Furthermore, the magnitude of CD14 expression in the mature macrophages is greater than that in the less mature macrophages ABT-263 in vitro [34]. It is of interest that CD14 expression was found to be more abundant in the PMs from cirrhotic patients compared to those of controls, and this difference in the magnitude of CD14 expression could contribute to the RB result. Consistent with other studies, our study has further confirmed the downregulatory effect of IFN-γ on CD14 expression [22] and [23]. CD14 binds LPS, and as a result, the release

of pro-inflammatory cytokines, including TNF-α, is mediated. Because TNF-α is involved in the pathogenesis of shock syndrome [23], the downregulatory effect of IFN-γ on CD14 expression may potentially have a protective effect on the host in complex situations such as shock syndrome. We have shown for the first time that the host defence of PMs from cirrhotic patients with ascites is altered. The predominance of activated CD14 expressing cells has generated a vigorous RB, which in turn had a downregulatory effect on endocytic receptors. This mechanism mTOR activation could account for the reduced phagocytosis reported. Such an alteration in host defence may in part play a role in the increased susceptibility of these patients to SBP. We are grateful to Anne Etches from Haematology Department at King’s College Hospital, London, UK, for her help with

macrophage characterisation studies. We are also grateful to Schering-Plough (UK) Ltd., MycoClean Mycoplasma Removal Kit Welwyn Garden City, Herts, UK, for providing the GM-CSF and to Boehringer Ingelheim (UK) Ltd., Bracknell, UK, for providing the interferon-gamma. “
“Betanodavirus is neuropathogenic and inflicts conspicuous damage that is characterized

by vacuolation and degeneration of neurons throughout the central nervous system [1] and [2]. Piscine nodavirus, a member of the Betanodavirdae family, is the causative agent of viral nervous necrosis or fish encephalitis that produces high mortalities in hatchery-reared larvae and juveniles of marine fishes in Taiwan, Japan, Australia, and Europe [3]. This virus is unenveloped, possesses a 25–30 nm diameter icosahedral capsid, and contains a genome composed of bipartite, single-stranded, and positive-sense RNA molecules [4]. Considerable progress in the understanding of the betanodavirdae pathogenesis has been made. The activation of the host immune response and direct invasion of cells are believed to contribute to this pathogenesis [5] and [6], which includes induction of inflammatory cells and the host’s immune response. For example, ubiquitin conjugating enzyme 7 interacting protein, which functions in apoptosis, and interferon induced with helicase C domain protein1, which contributes to apoptosis and mediates type I interferon production, are differentially expressed in infected and control cells [7]. However, the mechanisms underlying betanodavirdae pathogenesis are still not completely clear.