Disease Information
General Information of the Disease (ID: DIS00173)
Name |
Plasmodium vivax malaria
|
---|---|
ICD |
ICD-11: 1F41
|
Resistance Map |
Type(s) of Resistant Mechanism of This Disease
ADTT: Aberration of the Drug's Therapeutic Target
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
Pyrimethamine/Sulfadoxine
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Bifunctional dihydrofolate reductase-thymidylate synthase (PVDHFR) | [1] | |||
Resistant Disease | Plasmodium vivax malaria [ICD-11: 1F41.0] | |||
Molecule Alteration | SNP | . |
||
Resistant Drug | Pyrimethamine/Sulfadoxine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Red blood cells | Blood | Homo sapiens (Human) | N.A. |
Experiment for Molecule Alteration |
Whole genome sequencing assay | |||
Experiment for Drug Resistance |
Giemsa stain assay | |||
Mechanism Description | The lack of copy number variation of pvgch1 suggests that SP-resistant P. vivax may harbor alternative mechanisms to secure sufficient folate.The quadruple mutant haplotypes 57I/L/58R/61M/117T of pvdhfr gene were the most common (comprising 76% of cases in Myitsone and 43.7% of case in Laiza). The double mutant haplotype 383G/553G of pvdhps gene was also prevalent at each site. | |||
Key Molecule: Hydroxymethylpterin pyrophosphokinase-dihydropteroate synthetase (DHPS) | [1] | |||
Resistant Disease | Plasmodium vivax malaria [ICD-11: 1F41.0] | |||
Molecule Alteration | SNP | . |
||
Resistant Drug | Pyrimethamine/Sulfadoxine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Red blood cells | Blood | Homo sapiens (Human) | N.A. |
Experiment for Molecule Alteration |
Whole genome sequencing assay | |||
Experiment for Drug Resistance |
Giemsa stain assay | |||
Mechanism Description | The lack of copy number variation of pvgch1 suggests that SP-resistant P. vivax may harbor alternative mechanisms to secure sufficient folate.The quadruple mutant haplotypes 57I/L/58R/61M/117T of pvdhfr gene were the most common (comprising 76% of cases in Myitsone and 43.7% of case in Laiza). The double mutant haplotype 383G/553G of pvdhps gene was also prevalent at each site. |
References
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