Genetic resistance to vector-borne hemoprotozoa in livestock: molecular markers, host-parasite interactions, and implications for breeding and control.
PMID 40936275 | PMCID PMC12511894 | DOI 10.4142/jvs.25125 · Journal of veterinary science · 2025
IMPORTANCE: Vector-borne hemoparasitic diseases, such as Theileria, Babesia, Trypanosoma, Leishmania, and Anaplasma, pose significant constraints to livestock production, particularly in Africa and other tropical regions. These infections cause considerable economic losses from mortality, decreased productivity, and the high costs of treatment and control efforts. OBSERVATIONS: Resistance to hemoparasitic infections in livestock is strongly influenced by the genetic factors of the host. The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes. On the parasite side, the genes responsible for immune evasion (VSG and AP2), drug resistance (MDR1 and CYTB), and host cell invasion (AMA1 and HSP90) play pivotal roles in infection persistence and treatment failure. The advances in genomic and transcriptomic tools, including genome-wide association studies, CRISPR, and multi-omics profiling, have enhanced the understanding of these host-parasite interactions and enabled identification of the molecular markers for resistance traits. CONCLUSIONS AND RELEVANCE: Advanced genetic resistance offers a sustainable, long-term solution to managing vector-borne parasitic infections in livestock. The integration of resistance-associated markers into selective breeding programs, coupled with genome editing and real-time surveillance, can improve livestock resilience. Aligning these efforts with One Health strategies and collaborative genomic initiatives will be essential for achieving effective, regionally adapted disease control.
Validated evidence
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | TLR4 | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |
| gene | SOD2 | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |
| gene | GPX1 | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |
| gene | ABCB1 | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |
| gene | CYP3A4 | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |
| gene | MC1R | “The key host genes involved in immune responses (e.g., BoLA-DRB3 and TLR4), oxidative stress defense (SOD2 and GPX1), drug metabolism (ABCB1 and CYP3A4), and ectoparasite resistance (MC1R and MHC) have been identified as contributors to resistance phenotypes.” | 0.98 | hgnc_dict_v1 |