1/3. Determination of natural versus laboratory human infection with Mayaro virus by molecular analysis.A laboratory worker developed clinical signs of infection with Mayaro virus (togaviridae), an arbovirus of South and central america, 6 days after preparation of Mayaro viral antigen and 10 days after a trip to a rain forest. There was no evidence of skin lesions during the antigen preparation, and level 3 containment safety measures were followed. Therefore, molecular characterization of the virus was undertaken to identify the source of infection. RT-PCR and dna sequence comparisons proved the infection was with the laboratory strain. Airborne Mayaro virus contamination is thus a hazard to laboratory personnel.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/3. glomerulonephritis in the acute phase of ross river virus disease (epidemic polyarthritis).hematuria and proteinuria were detected at the peak of symptoms in a case of ross river virus (RRV) disease. No other infective cause was identified. A renal biopsy 28 days after the onset of nephritis showed mild mesangial proliferative changes and one segmental sclerotic lesion. Immunofluorescence showed widespread linear deposition of IgG in glomerular capillary walls with similar but weak staining for IgM, complement (C3) and fibrinogen; granular deposits of IgM and C3 in several arterioles; and IgM in a few mesangial cells. No electron-dense deposits were detected, nor was RRV antigen found in the renal tissue. Anti-glomerular basement membrane antibodies were not detected in the serum. Recovery from the renal disturbance was complete within three months although rheumatic symptoms persisted for 30 months.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |
3/3. The exanthem of ross river virus infection: histology, location of virus antigen and nature of inflammatory infiltrate.The exanthem of epidemic polyarthritis, a disease caused by Ross River (RR) virus, was examined three days after onset of the common erythematous and the rare purpuric forms of the eruption. The dermis showed a light perivascular infiltrate of mononuclear cells in both, with extravasation of erythrocytes in the latter. No immunoglobulins (IgM, IgG, IgA) or complement components (Clq, C3) were detected. Most of the infiltrating cells were T lymphocytes of the T suppressor-cytotoxic class. Their perivascular location, the scarcity of other lymphocytes or phagocytes, and rapid resolution of the rash indicated that the T lymphocytes were responsible for cytotoxic destruction of virus-infected cells. A few monocyte-macrophage cells were identified in the perivascular infiltrate. RR virus antigen was found in the basal epidermal and eccrine duct epithelial cells of both types of lesion and in the perivascular zone of the erythematous lesion, but appeared to have been eliminated from this region in the purpuric lesion. It is suggested that secondary effects of the T-cytotoxic reaction on nearby capillaries are responsible for erythema, oedema and purpura in the exanthem.- - - - - - - - - - ranking = 2.5keywords = antigen (Clic here for more details about this article) |