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The order Herpesvirales encompasses viruses that share structural, genetic, and biological properties. However, members of this order infect hosts ranging from molluscs to humans. It is currently divided into three phylogenetically related families. The Alloherpesviridae family contains viruses infecting fish and amphibians. There are 12 alloherpesviruses described to date, 10 of which infect fish. Over the last decade, cyprinid herpesvirus 3 (CyHV-3) infecting common and koi carp has emerged as the archetype of fish alloherpesviruses. Since its first description in the late 1990s, this virus has induced important economic losses in common and koi carp worldwide. It has also had negative environmental implications by affecting wild carp populations. These negative impacts and the importance of the host species have stimulated studies aimed at developing diagnostic and prophylactic tools. Unexpectedly, the data generated by these applied studies have stimulated interest in CyHV-3 as a model for fundamental research. This review intends to provide a complete overview of the knowledge currently available on CyHV-3., (© 2015 Elsevier Inc. All rights reserved.)

This paper utilises histological, ultrastructure and molecular phylogenetic data to describe a novel genus and species (Areospora rohanae n.gen., n.sp.) within the phylum Microsporidia. Phylogenetic and morphological distinction from other known lineages within the phylum also provide strong support for erection of a new family (Areosporiidae n. fam) to contain the parasite. Recognised via lesions observed by workers in king crab processing facilities in southern Chile, the parasite elicits giant cell formation in infected crabs. Merogony within haemocytes and fixed phagocytes proceeds apparent fusion of infected cells to produce multinucleate syncitia in which further development of the parasite occurs. Subsequent recruitment of adjacent cells within the haemal spaces of the hepatopancreas, the podocytes of the gill, and particularly in the subcuticular connective tissues, characterises the pathogenesis of A. rohanae. In late stages of infection, significant remodelling of the subcuticular tissues corresponds to the clinical lesions observed within processing plants. Sporogony of A. rohanae also occurs within the syncitial cytoplasm and culminates in production of bizarre spores, ornamented with distinctive tubular bristles. Spores occur in sets of 8 within a sporophorous vesicle. The description of A. rohanae offers considerable insight into the pathogenesis of giant-cell forming Microsporidia, signifies a new lineage of giant-cell forming Microsporidia in marine hosts, and may reflect emergence of a commercially-significant pathogen in the southern ocean Lithodes santolla fishery., (Crown Copyright © 2014. Published by Elsevier Inc. All rights reserved.)

We describe a microsporidian parasite infecting non-native Chinese mitten crabs (Eriochier sinensis) from Europe. Electron microscopy revealed merogonic and sporogonic life stages bound within a plasmalemma. The crab parasite develops polar tube precursors at the sporont stage but does not complete formation of the intact spore extrusion apparatus at the stage of the sporogonial plasmodium like Enterocytozoon bienuesi and other representatives of the Enterocytozoonidae. Its presence within an aquatic crustacean host, and a distinct molecular phylogeny based on partial small subunit ribosomal RNA (SSU rRNA) gene sequences also place it relatively close, though distinct to, existing genera within the Enterocytozoonidae. Consideration of morphological and phylogenetic characteristics of other hepatopancreas-infecting microsporidia from crustaceans suggests that certain ones (e.g. Enterospora canceri) are retained within the clade corresponding to the existing family Enterocytozoonidae, while others, including the parasite described here, may eventually be grouped in a sister taxon potentially of family rank. Based upon morphological and host similarity, it is likely that the parasite described here is the same as Endoreticulatus eriocheir (Wang and Chen, 2007), previously described from Chinese mitten crabs in Asia. However, using a combined taxonomic approach based upon morphological and phylogenetic data, we propose the formation of a new genus (Hepatospora) to replace the previous generic classification of the Asian parasite as Endoreticulatus. The microsporidian from the hepatopancreas of E. sinensis is named Hepatospora eriocheir (Wang and Chen, 2007) gen. et comb. nov. It is assumed that the parasite was introduced during initial invasions of this crab to Europe during the early 20th Century., (Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.)

Bovine leukemia virus (BLV) infection causes a significant polyclonal expansion of CD5(+), IgM+ B lymphocytes known as persistent lymphocytosis (PL) in approximately 30% of infected cattle. There is evidence that this expanded B cell population has altered signaling, and resistance to apoptosis has been proposed as one mechanism of B cell expansion. In human and murine B cells, antigen binding initiates movement of the B cell receptor (BCR) into membrane microdomains enriched in sphingolipids and cholesterol, termed lipid rafts. Lipid rafts include members of the Src-family kinases and exclude certain phosphatases. Inclusion of the BCR into lipid rafts plays an important role in regulation of early signaling events and subsequent antigen internalization. Viral proteins may also influence signaling events in lipid rafts. Here we demonstrate that the largely CD5(+) B cell population in PL cattle has different mobilization and internalization of the BCR when compared to the largely CD5-negative B cells in BLV-negative cattle. Unlike B cells from BLV-negative cattle, the BCR in B cells of BLV-infected, PL cattle resists movement into lipid rafts upon stimulation and is only weakly internalized. Expression of viral proteins as determined by detection of the BLV transmembrane (TM) envelope glycoprotein gp30 did not alter these events in cells from PL cattle. This exclusion of the BCR from lipid rafts may, in part, explain signaling differences seen between B cells of BLV-infected, PL, and BLV-negative cattle and the resistance to apoptosis speculated to contribute to persistent lymphocytosis.

Bovine leukemia virus (BLV) is an oncogenic retrovirus in the human T cell leukemia virus family. BLV infects B lymphocytes and induces a nonmalignant persistent lymphocytosis (PL) and leukemia/lymphoma in cattle. There is evidence that CD4 T lymphocytes are activated during BLV infection and promote the development of PL. How CD4 T lymphocytes are activated by BLV infection is not known. We observed that CD4 T lymphocytes from PL cattle proliferated in the presence of autologous, irradiated peripheral blood mononuclear cells (PBMC), whereas no proliferation occurred in cell cultures from BLV-infected non-PL cattle. Proliferation required direct contact with metabolically active irradiated PBMC but was not associated with viral protein expression or inhibited by antibodies to BLV. Unexpectedly, B lymphocytes alone failed to account for the irradiated PBMC stimulation of CD4 T lymphocytes. These observations and the magnitude of the proliferative response suggest that activation is polyclonal and involves mechanisms other than BLV antigen-specific stimulation., (Copyright 2000 Academic Press.)

Both human T lymphotropic virus (HTLV) and bovine leukemia virus (BLV) infections are characterized by in vitro proliferation of peripheral blood lymphocytes in the absence of exogenous antigens or mitogens. Differential expression of lymphocyte surface molecules in HTLV and BLV infection suggests that lymphocyte dysregulation may involve signaling through surface molecules involved in immune regulation. We examined the expression of adhesion and major histocompatibility (MHC) molecules on circulating lymphocytes from BLV-infected cows with persistent lymphocytosis and the ability of monoclonal antibodies to these molecules to modulate spontaneous lymphocyte proliferation. The integrin molecule, CD11c, and both MHC class I and MHC class II molecules were upregulated on B and T lymphocytes from PL cows. Anti-CD11c antibody was stimulatory to lymphocyte proliferation regardless of BLV status and had a greater stimulatory effect on spontaneously proliferating lymphocytes from persistently lymphocytotic cows than on normal bovine lymphocytes. Antibodies to bovine class I and class II inhibited spontaneous lymphocyte proliferation. Results suggest that lymphocyte dysregulation in BLV-induced persistent lymphocytosis involves upregulation of and signaling through lymphocyte surface molecules which are involved in immune activation of lymphocytes.

Recombinant mouse tryptophan hydroxylase (TPH) was expressed in large quantities in Escherichia coli strain MC 1061, using a bacterial expression vector, pKS, containing the full coding region of mouse TPH. Specific polyclonal antiserum to the subunit of the recombinant mouse TPH was produced in rabbit by injecting the TPH band cut from SDS-polyacrylamide slab gels. The resultant antiserum recognized a single identical protein band (MW = 54,000) from rat dorsal raphe area, pineal gland, and brain stem by Western blot analysis. The specific activity of recombinant mouse TPH obtained was equivalent to that of TPH purified from rat brain. The recombinant mouse TPH was stable for 3 days at 4 degrees C but lost 25% of the original activity for the same period at -20 degrees C. A serotonin concentration greater than 1 mM inhibited TPH activity under our assay conditions in a concentration-dependent fashion. The recombinant mouse TPH exhibited a charge isozyme corresponding to that of pineal gland TPH as applied to chromatofocusing column chromatography. Taken together, our results show that recombinant mouse TPH, expressed in large quantities in E. coli is not only enzymatically highly active but also shares many biochemical and immunochemical properties with native TPH.