bioRxiv Science⌕ Search

Biology subjects

Swift, N.

Publications and source records attributed to Swift, N..

2 recordsLinked to original sources

Reduction of Deformed Wing Virus-B levels in Colonies of the Honey bee Apis mellifera after Queen Vaccination with inactivated Paenibacillus larvae

Deformed wing virus (DWV) is a virulent and ubiquitous disease that affects honey bee colonies. DWV infects bees at all life stages, but is most noticeable in adult bees, where clinical symptoms include shriveled, non-functional wings, and a drastically shortened lifespan. DWV is recorded in upwards of 90% of honey bee colonies worldwide, and has been linked to colony loss in symptomatic hives. DWV is primarily spread by Varroa destructor mites, who feed on the fat bodies of honey bee adults and pupae. There is currently no direct treatment or preventative for DWV, with the primary method of reduction being vector control using acaracides. In this study, we tested the effect that vaccinating honey bee queens using killed Paenibacillus larvae bacterin, the causative agent of the honey bee disease American Foulbrood, had on deformed wing virus load in honey bee colonies. We placed vaccinated queens in 200 honey bee colonies, and unvaccinated queens in 200 colonies, and measured quantities of DWV-B in both groups immediately before, and 4 months after vaccination. We found that levels of DWV-B were identical before vaccination, but were significantly reduced in colonies 4 months post vaccination. This change was found despite no difference in mite quantities between groups. Overall, these data provide evidence that vaccination of queens with P. larvae bacterin is an effective method for reduction of DWV-B quantities in honey bee colonies in a commercially relevant field setting.

immunology↗

Infection-induced epilepsy is caused by increased expression of chondroitin sulfate proteoglycans in hippocampus and amygdala

Alterations in the extracellular matrix (ECM) are common in epilepsy, yet whether they are cause or consequence of disease is unknow. Using Theilers virus infection model of acquired epilepsy we find de novo expression of chondroitin sulfate proteoglycans (CSPGs), a major ECM component, in dentate gyrus (DG) and amygdala exclusively in mice with seizures. Preventing synthesis of CSPGs specifically in DG and amygdala by deletion of major CSPG aggrecan reduced seizure burden. Patch-clamp recordings from dentate granule cells (DGCs) revealed enhanced intrinsic and synaptic excitability in seizing mice that was normalized by aggrecan deletion. In situ experiments suggest that DGCs hyperexcitability results from negatively charged CSPGs increasing stationary cations (K+, Ca2+) on the membrane thereby depolarizing neurons, increasing their intrinsic and synaptic excitability. We show similar changes in CSPGs in pilocarpine-induced epilepsy suggesting enhanced CSPGs in the DG and amygdala may be a common ictogenic factor and novel therapeutic potential.

neuroscience↗