Abstract

BackgroundHost resilience (HR) to parasites can affect the performance of animals. Therefore, the aim of this study was to present a detailed investigation of the genetic mechanisms of HR to ticks (TICK), gastrointestinal nematodes (GIN), and Eimeria spp. (EIM) in Nellore cattle that were raised under natural infestation and a prophylactic parasite control strategy. In our study, HR was defined as the slope coefficient of body weight (BW) when TICK, GIN, and EIM burdens were used as environmental gradients in random regression models. In total, 1712 animals were evaluated at five measurement events (ME) at an average age of 331, 385, 443, 498, and 555 days, which generated 7307 body weight (BW) records. Of the 1712 animals, 1075 genotyped animals were used in genome-wide association studies to identify genomic regions associated with HR.ResultsPosterior means of the heritability estimates for BW ranged from 0.09 to 0.54 across parasites and ME. The single nucleotide polymorphism (SNP)-derived heritability for BW at each ME ranged from a low (0.09 at ME.331) to a moderate value (0.23 at ME.555). Those estimates show that genetic progress can be achieved for BW through selection. Both genetic and genomic associations between BW and HR to TICK, GIN, and EIM confirmed that parasite infestation impacted the performance of animals. Selection for BW under an environment with a controlled parasite burden is an alternative to improve both, BW and HR. There was no impact of age of measurement on the estimates of genetic variance for HR. Five quantitative trait loci (QTL) were associated with HR to EIM but none with HR to TICK and to GIN. These QTL contain genes that were previously shown to be associated with the production of antibody modulators and chemokines that are released in the intestinal epithelium.ConclusionsSelection for BW under natural infestation and controlled parasite burden, via prophylactic parasite control, contributes to the identification of animals that are resilient to nematodes and Eimeria ssp. Although we verified that sufficient genetic variation existed for HR, we did not find any genes associated with mechanisms that could justify the expression of HR to TICK and GIN.

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