Eight mares were infected with equid herpesvirus-1 subtype 1 isolated from a case of equine paresis. In two mares killed at 4 d.p.i. immunofluorescence showed endothelial cell infection together with thrombosis in the rete arteriosus of the nasal mucosa and also in the spinal cord of one of these mares. Circulating platelet counts in the other six mares fell as early as 2 d.p.i. and remained depressed for seven days. Circulating immune complexes started to appear at 2 d.p.i., reached maximum levels at 10 d.p.i., but were undetectable at 28 d.p.i. Three of the six remaining mares developed varying degrees of inco-ordination at 8 and 9 d.p.i. In the two inco-ordinate mares that were killed at 9 and 10 d.p.i. the haemorrhages in the spinal cord and brain were associated with extensive endothelial cell fluorescence and thrombus formation. Clinical paresis coincided with an increase in circulating complement fixing and neutralising antibodies which in all six mares were higher against the subtype 2 isolate than subtype 1. In five yearlings infected with a subtype 2 isolate of EHV-1 platelet counts remained normal and neither immune complexes nor viraemia, nor inco-ordination were detected.

No abstract

Summary Eight ponies were experimentally infected with equid herpesvirus 1 (EHV 1) (subtype 1). All animals showed clinical and serological evidence of infection and virus was isolated from nasal swabs and leucocytes. These ponies were kept in isolation for a further three months during which time complement fixing antibody decreased at least four‐fold. Following immunosuppression with dexamethasone and prednisolone subtype 1 virus was recovered from six of the eight animals within 14 days. Five of these six ponies were viraemic and three of them shed virus in nasal secretions; only four displayed significant rises in complement fixing antibody and only two in neutralising antibody. Clinical abnormalities were not detected during reactivation.

AIDS 5: [693][694][695][696][697][698] 1991). We now report that consistent with its improved anti-HIV activity, MDL 28,574 is more effective (50% inhibitory concentration [IC50],20 ,uM) than the parent molecule (ICso, 254 ,uM) at causing the accumulation of glucosylated oligosaccharides in HIV-infected cells by inhibition of glycoprotein processing. These were predominantly of the glucose 3 type, as determined by P4 Bio-Gel analysis after digestion with purified a-glucosidase I, indicating that, intracellularly, this enzyme is the major target for inhibition. MDL 28,574, however, was less active (IC50, 1.27 ,uM) than castanospermine (IC50, 0.12 ,uM) against the mutual target enzyme, cellular oi-glucosidase I, in a cell-free assay system. The increased effects of MDL 28,574 against a-glucosidase I in cell culture were attributed to the improved cellular uptake of the more lipophilic derivative. Inhibition of this enzyme activity in HIV-infected H9 cells impaired viral glycoprotein processing and resulted in the expression of abnormally configured gpl20. This did not affect virus production, but the virions had decreased infectivity which was partially related to a reduced ability to bind to CD4+ T cells.