Quantitative trait loci mapping for survival of virus infection and virus levels in honey bees

Authors: LU, ROBERT - University Of Alberta; BHATIA, SHILPI - North Carolina Agricultural And Technical State University; Simone-Finstrom, Michael; RUEPPELL, OLAV - University Of Alberta

Submitted to: Infection, Genetics and Evolution
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/25/2023
Publication Date: 11/28/2023
Citation: Lu, R.X., Bhatia, S., Simone-Finstrom, M., Rueppell, O. 2023. Quantitative trait loci mapping for survival of virus infection and virus levels in honey bees. Infection, Genetics and Evolution. 116. https://doi.org/10.1016/j.meegid.2023.105534
DOI: https://doi.org/10.1016/j.meegid.2023.105534

Interpretive Summary: Honey bees are commonly infected with viral pathogens that cause symptoms ranging from wing deformities to paralysis to death. Viral infections can also lead to colony death. However, it is known that some colonies and stocks have differential susceptibility to viral infections, though the genetic basis for this has yet to be determined. We setup and analyzed genetic differences to identify genes associated with susceptibility to Israeli acute paralysis virus (IAPV). Individual bees were treated with IAPV, those that died within 48h were deemed susceptible; those that received a second dose of IAPV and survived another 72h were determined to be non-susceptible. We identified several candidate genes that may be responsible for susceptibility to viral infection. Furthermore, our study shows that tolerance (i.e. the ability to withstand high level of infection) and resistance (i.e. ability to reduce or prevent infection) both affect honey bee virus susceptibility. Additional research needs to confirm the relationship of these genes to susceptibility to viral infection broadly and can be used within breeding programs focused on developing virus resistant stock.

Technical Abstract: Israeli acute paralysis virus (IAPV) is a highly virulent, Varroa-vectored virus that has been associated with global concern for honey bee health. Although our understanding of honey bee viruses and their interaction with the honey bees hosts is steadily increasing, little is known about the genetic basis of honey bees to withstand infection with IAPV or other viruses. We set up and analyzed a backcross between preselected honey bee colonies of low and high IAPV susceptibility to identify quantitative trait loci (QTL) associated with IAPV susceptibility. Experimentally inoculated adult worker bees were surveyed for survival and selectively sampled for QTL analysis based on SNPs identified by whole-genome resequencing and composite interval mapping. Additionally, natural titers of other viruses were quantified in these workers via qPCR and also used for QTL mapping. In addition to the full dataset, we analyzed the distinct subpopulations of susceptible and non-susceptible workers separately. These subpopulations are distinguished by a single, suggestive QTL on chromosome 6 but we identified numerous other QTL that influence the titer of IAPV after inoculation and of other naturally occurring viruses. Some of the QTL were of considerable strength despite the haphazard nature of natural virus titers. Some functional candidate genes are located in the QTL intervals, but the presence of many genes of unknown function and the complex nature of virus titers make any identification of candidate genes speculative. Our results reveal a complex genetic architecture of virus - honey bee interactions with some overlap among virus indicating a mixture of shared and specific genetic factors. Furthermore, our study shows that tolerance and resistance both affect honey bee virus susceptibility. The pronounced QTL differences between the susceptible and non-susceptible subpopulations indicate either an interaction between IAPV infection and the bees’ interaction with other viruses or heterogeneity among workers of a single age and colony that manifests itself as IAPV susceptibility and results in distinct groups that differ in their interaction with other viruses.