Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes
Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei para...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Christopher D Goodman [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016 |
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| Rechteinformationen: |
Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. |
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| Schlagwörter: |
Antimalarials - therapeutic use Plasmodium berghei - drug effects Plasmodium berghei - growth & development Genes, Mitochondrial - genetics |
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| Übergeordnetes Werk: |
Enthalten in: Science - Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883, 352(2016), 6283, Seite 349 |
|---|---|
| Übergeordnetes Werk: |
volume:352 ; year:2016 ; number:6283 ; pages:349 |
| Links: |
|---|
| DOI / URN: |
10.1126/science.aad9279 |
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| Katalog-ID: |
OLC1975103262 |
|---|
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| 520 | |a Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. | ||
| 540 | |a Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. | ||
| 650 | 4 | |a Parasites | |
| 650 | 4 | |a Malaria | |
| 650 | 4 | |a Mosquitoes | |
| 650 | 4 | |a Antiretroviral drugs | |
| 650 | 4 | |a Disease transmission | |
| 650 | 4 | |a Cytochromes b - genetics | |
| 650 | 4 | |a Antimalarials - therapeutic use | |
| 650 | 4 | |a Plasmodium berghei - drug effects | |
| 650 | 4 | |a Malaria - drug therapy | |
| 650 | 4 | |a Plasmodium berghei - genetics | |
| 650 | 4 | |a Atovaquone - pharmacology | |
| 650 | 4 | |a Malaria - parasitology | |
| 650 | 4 | |a Malaria - transmission | |
| 650 | 4 | |a Antimalarials - pharmacology | |
| 650 | 4 | |a Mitochondria - genetics | |
| 650 | 4 | |a Plasmodium berghei - growth & development | |
| 650 | 4 | |a Genes, Mitochondrial - genetics | |
| 650 | 4 | |a Anopheles - parasitology | |
| 650 | 4 | |a Atovaquone - therapeutic use | |
| 650 | 4 | |a Life Cycle Stages - drug effects | |
| 650 | 4 | |a Drug Resistance - genetics | |
| 650 | 4 | |a Life Cycle Stages - genetics | |
| 700 | 0 | |a Josephine E Siregar |4 oth | |
| 700 | 0 | |a Vanessa Mollard |4 oth | |
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| 700 | 0 | |a Hiroyuki Matsuoka |4 oth | |
| 700 | 0 | |a Motomichi Matsuzaki |4 oth | |
| 700 | 0 | |a Tomoko Toyama |4 oth | |
| 700 | 0 | |a Angelika Sturm |4 oth | |
| 700 | 0 | |a Anton Cozijnsen |4 oth | |
| 700 | 0 | |a Marcelo Jacobs-Lorena |4 oth | |
| 700 | 0 | |a Kiyoshi Kita |4 oth | |
| 700 | 0 | |a Sangkot Marzuki |4 oth | |
| 700 | 0 | |a Geoffrey I McFadden |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |t Science |d Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 |g 352(2016), 6283, Seite 349 |w (DE-627)12931482X |w (DE-600)128410-1 |w (DE-576)014533189 |x 0036-8075 |7 nnns |
| 773 | 1 | 8 | |g volume:352 |g year:2016 |g number:6283 |g pages:349 |
| 856 | 4 | 1 | |u http://dx.doi.org/10.1126/science.aad9279 |3 Volltext |
| 856 | 4 | 2 | |u http://www.ncbi.nlm.nih.gov/pubmed/27081071 |
| 856 | 4 | 2 | |u http://search.proquest.com/docview/1781203352 |
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10.1126/science.aad9279 doi PQ20160610 (DE-627)OLC1975103262 (DE-599)GBVOLC1975103262 (PRQ)p1046-49ab898d52426abc330d5cf20d9d960510b297bef4d8e90b81db3cbd7820c50e0 (KEY)0063888920160000352628300349parasitesresistanttotheantimalarialatovaquonefailt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Christopher D Goodman verfasserin aut Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics Josephine E Siregar oth Vanessa Mollard oth Joel Vega-Rodríguez oth Din Syafruddin oth Hiroyuki Matsuoka oth Motomichi Matsuzaki oth Tomoko Toyama oth Angelika Sturm oth Anton Cozijnsen oth Marcelo Jacobs-Lorena oth Kiyoshi Kita oth Sangkot Marzuki oth Geoffrey I McFadden oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6283, Seite 349 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6283 pages:349 http://dx.doi.org/10.1126/science.aad9279 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27081071 http://search.proquest.com/docview/1781203352 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6283 349 |
| spelling |
10.1126/science.aad9279 doi PQ20160610 (DE-627)OLC1975103262 (DE-599)GBVOLC1975103262 (PRQ)p1046-49ab898d52426abc330d5cf20d9d960510b297bef4d8e90b81db3cbd7820c50e0 (KEY)0063888920160000352628300349parasitesresistanttotheantimalarialatovaquonefailt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Christopher D Goodman verfasserin aut Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics Josephine E Siregar oth Vanessa Mollard oth Joel Vega-Rodríguez oth Din Syafruddin oth Hiroyuki Matsuoka oth Motomichi Matsuzaki oth Tomoko Toyama oth Angelika Sturm oth Anton Cozijnsen oth Marcelo Jacobs-Lorena oth Kiyoshi Kita oth Sangkot Marzuki oth Geoffrey I McFadden oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6283, Seite 349 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6283 pages:349 http://dx.doi.org/10.1126/science.aad9279 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27081071 http://search.proquest.com/docview/1781203352 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6283 349 |
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10.1126/science.aad9279 doi PQ20160610 (DE-627)OLC1975103262 (DE-599)GBVOLC1975103262 (PRQ)p1046-49ab898d52426abc330d5cf20d9d960510b297bef4d8e90b81db3cbd7820c50e0 (KEY)0063888920160000352628300349parasitesresistanttotheantimalarialatovaquonefailt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Christopher D Goodman verfasserin aut Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics Josephine E Siregar oth Vanessa Mollard oth Joel Vega-Rodríguez oth Din Syafruddin oth Hiroyuki Matsuoka oth Motomichi Matsuzaki oth Tomoko Toyama oth Angelika Sturm oth Anton Cozijnsen oth Marcelo Jacobs-Lorena oth Kiyoshi Kita oth Sangkot Marzuki oth Geoffrey I McFadden oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6283, Seite 349 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6283 pages:349 http://dx.doi.org/10.1126/science.aad9279 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27081071 http://search.proquest.com/docview/1781203352 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6283 349 |
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10.1126/science.aad9279 doi PQ20160610 (DE-627)OLC1975103262 (DE-599)GBVOLC1975103262 (PRQ)p1046-49ab898d52426abc330d5cf20d9d960510b297bef4d8e90b81db3cbd7820c50e0 (KEY)0063888920160000352628300349parasitesresistanttotheantimalarialatovaquonefailt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Christopher D Goodman verfasserin aut Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics Josephine E Siregar oth Vanessa Mollard oth Joel Vega-Rodríguez oth Din Syafruddin oth Hiroyuki Matsuoka oth Motomichi Matsuzaki oth Tomoko Toyama oth Angelika Sturm oth Anton Cozijnsen oth Marcelo Jacobs-Lorena oth Kiyoshi Kita oth Sangkot Marzuki oth Geoffrey I McFadden oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6283, Seite 349 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6283 pages:349 http://dx.doi.org/10.1126/science.aad9279 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27081071 http://search.proquest.com/docview/1781203352 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6283 349 |
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10.1126/science.aad9279 doi PQ20160610 (DE-627)OLC1975103262 (DE-599)GBVOLC1975103262 (PRQ)p1046-49ab898d52426abc330d5cf20d9d960510b297bef4d8e90b81db3cbd7820c50e0 (KEY)0063888920160000352628300349parasitesresistanttotheantimalarialatovaquonefailt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Christopher D Goodman verfasserin aut Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics Josephine E Siregar oth Vanessa Mollard oth Joel Vega-Rodríguez oth Din Syafruddin oth Hiroyuki Matsuoka oth Motomichi Matsuzaki oth Tomoko Toyama oth Angelika Sturm oth Anton Cozijnsen oth Marcelo Jacobs-Lorena oth Kiyoshi Kita oth Sangkot Marzuki oth Geoffrey I McFadden oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6283, Seite 349 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6283 pages:349 http://dx.doi.org/10.1126/science.aad9279 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27081071 http://search.proquest.com/docview/1781203352 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6283 349 |
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Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics |
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Christopher D Goodman @@aut@@ Josephine E Siregar @@oth@@ Vanessa Mollard @@oth@@ Joel Vega-Rodríguez @@oth@@ Din Syafruddin @@oth@@ Hiroyuki Matsuoka @@oth@@ Motomichi Matsuzaki @@oth@@ Tomoko Toyama @@oth@@ Angelika Sturm @@oth@@ Anton Cozijnsen @@oth@@ Marcelo Jacobs-Lorena @@oth@@ Kiyoshi Kita @@oth@@ Sangkot Marzuki @@oth@@ Geoffrey I McFadden @@oth@@ |
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500 DNB LING fid Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes Parasites Malaria Mosquitoes Antiretroviral drugs Disease transmission Cytochromes b - genetics Antimalarials - therapeutic use Plasmodium berghei - drug effects Malaria - drug therapy Plasmodium berghei - genetics Atovaquone - pharmacology Malaria - parasitology Malaria - transmission Antimalarials - pharmacology Mitochondria - genetics Plasmodium berghei - growth & development Genes, Mitochondrial - genetics Anopheles - parasitology Atovaquone - therapeutic use Life Cycle Stages - drug effects Drug Resistance - genetics Life Cycle Stages - genetics |
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Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes |
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Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes |
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parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes |
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Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes |
| abstract |
Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. |
| abstractGer |
Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. |
| abstract_unstemmed |
Resistance to the antimalarial drug atovaquone might prove to be this parasite's weak spot. Resistance develops rapidly via mutations in the drug's target: the parasite's mitochondrial cytochrome b complex. Goodman et al. have discovered that although resistant Plasmodium berghei parasites persist in mice, in blood-sucking malarial mosquitoes, the mutations disable female parasites too much for them to reproduce. The human-specific Plasmodium falciparum can only be investigated experimentally in mosquitoes, but a similar effect was seen. Thus, atovaquone-resistant parasites cannot be transmitted to another mammal or person. Science, this issue p. 349 Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control. |
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Parasites resistant to the antimalarial atovaquone fail to transmit by mosquitoes |
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Josephine E Siregar Vanessa Mollard Joel Vega-Rodríguez Din Syafruddin Hiroyuki Matsuoka Motomichi Matsuzaki Tomoko Toyama Angelika Sturm Anton Cozijnsen Marcelo Jacobs-Lorena Kiyoshi Kita Sangkot Marzuki Geoffrey I McFadden |
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