SYNOPSISA 3-year survey of wild fish in Loch Awe and the surrounding watershed has shown a restricted distribution and low prevalence of infection with infectious pancreatic necrosis virus. No signs of clinical disease were observed in infected fish. The restricted distribution close to a rainbow trout farm is consistent with the virus originating from this farm, where virus infected stocks have been found each year since 1971. The continuing low prevalence is also consistent with virus in wild fish resulting from the spread of infection from the farm. If infection is spreading between wild fish, it is slow within the time scale of the survey. The possible mechanisms of transmission of infection from the farm to wild fish are discussed.

The skin of the head of adult Atlantic salmon S. suluv L. was examined by light and electron microscopy. The general structure resembled that of most other vertebrates, but in common with other fish, the melanocytes were restricted to the papillary layer of the dermis. The mucus secreting cells were shown to elaborate a series of separate membrane bound vesicles of secretion. The basement-membrane was complex, with a system of primary, and secondary micro-papillae showing close adherence to the bases of the epithelial cells, which were modified to form a thick, electron dense basal plasma membrane. NO evidence to suggest a reason for the localization of the early lesions of ulcerative dermal necrosis to specific areas of the epithelium of the head was adduced.

Satellite cells (SCs) ensheathe neuronal cell bodies of sensory ganglia and provide mechanical and metabolic support for neurons. In mice, grossly detrimental stimuli such as nerve crush or cut, or explant culture of ganglia induce proliferation of SCs. It is unknown whether SC proliferation occurs in response to the less severe trauma that might commonly occur in a physiological situation. Our aim was to determine the response of SCs to mild trauma, such as scratching the skin. SC proliferation, measured by bromodeoxyuridine (BrdU) uptake, and immune cells, measured by CD45 labelling, were quantified at various times during the 7 days after scarification or abrasion of flank skin. We show that minimal skin trauma, such as scarification or light abrasion, triggers proliferation of SCs. Sections of control mice nervous tissue show <10 BrdU+ cells/ganglionic profile. In contrast, sections of traumatised mice show >50 BrdU+ cells/ganglionic profile, even after simply scratching the skin. The lack of CD45+ cells shows that the proliferating cells are not immune cells. We suggest that SCs in mice are a labile cell population able to proliferate rapidly in response to minimal nerve trauma. This finding has implications for the role of SCs in nervous system repair.

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Herpes simplex virus (HSV) is a virtually ubiquitous human pathogen that, following cutaneous infection, latently infects neurons of sensory ganglia. Satellite cells (SCs) ensheath and provide metabolic support for these neurons, and could potentially participate in controlling HSV disease. Although SCs are restrictive for HSV replication, hypercellularity of non-neuronal cells in ganglia is prominent during HSV infection in animal models. SCs proliferate in response to trauma, e.g. nerve cut or crush, but it is not known if proliferation occurs in response to viral infection. To address this issue, cell proliferation, measured by bromodeoxyuridine (BrdU) uptake, and immune infiltrate, measured by CD45 labelling, were examined during acute infection in a mouse model. Because SCs do not express CD45, the BrdU + CD45 2 cell subset represents the proliferating SC population. We report that during acute ganglionic HSV infection there is a substantial increase in SC numbers. We suggest that SC proliferation in response to HSV infection may occur in order to facilitate neuronal survival.Satellite cells (SCs) in the peripheral nervous system (PNS) physically and metabolically support neurons. Unlike neurons, SCs maintain the ability to divide in adult life, although these cells do not typically display evidence of rapid turnover. Consistent with this are findings of rare mitotic SCs and a small proportion of SCs labelled with tritiated thymidine present in ganglia of adult rodents and cats (Lieberman, 1976;Pannese, 1960;Wen et al., 1994). SCs proliferate in response to severe trauma, e.g. axotomy and nerve crush (Nathaniel & Nathaniel, 1973;Shinder et al., 1999), and proliferate in explant culture, in which ganglia are excised and cultured in vitro, eliminating invading blood cells while preserving structure (Wen et al., 1994). SCs proliferate in response to malnutrition, e.g. in vitamin E-deficient rats (Cecchini et al., 1999). It is proposed that proliferation of SCs in response to trauma facilitates neuronal recovery (Wen et al., 1994).The role of SCs in response to PNS infection by viruses, such as herpes simplex virus (HSV), is poorly characterized. During cutaneous infection HSV enters nerves and travels to sensory ganglia, where, after a brief bout of productive infection, it establishes latency in neurons. Neurons and SCs appear privileged in their response to HSV. In neurons this is reflected in an unusual ability to survive infection despite viral gene expression (Simmons & Tscharke, 1992), which in other cell types is typically associated with cell destruction (Roizman & Knipe, 2001). SCs undergo abortive infection with HSV, as shown by electron microscopy which finds only unenveloped virions in SCs (Hill et al., 1972) or no virions at all (Dillard et al., 1972). Viral antigens are rarely, if ever, found in SCs during acute ganglionic infection (Speck & Simmons, 1998). These studies suggest that efficient infection of SCs by HSV does not occur. Consistent with this are results of studies on infection of Sat....