Wight, A. | bioRxiv Science

bioRxiv2025

Discoloration of the Cephalothorax in Pandalus borealis and its Correlation with Internal Cadmium Concentration

This study investigates the correlation between discoloration of the cephalothorax in Pandalus borealis (P. borealis) shrimp and cadmium concentration. The data, obtained through Atomic Absorption Spectroscopy (AAS), was converted into weight-based cadmium concentrations and analyzed using both parametric and non-parametric statistical tests. Despite assumptions of normal distribution not being met, a two-sample Students t-test and Mann-Whitney test were performed to examine the differences in cadmium concentrations between pink and discolored shrimp. Results indicated no statistically significant differences between the two groups. Experimental analysis revealed considerable overlap in cadmium concentration ranges for both groups, with high standard deviations. Factors such as the period of exposure to cadmium and potential influences from other contaminants or microorganisms were also considered. Previous studies have linked discoloration in shrimp to heavy metals and infections, but this study found no correlation between cadmium concentration and discoloration in P. borealis. The conclusion suggests that cadmium may not be a sole factor in shrimp discoloration, and other variables should be explored. Recommendations for future research include examining other trace metals, microbial infections, shrimp age, and extent of exposure to provide a comprehensive understanding of cephalothorax discoloration in shrimp.

pathology↗

bioRxiv2020

Defective influenza A virus RNA products mediate MAVS-dependent upregulation of human leukocyte antigen class I proteins

Influenza A virus (IAV) increases presentation of class I human leukocyte antigen (HLA) proteins that limit antiviral responses mediated by natural killer (NK) cells, but molecular mechanisms have not yet been fully elucidated. We observed that infection with A/Fort Monmouth/1/1947 (H1N1) IAV significantly increased presentation of HLA-B, -C and -E on lung epithelial cells. Virus entry was not sufficient to induce HLA upregulation, because UV-inactivated virus had no effect. We found that HLA upregulation was elicited by aberrant internally-deleted viral RNAs (vRNAs) known as mini viral RNAs (mvRNAs) and defective interfering RNAs (DI RNAs), which bind to retinoic acid-inducible gene-I (RIG-I) and initiate mitochondrial antiviral signaling (MAVS) protein-dependent antiviral interferon (IFN) responses. Indeed, MAVS was required for HLA upregulation in response to IAV infection or ectopic mvRNA/DI RNA expression. The effect was partially due to paracrine signalling, as we observed that IAV infection or mvRNA/DI RNA-expression stimulated production of IFN-{beta} and IFN-{lambda}1, and conditioned media from these cells elicited a modest increase in HLA surface levels in naive epithelial cells. HLA upregulation in response to aberrant viral RNAs could be prevented by chemical blockade of IFN receptor signal transduction. While HLA upregulation would seem to be advantageous to the virus, it is kept in check by the viral non-structural 1 (NS1) protein; we determined that NS1 limits cell-intrinsic and paracrine mechanisms of HLA upregulation. Taken together, our findings indicate that aberrant IAV RNAs stimulate HLA presentation, which may aid viral evasion of innate immunity. IMPORTANCEHuman leukocyte antigens (HLA) are cell surface proteins that regulate innate and adaptive immune responses to viral infection by engaging with receptors on immune cells. Many viruses have evolved ways to evade host immune responses by modulating HLA expression and/or processing. Here, we provide evidence that aberrant RNA products of influenza virus genome replication can trigger RIG-I/MAVS-dependent remodeling of the cell surface, increasing surface presentation of HLA proteins known to inhibit the activation of an immune cell known as a natural killer (NK) cell. While this HLA upregulation would seem to be advantageous to the virus, it is kept in check by the viral non-structural 1 (NS1) protein, which limits RIG-I activation and interferon production by the infected cell.

microbiology↗