Infection of a chimeric simian and human immunodeficiency virus with CCR5-specific HIV-1 envelope to Rhesus macaques

Human immunodeficiency virus (HIV) infects lymphocytes and macrophages via CD4 and chemokine receptors. In this study, the infectivity of a chimeric simian and human immunodeficiency virus (SHIV) having a CCR5-specific HIV-1 envelope gene was examined. A SHIV strain termed SHIV-JRFL could enter cells via CD4 with a chemokine receptor CCR5, not CXCR4, and the viral replication was suppressed by recombinant human RANTES, one of beta-chemokines. The intravenous inoculation of SHIV-JRFL into two rhesus macaques resulted in a systemic infection, though it was rather weak. During the early infection, the production of RANTES from Con A-stimulated PBMCs of the infected monkeys increased. These results suggested that beta-chemokine has the potential to limit the infectivity of an R5-type SHIV.     

Histopathologic patterns of nephropathy in naturally acquired canine visceral leishmaniasis

Although the nephropathy of visceral leishmaniasis (VL) is known both in humans and dogs, histopathologic alterations have not been thoroughly studied. We examined renal alterations in 55 dogs with naturally acquired VL compared with five noninfected dogs from an endemic area in northeastern Brazil. Glomerulonephritis was found in 55 dogs, interstitial alterations in 53 dogs, and tubular changes in 43 dogs with VL. The glomerular alterations found were minor glomerular abnormalities (n = 8, 14.5%), focal segmental glomerulosclerosis (n = 10, 18.2%), mesangial proliferative glomerulonephritis (n = 17, 32.7%), membranoproliferative glomerulonephritis, (n = 18, 30.9%), crescentic glomerulonephritis (n = 1, 1.8%), and chronic glomerulonephritis (n = 1, 1.8%). Morphometric and ultrastructural studies complemented the analysis. The five control animals exhibited no glomerular alterations. The glomerular lesions were related to functional alterations. Considering that the alterations of canine and human nephropathy in VL are very similar, the data obtained in this study constitute an important contribution to the understanding of canine and human VL nephropathy.     

Cerebellar ataxia due to Toxocara infection in Mongolian gerbils,Meriones unguiculatus

We assessed the usefulness of gerbils as an experimental model for neurologic toxocarosis. Mongolian gerbils, Meriones unguiculatus, infected with Toxocara canis or Toxocara cati (1000 eggs/gerbil) showed progressive neurologic disorders from 50 days after infection in T. canis-infected gerbils or from 120 days after infection in T. cati-infected gerbils. The incidence of the onset was 6 of the 13 gerbils (49%) in the T. canis-gerbils and 5 of the 7 gerbils (71%) in the T. cati-gerbils. Histopathologically, the cerebellum was the most affected in both groups. We observed loss of Purkinje cells, glial nerve fibers, and nerve sheaths. We also found foci consisting of aggregated macrophages scattered in the white matter of the cerebellum. The affected gerbils showed ataxia and ultimately died of cachexia. Our findings suggest that irreversible neurologic toxocarosis in gerbils can be induced by infection with either T. canis or T. cati.     

Genetic and biological comparison of tick-borne encephalitis viruses from Hokkaido and far-eastern Russia

We compared the biological properties of Oshima 5-10 (tick-borne encephalitis [TBE] virus isolated in Hokkaido, Japan) and Sofjin-HO (Far-Eastern subtype TBE virus) including plaque formation, virus replication and virus protein synthesis in BHK-21 cell cultures to reveal strain differences. We also determined the complete nucleotide sequences of both strains and compared the deduced amino acid sequences. Plaques of Oshima 5-10 were smaller than those of Sofjin-HO. Virus titers in culture fluid of Oshima 5-10 were 1/100 of those of Sofjin-HO at 9 and 12 hr after infection. Less viral protein and RNA syntheses of strain Oshima 5-10 was observed than with Sofjin-HO. Genetic analysis revealed 1.4% of amino acids to differ with Sofjin-HO. No difference between the two strains was detected in the motif sequence of the viral enzyme, cleavage sites of viral protein or glycosylation sites of NS1.     

Amyloid angiopathy with cerebral hemorrhage and senile plaque in aged dogs

Amyloid angiopathy with cerebral hemorrhage and senile plaques was found in the brain of aged dogs. In all 9 cases examined, 13 to 19 years old, 6 males and 3 females, amyloid deposits were observed mostly in the wall of cerebral arterioles and capillaries showed hyaline degeneration. The accumulation of amyloid fibrils measuring about 10 nm in diameter was seen in the cerebral vessel wall by electron microscopy. The cerebral hemorrhage was observed in 6 of 9 dogs and 2 of them showed massive hemorrhage. The hemorrhagic foci were sometimes closely contact with the vessels involved in amyloid angiopathy. In addition, senile plaques being classified into 2 types were found in the cerebral cortex of 3 dogs. The first type was characterized by the accumulation of degenerative neurites and often contained granular argyrophilic material. The second type had a well-defined amyloid core with neuritic halo. Amyloid deposits were also found in or around intestinal vessel walls of 3 dogs. The amyloid deposited in the cerebral vessels, senile plaques and intestinal vessels showed characteristic green birefringence under the polarized light even after potassium permanganate treatment.