Molecular surveillance of anti-malarial resistance pfcrt, pfmdr1, and pfk13 polymorphisms in African Plasmodium falciparum imported parasites to Wuhan, China.
Molecular surveillance of anti-malarial resistance pfcrt, pfmdr1, and pfk13 polymorphisms in African Plasmodium falciparum imported parasites to Wuhan, China.
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中国武汉输入的非洲恶性疟原虫中抗疟疾耐药性 pfcrt、pfmdr1 和 pfk13 多态性的分子监测
DOI：
10.1186/s12936-021-03737-8
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发表时间：
2021-05-01
期刊：
影响因子：
3
通讯作者：
Li J
中科院分区：
文献类型：
--
作者：
Cheng W;Song X;Tan H;Wu K;Li J
来自非洲的具有抗疟药耐药性（ADR）的输入性疟原虫在包括中国武汉在内的非疟疾流行地区是一项严峻的公共卫生挑战。评估输入性疟疾病例中非洲恶性疟原虫分离株的抗疟药耐药状况至关重要，因为这将为合理用药和疟疾控制提供有价值的信息。
2017 - 2019年期间，在中国武汉开展了一项横断面研究。采集了从非洲回国的农民工的3毫升外周血。对pfcrt、pfmdr1和k13螺旋桨（pfk13）基因的目标片段进行扩增、测序和分析。
总共采集了106个样本。随后，这些样本中分别有98.11%（104/106）、100%（106/106）和86.79%（92/106）的pfcrt（72 - 76）、pfmdr1和pfk13基因成功扩增和测序。pfcrt 76T、pfmdr1 86Y和pfmdr1 184F突变的发生率分别为9.62%、4.72%和47.17%。在密码子72 - 76处，pfcrt位点呈现三种单倍型，CVMNK（野生型）、CVIET（突变型）、CVM/IN/EK/T（混合型），其发生率分别为87.50%、9.62%和2.88%。对于pfmdr1基因，NY（野生型）、NF和YF（突变型）、NY/F、YY/F和N/YY/F（混合型）分别占单倍型的34.91%、43.40%、3.77%、15.09%、0.94%和1.89%。在pfcrt和pfmdr1组合单倍型中总共发现了83个具有六种独特单倍型的分离株，其中NY - CVMNK和NF - CVMNK分别占40.96%（34/83）和43.37%（36/83）。此外，在pfcrt的93、97、101和145位点有90个样本成功测序（84.91%，90/106），在343、353和356位点有78个样本成功测序（73.58%，78/106）。然而，仅在356位点观察到突变，发生率为6.41%。对于pfk13，未观察到在东南亚（在474、476、493、508、527、533、537、539、543、553、568、574、578和580位点）和非洲（在550、561、575、579和589位点）所报道的突变。
来自pfcrt和pfmdr1的现有数据表明，包括氯喹、阿莫地喹和甲氟喹在内的抗疟药物对非洲的疟疾治疗仍然有效。与哌喹耐药相关的pfcrt新突变仍处于相对较低水平。另一个令人担忧的问题是pfmdr1的N86和184F与蒿甲醚 - 本芴醇耐药相关的情况。尽管未检测到pfk13的突变，但必须继续进行分子监测。
网络版包含补充材料，可在10.1186/s12936 - 021 - 03737 - 8获取。
Background
Imported malaria parasites with anti-malarial drug resistance (ADR) from Africa is a serious public health challenge in non-malarial regions, including Wuhan, China. It is crucial to assess the ADR status in African Plasmodium falciparum isolates from imported malaria cases, as this will provide valuable information for rational medication and malaria control.
Methods
During 2017–2019, a cross-sectional study was carried out in Wuhan, China. Peripheral blood 3 ml of returned migrant workers from Africa was collected. The target fragments from pfcrt, pfmdr1, and k13 propeller (pfk13) genes were amplified, sequenced, and analysed.
Results
In total, 106 samples were collected. Subsequently, 98.11% (104/106), 100% (106/106), and 86.79% (92/106) of these samples were successfully amplified and sequenced for the pfcrt (72–76), pfmdr1, and pfk13 genes, respectively. The prevalence of the pfcrt 76 T, pfmdr1 86Y, and pfmdr1 184F mutations was 9.62, 4.72, and 47.17%, respectively. At codons 72–76, the pfcrt locus displayed three haplotypes, CVMNK (wild-type), CVIET (mutation type), CV M/I N/E K/T (mixed type), with 87.50%, 9.62%, and 2.88% prevalence, respectively. For the pfmdr1 gene, NY (wild type), NF and YF (mutant type), N Y/F, Y Y/F, and N/Y Y/F (mixed type) accounted for 34.91, 43.40, 3.77, 15.09, 0.94, and 1.89% of the haplotypes, respectively. A total of 83 isolates with six unique haplotypes were found in pfcrt and pfmdr1 combined haplotypes, of which NY-CVMNK and NF-CVMNK accounted for 40.96% (34/83) and 43.37% (36/83), respectively. Furthermore, 90 cases were successfully sequenced (84.91%, 90/106) at loci 93, 97, 101, and 145, and 78 cases were successfully sequenced (73.58%, 78/106) at loci 343, 353, and 356 for pfcrt. However, the mutation was observed only in locus 356 with 6.41%. For pfk13, mutations reported in Southeast Asia (at loci 474, 476, 493, 508, 527, 533, 537, 539, 543, 553, 568, 574, 578, and 580) and Africa (at loci 550, 561, 575, 579, and 589) were not observed.
Conclusions
The present data from pfcrt and pfmdr1 demonstrate that anti-malarial drugs including chloroquine, amodiaquine, and mefloquine, remain effective against malaria treatment in Africa. The new mutations in pfcrt related to piperaquine resistance remain at relatively low levels. Another source of concern is the artemether-lumefantrine resistance-related profiles of N86 and 184F of pfmdr1. Although no mutation in pfk13 is detected, molecular surveillance must continue.
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