Virus particles in rubella infected tissue cultures

Replication complexes associated with the morphogenesis of rubella virus

“…Thus, it was important in this study to define the morphology and sites of maturation for RV virions so as to distinguish them from the RV replication complex vesicles. The morphological analysis of RV virions presented here correlated well with that reported by other investigators [13,[15][16][17], and provides clear evidence that RV virions and RV replication complex vesicles are separate entities. Firstly, the round or ovoid electron dense cores of RV virions were distinct from the irregular fibrous or thread-like inclusions that were observed within the RV replication complex vesicles.…”

“…Although the morphogenesis of RV has been examined in detail [13,[15][16][17], RV replication complexes have not been previously described. As the dimensions of the RV replication complex vesicles were similar to those of RV virions, these two entities may have been mistaken for one another and so contributed to RV replication complexes being overlooked.…”

Intracellular transport of rubella virus structural proteins expressed from cloned cDNA

“…It is not clear why some cells should be more permissive of transport than others; however, it is not possible to ascribe the variant reports in the literature as to the site of RV budding to the same cause as our observations of cell line variation in transport of RV proteins. Of the four lines in our study, BHK and RK13 cells allowed the most transport of E1 and E2 to the surface, yet the latter cell line has been consistently reported as showing only intracellular budding (Hamvas et al, 1969;Higashi, 1973;Holmes et al, 1968;Patrizi & Middlekamp, 1970). On the other hand, RV-infected RK13 cells form syncytia, suggesting that the viral fusion protein, at least, is found at the cell surface (Patrizi & Middlekamp, 1970).…”

“…Its replication is slow, taking 12 to 16 h after infection before viral structural proteins can be detected intracellularly (Hemphill et al, 1988), and without the shutoffof host protein synthesis exhibited by alphaviruses. In addition, although some authors have observed RV budding at the plasma membrane, particularly in BHK cells (Chatterji et al, 1969;Higashi, 1973;Murphy et al, 1968;Oshiro et al, 1969), most others (even using the same cell line) have failed to see budding at the plasma membrane of the host cell, finding it rather at internal membranes, possibly of Golgi origin (Bardeletti et al, 1979;Bonissol & Sisman, 1968;Hamvas et al, 1969;Higashi, 1973;Kouri et al, 1974;McCombs et al, 1968 ;Tuchinda et al, 1966;von Bonsdorff & Vaheri, 1969). The lipid composition of the virus (Bardeletti & Gautheron, 1976) lies midway between that of the endoplasmic reticulum (ER) and that of the plasma membrane (van Meer, 1989), particularly with regard to the cholesterol/phospholipid molar ratio, again suggesting that the virus buds from an intracellular compartment.…”

Rubella Virus Replication and Links to Teratogenicity

“…However, discrepancies with these findings exist. Cytoplasmic inclusions have been reported in RV-infected RK13 cells (65) but were never detected in a similar cell line studied by other investigators (51). Moreover, the significance of these cytoplasmic inclusions is not known.…”