Biology subjects

Sams, K. L.

Publications and source records attributed to Sams, K. L..

3 recordsLinked to original sources

bioRxiv2025

Identification of within-host deletions in domain 0 of the spike gene of highly pathogenic feline coronavirus type 2 from the United States

Feline coronavirus (FCoV) is known to gain pathogenicity within-host to cause the lethal disease feline infectious peritonitis (FIP). Most FIP cases are caused by viruses in genotype 1 (FCoV-1) via an internal mutation in the spike gene. However, genotype 2 (FCoV-2) has risen to prominence based on the emergence of FCoV-23, a highly pathogenic novel variant from Cyprus that has a deletion in the N-terminus (domain 0) of spike. Here, we conducted a retrospective molecular study of FCoV-2 detected in three cats in the U.S. during 2013 and 2016. Whole-genome sequencing revealed that the two cats exhibiting long-term signs each had an FCoV-2 with a distinct deletion in domain 0 of spike in all examined tissues. The epidemiologically-linked cat displaying signs for a short duration had an FCoV-2 with an intact spike. Our results suggest that this "internal deletion" in the spike gene is a biomarker of highly pathogenic FCoV-2. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/664542v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@1d10d9eorg.highwire.dtl.DTLVardef@1d53c7forg.highwire.dtl.DTLVardef@76ef35org.highwire.dtl.DTLVardef@528d1f_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2025

TITAN-RNA: A hybrid-capture sequencing panel detects known and unknown Flaviviridae for diagnostics and vector surveillance

The authors have withdrawn this manuscript because this preprint was merged with the preprint BIORXIV/2025/658355. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author. The correct preprint can be found at https://doi.org/10.1101/2025.06.06.658355

microbiology↗

bioRxiv2022

Disrupted development and altered hormone signaling in male Padi2/Padi4 double knockout mice

BackgroundPeptidylarginine deiminase enzymes (PADs) convert arginine residues to citrulline in a process called citrullination or deimination. Recently, two PADs, PAD2 and PAD4, have been linked to hormone signaling in vitro and the goal of this study was to test for links between PAD2/PAD4 and hormone signaling in vivo. MethodsPreliminary analysis of Padi2 and Padi4 single knockout (SKO) mice did not find any overt reproductive defects and we predicted that this was likely due to genetic compensation. To test this hypothesis, we created a Padi2/Padi4 double knockout (DKO) mouse model and tested these mice along with wild-type FVB/NJ (WT) and both strains of SKO mice for a range of reproductive defects. ResultsControlled breeding trials found that male DKO mice appeared to take longer to have their first litter than WT controls. This tendency was maintained when these mice were mated to either DKO and WT females. Additionally, unsexed 2-day old DKO pups and male DKO weanlings both weighed significantly less than their WT counterparts, took significantly longer than WT males to reach puberty, and had consistently lower serum testosterone levels. Furthermore, 90-day old adult DKO males had smaller testes than WT males with increased rates of germ cell apoptosis. ConclusionsThe Padi2/Padi4 DKO mouse model provides a new tool for investigating PAD function and outcomes from our studies provide the first in vivo evidence linking PADs with hormone signaling.

molecular biology↗