Comparison of Replicase Localization in Different Types of Mouse Hepatitis Virus (MHV)-infected Cells
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The replication complex (RC) of virtually all positive strand RNA viruses has been shown to be intimately associated with cellular membranes. However, different RNA viruses seem to target or recruit distinct membranes for the assembly of their RCs. For example, poliovirus replicates its RNA on the surface of membranous vesicles which seem to evolve from the endo-plasmic reticulum (ER). The vesicles form a rosette-like structure (Bienz et al 1992; Egger et al 1996). For tobacco etch potyvirus viral replication takes place at ER-derived vesicles and results in a collapse of the ER (Schaad et al 1997). In contrast, alphaviruses appear to use the cytosolic surface of endocytic organelles for the formation of their RCs (Froshauer et al 1988). For Nidoviruses such as arteriviruses and coronaviruses, the story is even more complex. Recently, it was shown that equine arteritis virus (EAV) generates ER-derived double-membrane vesicles (DMVs) (Pedersen et al 1999). In contrast, studies of the Coronavirus mouse hepatitis virus (MHV) implicated a role for late endosomes in the formation of the RC (van der Meer et al 1999). Recently, we have shown that translation products of the MHV replicase gene localized to different membrane structures in different cell lines. For a human cell line, viral replicase products colocalized with golgi markers, but in a murine cell line, the viral products and ER-derived membranes colocalized (Shi et al 1999). To extend our studies, we wanted to determine the viral and cellular factor(s) that drive the generation of the MHV RC at distinct membranes in the different cell lines.