Eileen Stillwaggon

Concurrent sexual partnerships do not explain the HIV epidemics in Africa: a systematic review of the evidence

The notion that concurrent sexual partnerships are especially common in sub-Saharan Africa and explain the regions high HIV prevalence is accepted by many as conventional wisdom. In this paper, we evaluate the quantitative and qualitative evidence offered by the principal proponents of the concurrency hypothesis and analyze the mathematical model they use to establish the plausibility of the hypothesis.We find that research seeking to establish a statistical correlation between concurrency and HIV prevalence either finds no correlation or has important limitations. Furthermore, in order to simulate rapid spread of HIV, mathematical models require unrealistic assumptions about frequency of sexual contact, gender symmetry, levels of concurrency, and per-act transmission rates. Moreover, quantitative evidence cited by proponents of the concurrency hypothesis is unconvincing since they exclude Demographic and Health Surveys and other data showing that concurrency in Africa is low, make broad statements about non-African concurrency based on very few surveys, report data incorrectly, report data from studies that have no information about concurrency as though they supported the hypothesis, report incomparable data and cite unpublished or unavailable studies. Qualitative evidence offered by proponents of the hypothesis is irrelevant since, among other reasons, there is no comparison of Africa with other regions.Promoters of the concurrency hypothesis have failed to establish that concurrency is unusually prevalent in Africa or that the kinds of concurrent partnerships found in Africa produce more rapid spread of HIV than other forms of sexual behaviour. Policy makers should turn attention to drivers of African HIV epidemics that are policy sensitive and for which there is substantial epidemiological evidence.

HIV/AIDS in Africa: Fertile Terrain

An interdisciplinary approach that incorporates biomedical data into an economic analysis provides the necessary foundation for HIV/AIDS policy in poor countries. This article examines the biomedical effects of economic conditions in Africa that contribute to high rates of HIV transmission. The results of statistical analysis show the correlation of economic and epidemiological variables (nutrition, distribution of income, and urbanisation) with rates of HIV. The economic/biomedical hypothesis implies a broad policy response for confronting HIV/AIDS in Africa and in Asia and Latin America.

Maternal Serologic Screening to Prevent Congenital Toxoplasmosis: A Decision-Analytic Economic Model

Objective To determine a cost-minimizing option for congenital toxoplasmosis in the United States. Methodology/Principal Findings A decision-analytic and cost-minimization model was constructed to compare monthly maternal serological screening, prenatal treatment, and post-natal follow-up and treatment according to the current French (Paris) protocol, versus no systematic screening or perinatal treatment. Costs are based on published estimates of lifetime societal costs of developmental disabilities and current diagnostic and treatment costs. Probabilities are based on published results and clinical practice in the United States and France. One- and two-way sensitivity analyses are used to evaluate robustness of results. Universal monthly maternal screening for congenital toxoplasmosis with follow-up and treatment, following the French protocol, is found to be cost-saving, with savings of

Complexity, cofactors, and the failure of AIDS policy in Africa

620 per child screened. Results are robust to changes in test costs, value of statistical life, seroprevalence in women of childbearing age, fetal loss due to amniocentesis, and to bivariate analysis of test costs and incidence of primary T. gondii infection in pregnancy. Given the parameters in this model and a maternal screening test cost of

HIV and concurrent sexual partnerships: modelling the role of coital dilution

12, screening is cost-saving for rates of congenital infection above 1 per 10,000 live births. If universal testing generates economies of scale in diagnostic tools—lowering test costs to about

Cofactor Infections and HIV Epidemics in Developing Countries: Implications for Treatment

2 per test—universal screening is cost-saving at rates of congenital infection well below the lowest reported rates in the United States of 1 per 10,000 live births. Conclusion/Significance Universal screening according to the French protocol is cost saving for the US population within broad parameters for costs and probabilities.

Living with uncertainty

Global AIDS policy still treats HIV as an exceptional case, abstracting from the context in which infection occurs. Policy is based on a simplistic theory of HIV causation, and evaluated using outdated tools of health economics. Recent calls for a health systems strategy – preventing and treating HIV within a programme of comprehensive health care – have not yet influenced the silo approach of AIDS policy.Evidence continues to accumulate, showing that multiple factors, such as malnutrition, malaria and helminthes, increase the risk of sexual and vertical transmission of HIV. Moreover, complementary interventions that reduce viral load, improve immune response, and interrupt pathways of transmission could increase the effectiveness of antiretroviral drugs and other tools of AIDS policy.In health economics, the omission of estimates of increasing returns generated by disease or treatment synergies biases cost-effectiveness analysis against multiple, yet inexpensive, interventions. Current tools of cost-effectiveness analysis only identify local maxima in a complex landscape, and can play, at best, a marginal role in the epidemic, especially where it is already generalized.Cost-effectiveness analyses for HIV that are based on the wrong epidemiological model can generate Type III errors: we get precise answers to the wrong questions about how to intervene. To control the epidemic, AIDS policy needs to utilize an epidemiological model that reflects the interactions of biological as well as behavioural variables that determine the course of HIV epidemics around the world. Cost-effectiveness analysis can benefit from using economic concepts of externalities and increasing returns to incorporate disease interactions and beneficial treatment spillovers for coinfections in HIV-prevention policy.

Race, Sex, and the Neglected Risks for Women and Girls in Sub-Saharan Africa

BackgroundThe concurrency hypothesis asserts that high prevalence of overlapping sexual partnerships explains extraordinarily high HIV levels in sub-Saharan Africa. Earlier simulation models show that the network effect of concurrency can increase HIV incidence, but those models do not account for the coital dilution effect (non-primary partnerships have lower coital frequency than primary partnerships).MethodsWe modify the model of Eaton et al (AIDS and Behavior, September 2010) to incorporate coital dilution by assigning lower coital frequencies to non-primary partnerships. We parameterize coital dilution based on the empirical work of Morris et al (PLoS ONE, December 2010) and others. Following Eaton et al, we simulate the daily transmission of HIV over 250 years for 10 levels of concurrency.ResultsAt every level of concurrency, our focal coital-dilution simulation produces epidemic extinction. Our sensitivity analysis shows that this result is quite robust; even modestly lower coital frequencies in non-primary partnerships lead to epidemic extinction.ConclusionsIn order to contribute usefully to the investigation of HIV prevalence, simulation models of concurrent partnering and HIV epidemics must incorporate realistic degrees of coital dilution. Doing so dramatically reduces the role that concurrency can play in accelerating the spread of HIV and suggests that concurrency cannot be an important driver of HIV epidemics in sub-Saharan Africa. Alternative explanations for HIV epidemics in sub-Saharan Africa are needed.

Rush to judgment: the STI-treatment trials and HIV in sub-Saharan Africa.

Abstract This article shows that the burden of certain tropical disease infections, after controlling for other factors, is positively correlated with HIV prevalence. Using cross-national data and multivariate linear regression analysis, we investigate the determinants of HIV prevalence in low- and middle-income countries. We begin with social and economic variables used in other cross-national studies and then incorporate data on parasitic and infectious diseases endemic in poor populations, which are found to be strongly and significantly correlated with – and are potent predictors of – HIV prevalence. The paper concludes by arguing that treating tropical diseases may be a cost-effective add-on to HIV-prevention and -treatment programs, thus slowing the spread of HIV in disease-burdened populations.

Congenital toxoplasmosis in Austria: Prenatal screening for prevention is cost-saving

The persistence of highly endemic parasitic, bacterial and viral diseases makes individuals and populations vulnerable to emerging and re-emerging diseases. Evaluating the role of multiple component, often interacting, causes of disease may be impossible with research tools designed to isolate single causes. Similarly, it may not be possible to identify statistically significant treatment effects, even for interventions known to be effective, when multiple morbidities are present. Evidence continues to accumulate that nutritional deficiencies, bacterial, viral and parasitic coinfections accelerate HIV transmission. Inclusion of antiparasitics and other beneficial interventions in HIV-prevention protocols is impeded by reliance on inappropriate methodologies. Lack of full scientific certainty is not a reason for postponing safe, cost-effective measures to prevent irreversible damage.