Induction of rainbow trout MH class I and accessory proteins by viral haemorrhagic septicaemia virus

Abstract

Major histocompatibility (MH) class I receptors are glycoproteins which play a critical role during responses to intracellular pathogens by presenting endogenous peptides to cytotoxic T cell lymphocytes (CD8+). To date, little is known about MH class I regulation at the protein level during viral infections in fish. In this study, we characterised the MH class I pathway response to polyinosinic–polycytidylic acid (poly I:C) and upon infection with viral haemorrhagic septicemia virus (VHSV) genotype IVa using the rainbow trout monocyte/macrophage cell line RTS11. A 14-day challenge with VHSV IVa at 14°C demonstrated enhanced expression of the class I heavy chain, β2 microglobulin (β2M) and tapasin, while the expression of other accessory molecules ERp57 and calreticulin remained unchanged. However, when infection occurred at 2°C no change in expression levels of any of these molecules was observed. β2M accumulated in the media of RTS11 over time, however the β2M concentrations were 2 fold higher in cultures infected with VHSV 14 days post infection. Strikingly, when cells were maintained at 2°C the secretion of β2M was significantly reduced in both infected and non-infected cultures. These results indicate that VHSV infection alters the kinetics of β2M release as well as the expression of MH class I and suggests that cellular immunity against VHSV can be compromised at low temperatures which may increase host susceptibility to this virus during the winter.