Dynamics of immune response and drug resistance in malaria infection
Abstract Background Malaria parasites that concurrently infect a host compete on the basis of their intrinsic growth rates and by stimulating cross-reactive immune responses that inhibit each others' growth. If the phenotypes also show different drug sensitivities ('sensitive' vs. ...
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ftdoajarticles:oai:doaj.org/article:16b2507549b14333a4a4aa717982c84f 2023-05-15T15:08:44+02:00 Dynamics of immune response and drug resistance in malaria infection Gurarie David McKenzie F Ellis 2006-10-01T00:00:00Z https://doi.org/10.1186/1475-2875-5-86 https://doaj.org/article/16b2507549b14333a4a4aa717982c84f EN eng BMC http://www.malariajournal.com/content/5/1/86 https://doaj.org/toc/1475-2875 doi:10.1186/1475-2875-5-86 1475-2875 https://doaj.org/article/16b2507549b14333a4a4aa717982c84f Malaria Journal, Vol 5, Iss 1, p 86 (2006) Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 article 2006 ftdoajarticles https://doi.org/10.1186/1475-2875-5-86 2022-12-31T07:23:48Z Abstract Background Malaria parasites that concurrently infect a host compete on the basis of their intrinsic growth rates and by stimulating cross-reactive immune responses that inhibit each others' growth. If the phenotypes also show different drug sensitivities ('sensitive' vs. 'resistant' strains), drug treatment can change their joint dynamics and the long-term outcome of the infection: most obviously, persistent drug pressure can permit the more resistant, but otherwise competitively-inferior, strains to dominate. Methods Here a mathematical model is developed to analyse how these and more subtle effects of antimalarial drug use are modulated by immune response, repeated re-inoculation of parasites, drug pharmacokinetic parameters, dose and treatment frequency. Results The model quantifies possible effects of single and multiple (periodic) treatment on the outcome of parasite competition. In the absence of further inoculation, the dosage and/or treatment frequency required for complete clearance can be estimated. With persistent superinfection, time-average parasite densities can be derived in terms of the basic immune-regulating parameters, the drug efficacy and treatment regimen. Conclusion The functional relations in the model are applicable to a wide range of conditions and transmission environments, allowing predictions to be made on both the individual and the community levels, and, in particular, transitions from drug-sensitive to drug-resistant parasite dominance to be projected on both levels. Article in Journal/Newspaper Arctic Directory of Open Access Journals: DOAJ Articles Arctic Malaria Journal 5 1 |
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Directory of Open Access Journals: DOAJ Articles |
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ftdoajarticles |
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English |
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Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 |
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Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 Gurarie David McKenzie F Ellis Dynamics of immune response and drug resistance in malaria infection |
topic_facet |
Arctic medicine. Tropical medicine RC955-962 Infectious and parasitic diseases RC109-216 |
description |
Abstract Background Malaria parasites that concurrently infect a host compete on the basis of their intrinsic growth rates and by stimulating cross-reactive immune responses that inhibit each others' growth. If the phenotypes also show different drug sensitivities ('sensitive' vs. 'resistant' strains), drug treatment can change their joint dynamics and the long-term outcome of the infection: most obviously, persistent drug pressure can permit the more resistant, but otherwise competitively-inferior, strains to dominate. Methods Here a mathematical model is developed to analyse how these and more subtle effects of antimalarial drug use are modulated by immune response, repeated re-inoculation of parasites, drug pharmacokinetic parameters, dose and treatment frequency. Results The model quantifies possible effects of single and multiple (periodic) treatment on the outcome of parasite competition. In the absence of further inoculation, the dosage and/or treatment frequency required for complete clearance can be estimated. With persistent superinfection, time-average parasite densities can be derived in terms of the basic immune-regulating parameters, the drug efficacy and treatment regimen. Conclusion The functional relations in the model are applicable to a wide range of conditions and transmission environments, allowing predictions to be made on both the individual and the community levels, and, in particular, transitions from drug-sensitive to drug-resistant parasite dominance to be projected on both levels. |
format |
Article in Journal/Newspaper |
author |
Gurarie David McKenzie F Ellis |
author_facet |
Gurarie David McKenzie F Ellis |
author_sort |
Gurarie David |
title |
Dynamics of immune response and drug resistance in malaria infection |
title_short |
Dynamics of immune response and drug resistance in malaria infection |
title_full |
Dynamics of immune response and drug resistance in malaria infection |
title_fullStr |
Dynamics of immune response and drug resistance in malaria infection |
title_full_unstemmed |
Dynamics of immune response and drug resistance in malaria infection |
title_sort |
dynamics of immune response and drug resistance in malaria infection |
publisher |
BMC |
publishDate |
2006 |
url |
https://doi.org/10.1186/1475-2875-5-86 https://doaj.org/article/16b2507549b14333a4a4aa717982c84f |
geographic |
Arctic |
geographic_facet |
Arctic |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
Malaria Journal, Vol 5, Iss 1, p 86 (2006) |
op_relation |
http://www.malariajournal.com/content/5/1/86 https://doaj.org/toc/1475-2875 doi:10.1186/1475-2875-5-86 1475-2875 https://doaj.org/article/16b2507549b14333a4a4aa717982c84f |
op_doi |
https://doi.org/10.1186/1475-2875-5-86 |
container_title |
Malaria Journal |
container_volume |
5 |
container_issue |
1 |
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1766340039570096128 |