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      Mapping HIV clustering: a strategy for identifying populations at high risk of HIV infection in sub-Saharan Africa

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          Abstract

          Background

          The geographical structure of an epidemic is ultimately a consequence of the drivers of the epidemic and the population susceptible to the infection. The ‘know your epidemic’ concept recognizes this geographical feature as a key element for identifying populations at higher risk of HIV infection where prevention interventions should be targeted. In an effort to clarify specific drivers of HIV transmission and identify priority populations for HIV prevention interventions, we conducted a comprehensive mapping of the spatial distribution of HIV infection across sub-Saharan Africa (SSA).

          Methods

          The main source of data for our study was the Demographic and Health Survey conducted in 20 countries from SSA. We identified and compared spatial clusters with high and low numbers of HIV infections in each country using Kulldorff spatial scan test. The test locates areas with higher and lower numbers of HIV infections than expected under spatial randomness. For each identified cluster, a likelihood ratio test was computed. A P-value was determined through Monte Carlo simulations to evaluate the statistical significance of each cluster.

          Results

          Our results suggest stark geographic variations in HIV transmission patterns within and across countries of SSA. About 14% of the population in SSA is located in areas of intense HIV epidemics. Meanwhile, another 16% of the population is located in areas of low HIV prevalence, where some behavioral or biological protective factors appear to have slowed HIV transmission.

          Conclusions

          Our study provides direct evidence for strong geographic clustering of HIV infection across SSA. This striking pattern of heterogeneity at the micro-geographical scale might reflect the fact that most HIV epidemics in the general population in SSA are not far from their epidemic threshold. Our findings identify priority geographic areas for HIV programming, and support the need for spatially targeted interventions in order to maximize the impact on the epidemic in SSA.

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          Most cited references19

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          Dual infection with HIV and malaria fuels the spread of both diseases in sub-Saharan Africa.

          Mounting evidence has revealed pathological interactions between HIV and malaria in dually infected patients, but the public health implications of the interplay have remained unclear. A transient almost one-log elevation in HIV viral load occurs during febrile malaria episodes; in addition, susceptibility to malaria is enhanced in HIV-infected patients. A mathematical model applied to a setting in Kenya with an adult population of roughly 200,000 estimated that, since 1980, the disease interaction may have been responsible for 8,500 excess HIV infections and 980,000 excess malaria episodes. Co-infection might also have facilitated the geographic expansion of malaria in areas where HIV prevalence is high. Hence, transient and repeated increases in HIV viral load resulting from recurrent co-infection with malaria may be an important factor in promoting the spread of HIV in sub-Saharan Africa.
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            Concurrent partnerships and the spread of HIV.

            To examine how concurrent partnerships amplify the rate of HIV spread, using methods that can be supported by feasible data collection. A fully stochastic simulation is used to represent a population of individuals, the sexual partnerships that they form and dissolve over time, and the spread of an infectious disease. Sequential monogamy is compared with various levels of concurrency, holding all other features of the infection process constant. Effective summary measures of concurrency are developed that can be estimated on the basis of simple local network data. Concurrent partnerships exponentially increase the number of infected individuals and the growth rate of the epidemic during its initial phase. For example, when one-half of the partnerships in a population are concurrent, the size of the epidemic after 5 years is 10 times as large as under sequential monogamy. The primary cause of this amplification is the growth in the number of people connected in the network at any point in time: the size of the largest "component'. Concurrency increases the size of this component, and the result is that the infectious agent is no longer trapped in a monogamous partnership after transmission occurs, but can spread immediately beyond this partnership to infect others. The summary measure of concurrency developed here does a good job in predicting the size of the amplification effect, and may therefore be a useful and practical tool for evaluation and intervention at the beginning of an epidemic. Concurrent partnerships may be as important as multiple partners or cofactor infections in amplifying the spread of HIV. The public health implications are that data must be collected properly to measure the levels of concurrency in a population, and that messages promoting one partner at a time are as important as messages promoting fewer partners.
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              Genital Herpes Has Played a More Important Role than Any Other Sexually Transmitted Infection in Driving HIV Prevalence in Africa

              Background Extensive evidence from observational studies suggests a role for genital herpes in the HIV epidemic. A number of herpes vaccines are under development and several trials of the efficacy of HSV-2 treatment with acyclovir in reducing HIV acquisition, transmission, and disease progression have just reported their results or will report their results in the next year. The potential impact of these interventions requires a quantitative assessment of the magnitude of the synergy between HIV and HSV-2 at the population level. Methods and Findings A deterministic compartmental model of HIV and HSV-2 dynamics and interactions was constructed. The nature of the epidemiologic synergy was explored qualitatively and quantitatively and compared to other sexually transmitted infections (STIs). The results suggest a more substantial role for HSV-2 in fueling HIV spread in sub-Saharan Africa than other STIs. We estimate that in settings of high HSV-2 prevalence, such as Kisumu, Kenya, more than a quarter of incident HIV infections may have been attributed directly to HSV-2. HSV-2 has also contributed considerably to the onward transmission of HIV by increasing the pool of HIV positive persons in the population and may explain one-third of the differential HIV prevalence among the cities of the Four City study. Conversely, we estimate that HIV had only a small net impact on HSV-2 prevalence. Conclusions HSV-2 role as a biological cofactor in HIV acquisition and transmission may have contributed substantially to HIV particularly by facilitating HIV spread among the low-risk population with stable long-term sexual partnerships. This finding suggests that prevention of HSV-2 infection through a prophylactic vaccine may be an effective intervention both in nascent epidemics with high HIV incidence in the high risk groups, and in established epidemics where a large portion of HIV transmission occurs in stable partnerships.
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                Author and article information

                Journal
                Int J Health Geogr
                Int J Health Geogr
                International Journal of Health Geographics
                BioMed Central
                1476-072X
                2013
                22 May 2013
                : 12
                : 28
                Affiliations
                [1 ]Infectious Disease Epidemiology Group, Weill Cornell Medical College – Qatar, Qatar Foundation - Education City, P.O. Box 24144, Doha, Qatar
                [2 ]Department of Public Health, Weill Cornell Medical College, Cornell University, New York, NY, USA
                [3 ]Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA
                Article
                1476-072X-12-28
                10.1186/1476-072X-12-28
                3669110
                23692994
                f7ee11ae-6f34-482e-9a98-8eb98160b55c
                Copyright ©2013 Cuadros et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 2 March 2013
                : 15 May 2013
                Categories
                Research

                Public health
                hiv,spatial epidemiology,disease mapping,sub-saharan africa,mathematical modeling
                Public health
                hiv, spatial epidemiology, disease mapping, sub-saharan africa, mathematical modeling

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