The growth of Ross River virus in cultured mosquito () and monkey kidney (Vero) cells shows similar latent periods (5 to 6 h) and maximum yields.

In cells the virus establishes a persistent, non-cytopathic infection with no significant change in cell division rate. Virus matures within large, electron-dense cytoplasmic inclusions and also at the cell membrane. Virus accumulates within the inclusions but nucleocapsids do not. ‘Type-1 cytopathic vacuoles’ (Grimley, Berezesky & Friedman, 1968) are not found. Between 40 and 60 h after infection, the cell-associated virus titre falls by 1 log unit. Cytoplasmic inclusions lose electron-dense material and are transformed into microvesiculated vacuoles. Virus progressively disappears from these structures and from the cell membrane. It is suggested that during the establishment of the persistent infection, digestion of the contents of the inclusions occurs, resulting from fusion of lysosomal microvesicles with the inclusions.

In Vero cells infection leads to cell lysis. Early in infection virus is found in small cytoplasmic vesicles: ‘type-1 cytopathic vacuoles’ are also present. Accumulation of nucleocapsids is marked, particularly late in infection. Thus, although the pathogenesis of Ross River virus in mice is atypical (Mims 1973; Murphy 1973), its ultrastructural development is similar to that of other alphaviruses in cultured vertebrate cells.


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