Complementary hypothesis concerning the community sexually transmitted disease mass treatment puzzle in Rakai, Uganda

Citation
Mc. Boily et al., Complementary hypothesis concerning the community sexually transmitted disease mass treatment puzzle in Rakai, Uganda, AIDS, 14(16), 2000, pp. 2583-2592
Citations number
18
Categorie Soggetti
Immunology
Journal title
AIDS
ISSN journal
02699370 → ACNP
Volume
14
Issue
16
Year of publication
2000
Pages
2583 - 2592
Database
ISI
SICI code
0269-9370(20001110)14:16<2583:CHCTCS>2.0.ZU;2-E
Abstract
Objectives: To study the dynamics of a mass treatment programme for sexuall y transmitted diseases (STD) on prevalence of STD and HIV incidence in orde r to help explain the results of the STD mass treatment community trial in Rakai, Uganda. Methods: The analysis is based on simulations of STD mass treatment interve ntions using a deterministic model describing the course of STD and HIV tra nsmission over time and incorporating demographic, biological and behaviour al parameters. The mass intervention modelled mimics that used in the Rakai community trial. Results: Mass treatment decreases STD prevalence to a very low level compar ed with baseline but is unsuccessful at eradicating the infection. STD prev alences return to baseline fairly rapidly after each round of mass treatmen t. Under different realistic scenarios, the fraction of HIV cases prevented by STD mass treatment assuming uniform 80% coverage of high- and low- risk groups, over the 20-month period following the first round of treatment, w as greater than 35%. If, however, differential coverage is assumed, for exa mple that while the total coverage is still 80%, only 40 or 25% of those at high risk are treated, the HIV preventable fraction is reduced, to 19 and 15% respectively (undetectable given the statistical power of the study). T he tremendous impact of differential coverage can also be observed even in the early stage of the HIV epidemic. Conclusions: In the Rakai trial, mass treatment may have had an effect, alt hough transient, on all STD prevalences, which could have had positive repe rcussions for HIV incidence. This modelling exercise suggests that although an 80% coverage appears high, the differential coverage of low- and high-r isk populations may seriously impair our ability to test the STD-HIV intera ction hypothesis. (C) 2000 Lippincott Williams & Wilkins.