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**Molecular Diagnosis and Monitoring of** 

*1Department of Parasitology and Entomology, Faculty of Public Health,* 

*4Ministry of Public Health, Department of Disease Control, Office of* 

*Faculty of Public Health, Mahidol University, Bangkok* 

*Disease Prevention and Control 11 Nakhon Si Thammarat* 

 *Mahidol University, Bangkok* 

*-tubulin* gene of human and

*Thailand* 

Adisak Bhumiratana1,2,3, Apiradee Intarapuk3, Danai Sangthong3, Surachart Koyadun4, Prapassorn Pechgit1 and Jinrapa Pothikasikorn5

*2Center for EcoHealth Disease Modeling and Intervention Development Research,* 

*3Environmental Pathogen Molecular Biology and Epidemiology Research Unit, Faculty of Veterinary Medicine, Mahanakorn University of Technology, Bangkok* 

*5Department of Microbiology, Faculty of Science, Mahidol University, Bangkok* 

Lymphatic filarial nematode parasites, mainly *Wuchereria bancrofti* and *Brugia malayi,* are causing agents of lymphatic filariasis in humans, which can be effectively treated with antifilarial drugs including diethylcarbamazine (DEC) and ivermectin. Albendazole, an effective benzimidazole compound, acts as a board-spectrum anthelminthic drug, and when combined with either one of antifilarial drugs, it exerts synergistic effects on reduction of peripheral microfilaremia in lymphatic filariasis cases. However, the varying parasite infection levels in those treated with DEC or ivermectin alone or in combination with albendazole are due to differences in drug responses. The additional clearance of infection with albendazole relative to what is observed with DEC or ivermectin alone suggests that

veterinary filariids that β-tubulin homologs have conserved domains structurally related to other orthologs among the nematodes, cestodes, trematodes and vertebrate hosts, is responsible for benzimidazole susceptibility. The genetic inheritance of resistance in nematode parasites can undergo under selection of benzimidazole compounds in a way that albendazole resistance mechanism involves one of two single amino acid substitutions from phenylalanine to tyrosine in parasite β-tubulin at position 167 or 200. This genetically-stable marker has shown promise for molecular diagnosis and monitoring of *W. bancrofti* infections that carry responsible genotypes associated with benzimidazole susceptibility or resistance. In particular, this approach can augment the surveillance and monitoring of mass treatment impacts on the parasite populations in target areas where long-running elimination programs for lymphatic filariasis are implemented at a large-scale by using a regionally-adopted combination therapy with

albendazole has different parasite target(s). The homologous

antifilarial drugs, recommended by the World Health Organization.

**1. Introduction** 

**Benzimidazole Susceptibility of Human Filariids** 

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