiro ou menos. Para o clareamento de HPV não-oncogênicos tivemos como fator que indica um clareamento mais lento o hábito tabagista em que, supondo fragilidades iguais, pacientes fumantes tem a taxa de clareamento 0.53 (IC 90%, 0.32; 0.87) vezes a taxa referente à uma mulher que não fuma.We evaluated the incidence and clearance for oncogenic and non-oncogenic human papilloma virus (HPV) in an open cohort of 202 women infected with human immunodeficiency virus (HIV), and we identified some risk factors and protective factors for each outcome using Gamma frailty models. In the incidence model, we studied the incidence of stroke by oncogenic and non-oncogenic HPV for each woman; in the clearance model, the corresponding times to clearance were studied. We compared the standard errors estimated by the observed information matrix with bootstrap standard errors for both models and found that the variance and covariance matrix of the parameters proposed by Verweij & Houwelingen (1994) is more appropriate. For the incidence of oncogenic HPV, identified as a risk factor drug use and the incidence rate for patients who use drugs is 1.88 (90% CI, 1.01; 3.5) times the rate for those who do not use and as a protective factor income where the incidence rate is 0.62 (90% CI, 0.38; 1.00) times the rate for those earning less than 3 minimum wages. For the incidence of non-oncogenic HPV identified as risk factors schooling and total pregnancies, in which, for the latter, the incidence rate for women who had more than one pregnancy is 1.76 (90% CI, 1.09; 2.86) times the rate for those which have one or none. For clearance of oncogenic HPV identified as factors that indicate a faster clearance income, age and antiretroviral therapy (ART), in which, to the last, with women assuming equal frailties, the rate of clearance for patients who were treated with the protease inhibitor (IP) regimen is 1.79 (90% CI, 1.1; 2.9) times the rate for those who were not treated with any antiretroviral regimen and as a factor that indicates slower clearance the number of sexual partners in the last year, and for patients with more than one partner the clearance rate 0.39 (IC 90%, 0.16; 0.98) times the rate referring to a woman who had up to a partner. For the clearance of non-oncogenic HPV had a factor which indicates a slower clearance smoking habit, assuming equal frailties, smokers have the clearance rate 0.53 (90% CI, 0.32; 0.87) times the rate referring to a woman who does not smoke.
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Gao, Zhanhai School of Mathematics UNSW. "Modelling Human Immunodeficiency Virus and Hepatitis C Virus Epidemics in Australia." Awarded by:University of New South Wales. School of Mathematics, 2001. http://handle.unsw.edu.au/1959.4/18187.
Full textAbstract:
This thesis is concerned with the mathematical modelling for human immunodeficiency virus (HIV) and hepatitis C virus (HCV) epidemics in Australia. There are two parts to this thesis. Part I is aimed at modelling the transmission of HIV and HCV via needle sharing among injecting drug users (IDUs). The dynamical model of an epidemic through needle sharing among IDUs is derived. This model reveals the correlation between needle sharing and the epidemic prevalence among IDUs. The simulations of HIV and HCV prevalence and incidence among IDUs in Australia are made with this model. The comparison of simulated results with literature estimates shows that the modelled results are consistent with the literature estimates. The effects of needle sharing and cleaning on HIV and HCV prevalence and incidence among IDUs in Australia are evaluated. Part II is devoted to modelling the spread of HIV in the general community in Australia. A mathematical model is formulated to assess the epidemiological consequences of injecting drug use and sexual transmission in Australia. The effects of highly active antiretroviral therapies (HAART) on the HIV epidemic are included. The modelled results are in broad agreement with the literature estimates and observed data. The long-term effects of HAART are also discussed.
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Konrad, Bernhard Paul. "On the dynamics of HIV and malaria infection : insights from mathematical models." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54829.
Full textAbstract:
We develop and apply mathematical models to obtain insights into the dynamics of HIV and malaria infection. We consider three case studies.
1. The duration of the time between exposure and detectability of HIV infection is difficult to estimate because precise dates of exposure are rarely known. Therefore, the reliability of clinical HIV testing during the first few weeks of infections is unknown, creating anxiety among HIV-exposed individuals and their physicians. We address this knowledge gap by fitting stochastic models of early HIV infection to detailed viral load time-courses, taken shortly after exposure, from 78 plasma donors. Since every plasma donor in our data eventually becomes infected, we condition our model to reflect this bias before fitting to the data. Our model prediction for the mean eclipse period is 8-10 days. We further quantify the reliability of a negative test t days after potential exposure to inform physicians about the value of initial and follow-up testing.
2. The recently launched Get Checked Online (GCO) program aims at increasing the HIV testing rate in the Vancouver men who have sex with men population by facilitating test taking and result delivery. We develop mathematical models and extract parameter values from surveys and interviews to quantify GCO's population-level impact. Our models predict that the epidemic is growing overall, that its severeness is increased by the presence of a high-risk group and that, even at modest effectiveness, GCO might avert 34-66 new infections in the next five years.
3. Metarhizium anisopliae is a naturally occurring fungal pathogen of mosquitoes that has been engineered to act against malaria by effectively blocking onward transmission from the mosquito vector. We develop and analyse two mathematical models to examine the efficacy of this fungal pathogen. We find that, in many plausible scenarios, the best effects are achieved with a reduced or minimal pathogen virulence, even if the likelihood of resistance to the fungus is negligible. The results depend on the interplay between two main effects: the ability of the fungus to reduce the mosquito population, and the ability of fungus-infected mosquitoes to compete for resources with non-fungus-infected mosquitoes.Science, Faculty of
Mathematics, Department of
Graduate
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Immonen, Taina Tuulia. "Computational Models of Ex Vivo HIV-1 Dynamics and Fitness Across Scales." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1365173809.
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Malaquias, Angelo Miguel 1978. "Explorando longo período de interação entre sistema imunológico e HIV." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/307214.
Full textAbstract:
Orientadores: Hyun Mo Yang, Norberto Anibal MaidanaTese (doutorado) - Universidade Estadual de Campinas, Instituto de Matemática, Estatística e Computação Científica
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Resumo: Esta tese tem como objetivo abordar, matematicamente, a mutação do vírus da imunodeficiência humana (HIV) por meio de um processo de difusão e advecção. é dividida em três partes: estudo e compreensão do fenômeno biológico; formulação e análise de um primeiro sistema de equações diferenciais ordinárias para estudar o tema e, finalmente, construção e análise de um modelo de equações diferenciais parciais envolvendo a mutação. Os modelos são formulados com base em características biológicas, e procurando, sempre que possível, estabelecer um paralelo entre Biologia e Matemática. Com o modelo de equações diferenciais ordinárias mostrou-se que um sistema imunológico que perde sua capacidade de resposta permite a persistência do vírus HIV no organismo infectado. Também, do modelo com equações diferenciais parciais, concluímos que usar as próprias mutações para combater o vírus pode ser uma alternativa, assim como na idéia de mutagênese letal
Abstract: The aim of this thesis is to study mathematically the mutation of the human immunodeficiency virus (HIV) taking into account the process of diffusion and advection. The thesis is divided in three parts: the current understand of the HIV biology; formulation and analysis of a system of ordinary differential equations to understanding the persistent HIV infection; and, finally, construction and analysis of a model of partial differential equations considering the mutation. The models are formulated based on biological characteristics and whenever it is possible, a parallel between biology and mathematics was established. From system of ordinary differential equations, the persistent HIV infection can be explained by exhausting immune system response. From partial differential equations, the main conclusion is that mutations themselves can be used to fight the virus based on the idea of lethal mutagenesis
Doutorado
Matematica Aplicada
Doutor em Matemática Aplicada
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Jia, Yujiang. "Monitoring the status of HIV/AIDS in China." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/jia.pdf.
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Ejigu, Amsalework Ayele. "Mathematical modelling of HIV/AIDS transmission under treatment structured by age of infection." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/6628.
Full textAbstract:
Thesis (MSc (Mathematical Sciences))--University of Stellenbosch, 2011.Includes bibliography.
ENGLISH ABSTRACT: This thesis takes into account the different levels of infectiousness of the human immunodeficiency virus (HIV) infected individuals throughout their period of infection. Infectiousness depends on the time since infection. It is high shortly after the infection occurs and then much lower for several years, and thereafter a higher plateau is reached before the acquired immunodeficiency syndrome (AIDS) phase sets in. In line with this, we formulated a mathematical model which is structured according to the age of infection. To understand the dynamics of the disease, we first discuss and analyse a simple model in which the age of infection is not considered, but progression of the HIV-AIDS transmission is taken into consideration by introducing three stages of infection. Analysis of these models tells us that the disease can be eradicated from the population only if on average one infected individual infects less than one person in his or her infectious period, otherwise the disease persists. To investigate the reduction of the number of infections caused by a single infectious individual to less than one, we introduce different treatment strategies for a model which depends on the age of infection, and we analyse it numerically. Current strategies amount to introducing treatment only at a late stage of infection when the infected individual has already lived through most of the infectious period. From our numerical results, this strategy does not result in eradication of the disease, even though it does reduce the burden for the individual. To eradicate the disease from the population, everyone would need to be HIV tested regularly and undergo immediate treatment if found positive.
AFRIKAANSE OPSOMMING: Hierdie tesis hou rekening met die verskillende aansteeklikheidsvlakke van die menslike immuniteitsgebreksvirus (MIV) deur besmette individue gedurende hulle aansteeklikheidstydperk. Die graad van aansteeklikheid hang af van die tydperk sedert infeksie. Dit is hoog kort nadat die infeksie plaasvind en daarna heelwat laer vir etlike jare, en dan volg n hoer plato voordat uiteindelik die Verworwe-Immuniteitsgebreksindroom (VIGS) fase intree. In ooreenstemming hiermee, formuleer ons n wiskundige model van MIV-VIGSoordrag met n struktureer waarin die tydperk sedert infeksie bevat is. Om die dinamika van die siekte te verstaan, bespreek en analiseer ons eers n eenvoudige model sonder inagneming van die tydperk sedert infeksie, terwyl die progressie van MIV-VIGS-oordrag egter wel in ag geneem word deur die beskouing van drie stadiums van infeksie. Analise van die modelle wys dat die siekte in die bevolking slegs uitgeroei kan word as elke besmette mens gemiddeld minder as een ander individu aansteek gedurende die tydperk waarin hy of sy self besmet is, anders sal die siekte voortduur. Vir die ondersoek oor hoe om die aantal infeksies per besmette individu tot onder die waarde van een te verlaag, beskou ons verskeie behandelingsstrategiee binne die model, wat afhang van die tydperk sedert infeksie, en ondersoek hulle numeries. Die huidige behandelingstrategiee kom neer op behandeling slegs gedurende die laat sta- dium van infeksie, wanneer die besmette individu reeds die grootste deel van die aansteeklikheidsperiode deurleef het. Ons numeriese resultate toon dat hierdie strategie nie lei tot uitroeiing van die siekte nie, alhoewel dit wel die las van die siekte vir die individu verminder. Om die siekte binne die bevolking uit te roei, sou elkeen gereeld vir MIV getoets moes word en indien positief gevind, dadelik met behandeling moes begin.
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Parker, Christopher Gareth. "Mathematical frameworks for the transmission dynamics of HIV on a concurrent partnership network." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318805.
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Chen, Ren. "Bayesian Inference on Mixed-effects Models with Skewed Distributions for HIV longitudinal Data." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4298.
Full textAbstract:
Statistical models have greatly improved our understanding of the pathogenesis of HIV-1 infection
and guided for the treatment of AIDS patients and evaluation of antiretroviral (ARV) therapies.
Although various statistical modeling and analysis methods have been applied for estimating the
parameters of HIV dynamics via mixed-effects models, a common assumption of distribution is
normal for random errors and random-effects. This assumption may lack the robustness against
departures from normality so may lead misleading or biased inference. Moreover, some covariates
such as CD4 cell count may be often measured with substantial errors. Bivariate clustered
(correlated) data are also commonly encountered in HIV dynamic studies, in which the data set particularly
exhibits skewness and heavy tails. In the literature, there has been considerable interest in,
via tangible computation methods, comparing different proposed models related to HIV dynamics,
accommodating skewness (in univariate) and covariate measurement errors, or considering skewness
in multivariate outcomes observed in longitudinal studies. However, there have been limited
studies that address these issues simultaneously.
One way to incorporate skewness is to use a more general distribution family that can provide
flexibility in distributional assumptions of random-effects and model random errors to produce robust
parameter estimates. In this research, we developed Bayesian hierarchical models in which the
skewness was incorporated by using skew-elliptical (SE) distribution and all of the inferences were
carried out through Bayesian approach via Markov chain Monte Carlo (MCMC). Two real data set
from HIV/AIDS clinical trial were used to illustrate the proposed models and methods.
This dissertation explored three topics. First, with an SE distribution assumption, we compared
models with different time-varying viral decay rate functions. The effect of skewness on the model
fitting was also evaluated. The associations between the estimated decay rates based on the best
fitted model and clinical related variables such as baseline HIV viral load, CD4 cell count and longterm
response status were also evaluated. Second, by jointly modeling via a Bayesian approach,
we simultaneously addressed the issues of outcome with skewness and a covariate process with measurement errors. We also investigated how estimated parameters were changed under linear,
nonlinear and semiparametric mixed-effects models. Third, in order to accommodate individual
clustering within subjects as well as the correlation between bivariate measurements such as CD4
and CD8 cell count measured during the ARV therapies, bivariate linear mixed-effects models with
skewed distributions were investigated. Extended underlying normality assumption with SE distribution
assumption was proposed. The impacts of different distributions in SE family on the model
fit were also evaluated and compared.
Real data sets from AIDS clinical trial studies were used to illustrate the proposed methodologies
based on the three topics and compare various potential models with different distribution
specifications. The results may be important for HIV/AIDS studies in providing guidance to better
understand the virologic responses to antiretroviral treatment. Although this research is motivated
by HIV/AIDS studies, the basic concepts of the methods developed here can have generally broader
applications in other fields as long as the relevant technical specifications are met. In addition, the
proposed methods can be easily implemented by using the publicly available WinBUGS package,
and this makes our approach quite accessible to practicing statisticians in the fields.
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Xu, Liang, and 许亮. "A functional analytic approach to the power series solutions of an HIVmodel." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44912663.
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Nichols, Carmen Nicola. "Poliovirus/SIV antigen chimaeras." Thesis, University of Reading, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339507.
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Blay, Wendy Marie. "Human immunodeficiency virus type I (HIV-1) envelope evolution and the relationship to neutralizing antibodies /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/9296.
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Freitas, Luiz Fernando de Souza 1988. "Modelagem matemática da resposta imunológica na co-infecçãoTrypanosoma cruzi e HIV." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/307201.
Full textAbstract:
Orientador: Hyun Mo YangDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Matemática, Estatística e Computação Científica
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Resumo: O organismo humano possui um complexo sistema de defesa: o sistema imunológico. Tal sistema apresenta diferentes respostas para diferentes ataques ao organismo. A co-infecção por parasitas como protozoário Tripanossoma cruzi e o vírus HIV aciona dois importantes mecanismos de defesa: a imunidade humoral a imunidade celular. Devido à fase crônica da Doença de Chagas, na maioria dos casos assintomática, esta é reativada quando as principais células de defesa do corpo, linfócitos T CD4 não ativos, sucumbem pela ação do vírus HIV. Com o objetivo de estudar a dinâmica de co-infecção por parte das doenças, Doença de Chagas e Síndrome da Imunodeficiência Adquirida, a resposta do sistema imunológico humano, um modelo matemático de equações diferenciais ordinárias autônomas não linear é elaborado. Tal modelo apresenta de forma simplificada a dinâmica entre sistema imunológico, protozoário Tripanossoma cruzi, vírus HIV e células alvo. Após simplificações, obtemos dois sub modelos, com o objetivo de elucidar os mecanismos de defesa do sistema imunológico: imunidade humoral e imunidade celular. A análise quantitativa dos modelos de imunidade faz-se necessária devido a suas complexidades. Sub casos são abordados, com o objetivo de avaliar a eficiência de anticorpos e células que secretam citocinas
Abstract: The human body has a complex system of defense: the immune system. Such a system has different answers for different attacks to the body. Co-infection by parasites such as Trypanossoma cruzi and HIV triggers two important defense mechanisms: humoral immunity cellular immunity. Due to the chronic phase of Chagas's disease, in most cases asymptomatic, it is reactivated, when the main defense cells of the body, linfocity T CD4 no active, succumb by the action of HIV. Aiming to study the dynamics of co-infection by the disease, Chagas's Disease and Acquired Immunode ficiency Syndrome, the response of the human immune system, a mathematical model of autonomous ordinary differential equations nonlinear is elaborate. This model presents a simplified dynamic among the immune system, protozoan Trypanossoma cruzi, HIV and target cells. After simplifications, we get two sub models, aiming to elucidate the defense mechanisms of the immune system: humoral and cellular immunity. Quantitative analysis of models of immunity is necessary due to its complexities. Sub cases are dealt with to evaluate the effectiveness of antibodies and cells that secrete cytokines
Mestrado
Matematica Aplicada
Mestre em Matemática Aplicada
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Hove, Fidelis M. "HIV prevalence estimates and their use in regression models: cautionary evidence from Zimbabwe and studies of the relationship between armed conflict and HIV." Doctoral thesis, University of Cape Town, 2012. http://hdl.handle.net/11427/11777.
Full textAbstract:
Includes abstract.Includes bibliographical references.
This dissertation makes two central arguments. The first is that regressions on country-level HIV prevalence are compromised by the fact that the HIV data used are estimates and not empirical data points. The HIV prevalence rates published by UNAIDS are estimates derived from epidemiological modelling (using EPP and Spectrum) in which data from antenatal clinics (sometimes supplemented by population survey data) are translated into adult HIV prevalence estimates.
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Culshaw, Rebecca Veronica. "Mathematical models of cell-to-cell and cell-free viral spread of HIV infection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq24826.pdf.
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Holtzhausen, Tresia Louisa. "A mathematical investigation of the effects of sexual orientation and HIV status on HPV transmission and vaccination." Thesis, Nelson Mandela Metropolitan University, 2013. http://hdl.handle.net/10948/3946.
Full textAbstract:
The effect of the inclusion of sexual behaviour, particularly three sexual orientation classes, on the transmission dynamics of HPV and cervical cancer incidence was investigated. A comprehensive literature review of mathematical models of HPV transmission and the natural history of cervical cancer was concluded. A mathematical model using ordinary differential equations was developed, which incorporated the three sexual orientation classes, and a sexual mixing algorithm for modelling the transmission dynamics. Reproduction numbers, determined through a simplified version of the developed model, indicated that the bisexual population could form a bridge between the heterosexual and homosexual population. The level of interaction is determined by the selection preferences of a bisexual individual to form a partnership with an individual of the same or opposite sex. The model was simulated, with parameters based on a South African population and HPV type 16/18, to investigate the effects of HIV status, sexual orientation and various vaccination strategies on HPV transmission and cervical cancer incidence. The results indicated that HIV status is a significant factor when determining cervical cancer incidence. The results regarding vaccination strategies agreed with results from the literature review with a two sex before sexual debut and catch up program the most effective, noting that with increased vaccination coverage of females the marginal impact on cervical cancer incidence of this approach diminished.
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Eggett, Christopher James. "Development and use of in vitro models for the investigation of the neurotoxic properties of a tryptophan metabolite." Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245562.
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Cunnama, Lucy. "Economic evaluation of models of prevention of mother-to-child transmission of HIV intervention for large scale implementation." Doctoral thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/33604.
Full textAbstract:
Background: Huge successes have been seen in the prevention of mother-to-child transmission of HIV (PMTCT) towards its elimination. Now amidst a landscape of universal antiretroviral therapy (ART), focus has been placed on different models of care to support and retain mother-infant pairs in the vulnerable postpartum phase. Methods The aim was to establish economic evidence for scaling-up approaches and models of care for PMTCT particularly during the postpartum period in Southern Africa. The economic data were collected during three studies, Safe Generations (Eswatini), MCH-ART and PACER (South Africa), using mixed bottom-up and top-down methodology. Outcomes of these studies were used to estimate the cost-effectiveness using an incremental cost effectiveness ratio (ICER, calculated by the difference in cost divided by the difference in effects) of lifelong ART in comparison to Option A (the standard of care at the time) in Eswatini; and to estimate the annual costs, costeffectiveness and budget impact of three models of care (Model I: Routine Care - mothers in general ART and infants in well-baby clinics; Model II: Integrated Care - mothers-infant pairs in integrated care in midwife obstetric unit; and Model III: Community Care - mothers in community adherence clubs and infants in well-baby clinics) in South Africa, from the provider and patient's perspectives. Costs are presented in 2019 United States Dollars (US $). Results Lifelong ART can be considered cost-effective in Eswatini with an ICER of US $984 per mother retained in care to six months postpartum. In Cape Town, South Africa, Routine Care cost US $226 per mother-infant pair per annum; Integrated Care cost US $341; and Community Care cost US $254. Annual patient costs (direct and indirect costs) for Models I-III, were US $30-55, US $23-45 and US $76 per mother-infant pair respectively. Comparatively Community Care was the most cost-effective model with an ICER of US $97 per mother-infant pair retained and mother virally suppressed. Scaling-up Community Care nationally in South Africa would require US $5 720 096 more than Routine Care, 0.2% of the total health budget for 2020/21. Conclusions This work has generated novel empirical data in the form of new cost estimates and cost comparisons across different models of care. It has also provided a unique comparison of the different models of care using a cost-effectiveness analysis; and further a novel budget impact analysis of different approaches to rolling these strategies out. This data has helped to fill the gap in the evidence base for instance lifelong ART was implemented in Eswatini as a direct result of the Safe Generations study findings. Community Care was found to be cost-effective and if scaled up nationally in South Africa would only require a small increment of the total health budget. However, we recommend a mixture of models of care to cater for the needs and preferences of patients. Decision makers can use the empirical findings to help set realistic budgets in Southern Africa and explore ideal model implementation to support mother-infant pairs in the crucial postpartum phase.
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Byrne, Catherine Margaret McCombe. "Spatial stochastic models of HSV-2 lesion dynamics and their link with HIV-1 acquisition." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58436.
Full textAbstract:
Patients with Herpes Simplex Virus-2 (HSV-2) infection face a significantly higher risk of contracting HIV-1. This marked increase is thought to be due not only to herpetic lesions serving as an entry point for the HIV-1 virus, but also to the increase in CD4+ T cells in the human genital mucosa during HSV-2 lesional events. By creating a stochastic, spatial, mathematical model describing the behaviour of the HSV-2 infection and immune response in the genital mucosa, I first capture the dynamics that occur during the development of an HSV-2 lesion. I then use this model to quantify the risk of acquiring HIV-1 in HSV-2 positive patients upon sexual exposure, and determine whether antivirals meant to control HSV-2 can decrease HIV-1 infectivity. While theory predicts that HSV-2 treatment should lower HIV-1 infection probability, my results show that this may not be the case unless a critical dosage of HSV-2 treatment is given to the patient. These results help to explain the conflicting data on HIV-1 infection probability in HSV-2 patients and allow for further insight into the type of treatment HSV-2 positive patients should receive to prevent HIV-1 infection.Science, Faculty of
Mathematics, Department of
Graduate
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Mugwagwa, Tendai. "Mathematical models of coreceptor usage and a dendritic cell-based vaccine during HIV-1 infection." Master's thesis, University of Cape Town, 2005. http://hdl.handle.net/11427/8733.
Full textAbstract:
Includes bibliographical references.While most of Europe is affected by HIV-1 subtype B, sub-Saharan African is dominated by HIV-1 subtype C. Due to costs, most vaccine development is carried out Europe rather than sub-Saharan countries. However since the mechanisms of disease progression in HIV-1 subtype B may be different from those in HIV-1 subtype C, it is interesting to investigate if and how a dendritic cells based vaccine such as the one developed in France and tested on Brazilians (Lu et al, Nature; 2004) can be used on individuals in sub-Saharan Africa. To investigate this, mathematical models and sensitivity analysis techniques are used to understand the mechanisms of disease progression in two HIV-1 subtypes. These models are then extended to explore the ways in which the vaccine could be used to treat these different HIV-1 subtypes. It is found that the level of immune activation plays a large role in determining the mechanism of disease progression and can itself be a means to the development of AIDS. Furthermore, it is also shown that the dendritic cells based vaccine could reduce the viral load but not eliminate the virus resulting in a viral rebound. To maintain a low viral load, vaccination would have to be repeated. Unfortunately, repeated vaccination may lead to the overproduction of proinflamatory cytokines resulting in severe side effects. However this could be avoided by using a carefully planned treatment schedule. We conclude that the dendritic cells based vaccine can be used in individuals in either subtype B or subtype C region as long as the correct treatment schedule is followed.
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Qian, Lei. "Bayesian semiparametric correlation models for longitudinal data with applications to an HIV/AIDS biomarker study." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1973896431&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Aboagye-Sarfo, Patrick. "Time series analysis of HIV incidence cases in Ghana : trends, predictions and impact of interventions." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2009. https://ro.ecu.edu.au/theses/1889.
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The HIV/AIDS epidemic is one of the world’s leading causes of death, particularly in sub-Saharan African nations like Ghana, and threatens socio-economic development in many developing countries. In this thesis Ghanaian HIV data, comprising monthly number of serologically confirmed reported new HIV cases since 1996, was subdivided into northern and southern sectors based on the geographical location of the ten administrative regions. Potential bias in the collection is considered given the strategic location of the two specialist teaching hospital, one in each sector, which receive referrals from the regions.
Time series modelling was applied to the monthly number of new HIV cases in each sector. Moving average of time series analysis of equal weight was applied to determine the trend for cases of incidence of HIV infection in the northern and southern sectors while Box-Jenkins modelling identification and Holt’s (double) exponential smoothing modelling methods were employed to predict of new incidence of HIV cases for both sectors in respect to sex and age groups. The effectiveness of three existing major interventions was examined using intervention modelling whereas cointegration modelling was used to determine the long-run impact of condom utilisation on the incidence cases of HIV infection. The trend analysis and predictions for the next three years reveal a slow increase in the number of new incidence of HIV cases. Although, various interventions have influenced the number of cases of HIV infection, the magnitude of impact fluctuated and declined with time. The analysis of the long-run impact of condom utilisation, on the reduction of new HIV incidence cases, indicates that new cases of infection will actually increase monthly by factor of 0.4 -0.6 for every 1000 condoms issued. These perplexing results may be because issuing of condoms does not ensure usage.
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CHERUVU, VINAY KUMAR. "CONTINUOUS ANTEDEPENDENCE MODELS FOR SPARSE LONGITUDINAL DATA." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1315579803.
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Azizi, Ali. "Humoral and cellular immune responses in RNA viral infections: Immunogenicity of HIV-1, HCV and SARS-CoV candidate vaccines in animal models." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29278.
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It is difficult to induce protective immunity against most RNA viruses. However, there is strong evidence that humoral and especially cellular immune responses play crucial roles in the control of established RNA viral infections. Thus, an ideal vaccine should be able to induce strong specific antibody titer as well as a robust T-helper and T-cell cytotoxic response. Here, correlates of protective immunity against HIV-1, HCV and SARS-CoV were assessed.
Monocistronic and polycistronic DNA constructs containing structural HIV-l, and SARS genes were designed. The structural proteins (HIV- gpl20, gag, pol, HCV-core, E1/E2 and SARS-NC) were also expressed, purified and characterized in mammalian and bacterial cell lines. HLA-A2.1 and B6 mice were immunized with different combinations of DNA constructs, recombinant proteins and novel adjuvants. Humoral responses were measured by titrating of specific antibodies and cell-mediated immune responses were identified by Th1/Th2 cytokine expression, lymphocyte proliferation, intracellular cytokine staining, HLA-peptide dimer assay, and ELISPOT. The first study in HIV-1 showed that a combination of DNA single constructs, protein and adjuvant induce a higher immune response compared to the DNA or/and protein alone. In the second HIV-1 approach, a synergistic effect between HIV/HCV antigens was detected that may lead to induction of multi-specific immune responses against both HIV and HCV. In the third study (SARS project), a high level of specific SARS-CD8+ T-cell response was demonstrated in mice that received DNA encoding the SARS-nucleocapsid, protein and XIAP (X-link inhibitor of apoptosis) as an adjuvant.
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Cuadros, Diego Fernando. "THE ROLE OF CO-INFECTION IN THE SPREAD OF HIV IN SUB-SAHARAN AFRICA." UKnowledge, 2011. http://uknowledge.uky.edu/biology_etds/1.
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The cause of the high HIV prevalence in sub-Saharan Africa is incompletely understood, with heterosexual penile-vaginal transmission proposed as the main mechanism. Heterosexual HIV transmission has a very low probability; further, a single estimation of heterosexual probability of HIV transmission fails to reproduce the variation associated with important biological cofactors. In particular, studies of HIV incidence suggest that co-infection with other infectious diseases influence the HIV transmission, and therefore might substantially vary the pattern of the spread of the infection. To assess the effect of co-infection on the spread of HIV, I developed and analyzed several mathematical and statistical models based on published data. The results show that despite the low probability of heterosexual transmission per sexual contact, the inclusion of individual variation generated by transient but repeated increases in HIV viral load associated with co-infections may provide a biological basis for the accelerated spread of HIV in sub-Saharan Africa, and raises the possibility that that the natural history of HIV in sub-Saharan Africa cannot be fully understood if individual variation in infectiousness is neglected.
Co-infection might be a key explanatory variable for the rapid spread of HIV infection in sub-Saharan Africa; in fact, co-infection may be a necessary factor, rather than merely being a contributing factor, in the successful spread and survival of HIV in populations where heterosexual vaginal-penile contact is the main mechanism of transmission. Consequently, broad population based control strategies to decrease infectivity and reduce the incidence of other sexual and parasitic infectious diseases might be effective strategies in diminishing the spread of HIV in sub-Saharan Africa.
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Farr, Christina. "A Caulobacter crescentus microbicide prevents vaginal infection with HIV-1 and HSV-2 in preclinical models." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/57896.
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Over 2 million people are infected with HIV each year. The majority of these infections occur in women residing in low-income countries, where their access to and control over preventative measures is often limited. This suggests that female-controlled prevention options for HIV-1 are urgently needed. Microbicides, which can be topically applied to the vaginal tract in advance of sexual activity to protect from HIV-1 infection, represent a promising female-controlled prevention option. We have investigated the development of an HIV-1 specific microbicide using the non-pathogenic, freshwater bacterium Caulobacter crescentus. C. crescentus contains a Surface or S-layer that is easily modified for high-density display of recombinant proteins. We have developed 18 recombinant C. crescentus that display anti-HIV proteins, including decoy receptors and ligands, anti-viral lectins and fusion inhibitors, that can prevent various steps of the HIV-1 attachment and entry process. In vitro testing with these recombinant C. crescentus indicated that 15 were able to provide substantial protection from HIV-1 infection. Studies with immune-competent mice demonstrated that application of C. crescentus to the vaginal tract does not induce the production of inflammatory cytokines or recruitment of immune cells. To test for protection against HIV-1 in vivo we have combined the implantation of human fetal liver and thymus tissue with the intravenous injection of autologous CD34+ cells into NOD-scid IL2Rγnull mice to create humanized Bone Marrow-Liver-Thymus (BLT) mice and we have demonstrated that the peripheral blood of these mice contains human CD45+ cells, including CD4+ and CD8+ T cells, B cells, myeloid cells, and NK cells. Our data indicates that vaginal application of recombinant C. crescentus at the time of HIV-1JR-CSF infection provides protection from HIV-1 infection. Seven of the recombinant C. crescentus were predicted to also prevent infection with herpes simplex virus 2 (HSV-2). HSV-2 is a major co-morbidity for HIV-1 infection, contributing to a 2-4 fold increase in acquisition. Four recombinant C. crescentus provided significant protection from HSV-2 infection in vivo. Taken together this data suggests that a C. crescentus based microbicide could be a safe and effective method to prevent infection with HIV-1 and HSV-2, having considerable impact on public health.Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Goyal, Ravi. "Estimating Network Features and Associated Measures of Uncertainty and Their Incorporation in Network Generation and Analysis." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10605.
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The efficacy of interventions to control HIV spread depends upon many features of the communities where they are implemented, including not only prevalence, incidence, and per contact risk of transmission, but also properties of the sexual or transmission network. For this reason, HIV epidemic models have to take into account network properties including degree distribution and mixing patterns. The use of sampled data to estimate properties of a network is a common practice; however, current network generation methods do not account for the uncertainty in the estimates due to sampling. In chapter 1, we present a framework for constructing collections of networks using sampled data collected from ego-centric surveys. The constructed networks not only target estimates for density, degree distributions and mixing frequencies, but also incorporate the uncertainty due to sampling. Our method is applied to the National Longitudinal Study of Adolescent Health and considers two sampling procedures. We demonstrate how a collection of constructed networks using the proposed methods are useful in investigating variation in unobserved network topology, and therefore also insightful for studying processes that operate on networks. In chapter 2, we focus on the degree to which impact of concurrency on HIV incidence in a community may be overshadowed by differences in unobserved, but local, network properties. Our results demonstrate that even after controlling for cumulative ego-centric properties, i.e. degree distribution and concurrency, other network properties, which include degree mixing and clustering, can be very influential on the size of the potential epidemic. In chapter 3, we demonstrate the need to incorporate information about degree mixing patterns in such modeling. We present a procedure to construct collections of bipartite networks, given point estimates for degree distribution, that either makes use of information on the degree mixing matrix or assumes that no such information is available. These methods permit a demonstration of the differences between these two network collections, even when degree sequence is fixed. Methods are also developed to estimate degree mixing patterns, given a point estimate for the degree distribution.
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Gilbert, Peter Brian. "Sieve analysis : statistical methods for assessing differential vaccine protection against human immunodeficiency virus types /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/9551.
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Al, Mazari Ali. "Computational methods for the analysis of HIV drug resistance dynamics." Connect to full text, 2007. http://hdl.handle.net/2123/1907.
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Doctor of Philosophy(PhD)ABSTRACT Despite the extensive quantitative and qualitative knowledge about therapeutic regimens and the molecular biology of HIV/AIDS, the eradication of HIV infection cannot be achieved with available antiretroviral regimens. HIV drug resistance remains the most challenging factor in the application of approved antiretroviral agents. Previous investigations and existing HIV/AIDS models and algorithms have not enabled the development of long-lasting and preventive drug agents. Therefore, the analysis of the dynamics of drug resistance and the development of sophisticated HIV/AIDS analytical algorithms and models are critical for the development of new, potent antiviral agents, and for the greater understanding of the evolutionary behaviours of HIV. This study presents novel computational methods for the analysis of drug-resistance dynamics, including: viral sequences, phenotypic resistance, immunological and virological responses and key clinical data, from HIV-infected patients at Royal Prince Alfred Hospital in Sydney. The lability of immunological and virological responses is analysed in the context of the evolution of antiretroviral drug-resistance mutations. A novel Bayesian algorithm is developed for the detection and classification of neutral and adaptive mutational patterns associated with HIV drug resistance. To simplify and provide insights into the multifactorial interactions between viral populations, immune-system cells, drug resistance and treatment parameters, a Bayesian graphical model of drug-resistance dynamics is developed; the model supports the exploration of the interdependent associations among these dynamics.
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Traore, Fatoumata. "Understanding sexual risk behavoirs among persons living with HIV/AIDS in Abidjan, Cote d'Ivoire." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1112511160.
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Thesis (Ph. D.)--Case Western Reserve University, 2005.[School of Medicine] Department of Epidemiology and Biostatistics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
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Rahim, Mir Munir Ahmed 1975. "Pathogenesis of HIV-1 nef in adult mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115698.
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Development of a suitable animal model of AIDS is much needed in AIDS research to study infection and pathogenesis as well as to evaluate methods of prevention and treatment of HIV infection. Small animals such as rodents are attractive candidates for AIDS research due to the availability of various inbred and genetically engineered strains, extensive knowledge or their immune system, especially in mice, and the relative ease of breeding and maintaining animal colonies. Transgenic small animal models carrying entire HIV genome or selected genes have been instrumental to understand functions of HIV genes in vivo and their role in HIV pathogenesis. The type of cells in which HIV genes are expressed seems to be an import prerequisite for the study of HIV gene functions in transgenic mice. Mice constitutively expressing the entire HIV-1 genome or HIV-1 nef gene in CD4 + T cells and in the cells of macrophage/dendritic lineage develop an AIDS-like disease very similar to AIDS disease in humans. Similarly, expression of Nef in adult mice, using inducible system, results in the AIDS-like disease. This disease is characterized by thymic atrophy, impaired thymocyte maturation, loss of CD4+ T cells, increased activation and turnover of T cells, which can occur in the absence of lymphypenia, and non-lymphoid organ disease involving the lungs and kidneys. Susceptibility of adult mice to the pathological effects of Nef suggests that the AIDS-like disease in the constitutively expressing Nef Tg mice is not due to developmental defects caused by early expression of Nef. This model highlights the important role of Nef in HIV-1 pathogenesis. The high similarity in the disease in these Tg mice with human AIDS strongly suggest that these mice are a relevant model to study AIDS. This study further evidence that mouse cells can support functions of Nef and these Tg mice represent a unique model to study Nef functions in vivo in the context of the primary immune system. Moreover, the inducible Nef Tg model has given us the ability to control the level and time of expression of Nef which was impossible to do in the previously reported constitutive Nef Tg mouse models. These mice will be useful to study immune reconstitution since Nef expression can be turned off after withdrawal from dox.
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Grimsrud, Anna Thora. "Loss to follow-up from South Africa's antiretroviral treatment programme: Trends, risk factors, and models of care to improve retention." Doctoral thesis, University of Cape Town, 2015. http://hdl.handle.net/11427/14578.
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Includes bibliographical referencesOver the past decade, antiretroviral therapy (ART) programmes have rapidly expanded in resource-limited settings. Access to ART has been accelerated through a public health approach to reduce morbidity and mortality, thereby transforming HIV from a humanitarian crisis to a chronic disease. However, the benefits of ART to patients and communities are dependent on patients being retained in care. This thesis investigates loss to follow-up (LTFU) after ART initiation, in the context of scale-up and limited resources and evaluates models of ART delivery to improve retention. After a brief introduction that offers orientation to the key issues and concepts in the field, Chapter 2 provides a comprehensive literature review discussing the public health concerns related to LTFU in ART programmes, as well as the methodological concerns encountered in studying LTFU. Six results chapters (Chapters 3-8) are presented using complementary cohort data from two collaborative datasets (one from programmes in resource-limited settings and one including only South African cohorts) and from a single ART programme at a community health centre. How to define LTFU is the focus of Chapter 3, demonstrating that definitions can have an appreciable impact on estimates of LTFU. In Chapter 4, temporal factors related to the expansion of ART programmes are investigated, with evidence that the risk of patient LTFU increases with each successive calendar year of ART initiation, and that the rate of programme expansion has a stronger association with the risk of LTFU than absolute programme size. Analyses in Chapter 5 suggest that patients initiating ART at higher CD4 cell counts, above 300 cells/μl, may have an increased risk of LTFU compared to patients initiating ART with lower CD4 cell counts. Taken together, these findings underscore the notion that LTFU is a burgeoning threat to the long-term successes of ART programmes in South Africa and other resource-limited settings. Chapters 6-8 report on the implementation and outcomes from innovative models of ART delivery for stable ART patients. Patient outcomes from (i) a nurse-managed ART service and then (ii) community-based 'Adherence Clubs' highlight that comparable and, in some cases, favourable patient outcomes may be achieved when ART delivery is decentralised. This thesis concludes that LTFU is a significant challenge faced by ART programmes. In the context of ambitious targets and evidence of the potential benefits of ART for individuals and communities, concurrent changes to the health system are necessary to support retention in care. The successes of ART programmes in treating a chronic condition in resource-limited settings can be built upon by expanding community-based ART provision and potentially integrating management of other adulthood illnesses.
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Ekhagen, Johanna. "HIV/AIDS in economic growth models : how does HIV/AIDS influence the Solow Growth Model and what are the implications of the pandemic for the fight against poverty for countries in Sub-Saharan Africa?" Thesis, Uppsala University, Department of Economics, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-106150.
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This thesis studies the impact from HIV/AIDS on economic growth in sub-Saharan Africa. This is an important region for investigation since HIV/AIDS is more common in poor countries where economic growth levels are initially low.
The theoretical framework for the analysis is the Solow Growth Model. The analysis also considers the impact on changes to human capital and adds this factor to the Solow equation.
The analysis concludes that the HIV/AIDS epidemic has negative effects on per capita GDP growth through the parameters of the Solow Growth Model, including human capital. The thesis also deduces that the pandemic enhances income and gender inequality.