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Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa
BACKGROUND: 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 been estimated to have a very low probability; but effects of cofactors that vary in spac...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175213/ https://www.ncbi.nlm.nih.gov/pubmed/21834977 http://dx.doi.org/10.1186/1471-2334-11-216 |
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author | Cuadros, Diego F Crowley, Philip H Augustine, Ben Stewart, Sarah L García-Ramos, Gisela |
author_facet | Cuadros, Diego F Crowley, Philip H Augustine, Ben Stewart, Sarah L García-Ramos, Gisela |
author_sort | Cuadros, Diego F |
collection | PubMed |
description | BACKGROUND: 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 been estimated to have a very low probability; but effects of cofactors that vary in space and time may substantially alter this pattern. METHODS: To test the effect of individual variation in the HIV infectiousness generated by co-infection, we developed and analyzed a mathematical sexual network model that simulates the behavioral components of a population from Malawi, as well as the dynamics of HIV and the co-infection effect caused by other infectious diseases, including herpes simplex virus type-2, gonorrhea, syphilis and malaria. RESULTS: The analysis shows that without the amplification effect caused by co-infection, no epidemic is generated, and HIV prevalence decreases to extinction. But the model indicates that an epidemic can be generated by the amplification effect on HIV transmission caused by co-infection. CONCLUSION: The simulated sexual network demonstrated that a single value for HIV infectivity fails to describe the dynamics of the epidemic. Regardless of 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. Moreover, our work raises the possibility that the natural history of HIV in sub-Saharan Africa cannot be fully understood if individual variation in infectiousness is neglected. |
format | Online Article Text |
id | pubmed-3175213 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31752132011-09-18 Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa Cuadros, Diego F Crowley, Philip H Augustine, Ben Stewart, Sarah L García-Ramos, Gisela BMC Infect Dis Research Article BACKGROUND: 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 been estimated to have a very low probability; but effects of cofactors that vary in space and time may substantially alter this pattern. METHODS: To test the effect of individual variation in the HIV infectiousness generated by co-infection, we developed and analyzed a mathematical sexual network model that simulates the behavioral components of a population from Malawi, as well as the dynamics of HIV and the co-infection effect caused by other infectious diseases, including herpes simplex virus type-2, gonorrhea, syphilis and malaria. RESULTS: The analysis shows that without the amplification effect caused by co-infection, no epidemic is generated, and HIV prevalence decreases to extinction. But the model indicates that an epidemic can be generated by the amplification effect on HIV transmission caused by co-infection. CONCLUSION: The simulated sexual network demonstrated that a single value for HIV infectivity fails to describe the dynamics of the epidemic. Regardless of 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. Moreover, our work raises the possibility that the natural history of HIV in sub-Saharan Africa cannot be fully understood if individual variation in infectiousness is neglected. BioMed Central 2011-08-11 /pmc/articles/PMC3175213/ /pubmed/21834977 http://dx.doi.org/10.1186/1471-2334-11-216 Text en Copyright ©2011 Cuadros et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 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. |
spellingShingle | Research Article Cuadros, Diego F Crowley, Philip H Augustine, Ben Stewart, Sarah L García-Ramos, Gisela Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title | Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title_full | Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title_fullStr | Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title_full_unstemmed | Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title_short | Effect of variable transmission rate on the dynamics of HIV in sub-Saharan Africa |
title_sort | effect of variable transmission rate on the dynamics of hiv in sub-saharan africa |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175213/ https://www.ncbi.nlm.nih.gov/pubmed/21834977 http://dx.doi.org/10.1186/1471-2334-11-216 |
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