Morphogenesis of Dengue‐1 Virus in Cultures of a Human Leukemic Leukocyte Line (J‐111)

SummaryIn dengue virus infected Aedes albopictus cells, electron-dense particles, larger than single ribosomes, were arranged on the cytoplasmic sides of rough endoplasmic reticulum (I~ER) membranes. Mature virions 40---45 nm in diameter as well as vesieulotubular structures 50--120 nm in diameter appeared in enlarged cisternae of I~EI~ filled with fine granular substance. Many of the mature virions and somewhat degenerated vesiculotubular structures remained to be enclosed in membranous structures presumably derived from I~.EI~, even after degeneration of infected cells. The findings suggest that development of dengue viruses in cultured A. albopictus cells takes place in close relationship with the activated membranes of RELY.Other morphological changes observed in dengue infected A. albopictus cells were 1. electron-dense "double-track structures" in areas of virion morphogenesis, 2. fine crystalline structures in type-2 dengue infected cells, and 3. aggregates of nucleoid structures, in cells persistently infected with type 2 dengue virus. The implication and nature of these structures in relation to virion morphogenesis remain to be investigated.

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Electron microscopic observations onAedes albopictus cells infected with dengue viruses

Igarashi

Fukai

1979

“…Electron microscopic studies have shown consistently the presence of mature virus particles within the lumen of the endoplasmic reticulum [7,12,14,19]. Egression of virus particles at the plasma membrane was rarely observed.…”

Section: Discussionmentioning

confidence: 97%

Flavivirus West Nile (Sarafend) egress at the plasma membrane

Howe

Sreenivasan

et al. 1994

West Nile (Sarafend) virus was distinctly observed to bud from the plasma membrane rather than mature intracellularly. This has been observed with transmission electron microscopy. Using conventional scanning electron microscopy, budding at the plasma membrane especially at the filopodia was clearly illustrated. Immunogold labelling against the virus envelope protein was also performed to confirm this mode of exit. The gold particles were observed to be located at the sites where virus budding was seen under the field emission scanning electron microscope.

“…An area of inconsistency involves the sit~e of nueleocapsid assembly. Several studies have demonstrated flavivirus nueleocapsids in the cytosol (7,9,11), while others have demonstrated them in the cisternae of rough endoplasmic retieulum (RER) (4,8,10,12). Recently, we have shown that, during infection of C6/36 mosquito cells with dengue-2 (DEN-2) virus, nueleocapsids assemble themselves in the eytosol and subsequently mature b y b u d d i n g t h r o u g h h o s t p l a s m a or c y t o p l a s m i c m e m b r a n e s , a c q u i r i n g v i r a l m e m b r a n e e n v e l o p e s in t h e p r o c e s s (7).…”

Section: Introductionmentioning

confidence: 98%

Maturation process of Japanese encephalitis virus in cultured mosquito cells in vitro and mouse brain cells in vivo

Hase

Summers

Eckels

et al. 1987

The maturation process of Japanese encephalitis (JE) virus in C6/36 cells in vitro and in mouse brain cells in vivo was studied by electron microscopy. In the C6/36 cell infection, 500 to 2250 virions per cell were released into the medium during the period of study; yet, no virus budding process was observed at the host cell membranes. JE virions at various maturation stages appeared within the cisternae of rough endoplasmic reticulum (RER) of infected cells at 24 hours p.i.; and, although C6/36 cells did not show a well-developed Golgi apparatus, the virions appeared to be carried to the cell surface within host-cell secretory vesicles for extracellular release as early as 24 hours p.i. The occurrence of a secretory-type intracellular transport of maturing JE virus particles was well recognizable in brain cells of infected mice, in which JE virus particles were found almost exclusively in the cisternae of RER, in the Golgi apparatus, and in various vesicles, including coated vesicles, in the vicinity of the Golgi apparatus. Our previous study of dengue-2 virus morphogenesis and our present study of JE virus morphogenesis differed substantially at various stages of maturation. Possible mechanisms which explain these differences were discussed.