Biochemical Properties of Polyhedra and Virus Particles of the Cytoplasmic Polyhedrosis Virus of Bombyx mori

Intervirology ◽  
1974 ◽  
Vol 4 (6) ◽  
pp. 354-364 ◽  
Author(s):  
Christopher C. Payne ◽  
James Kalmakoff
1965 ◽  
Vol 11 (3) ◽  
pp. 497-501 ◽  
Author(s):  
F. T. Bird

The cytoplasmic-polyhedrosis virus particle is an icosahedron about 68 mμ in diameter. It consists of a capsid, made up of two concentric rings, and an inner core. The capsid has 12 projections.Large masses consisting mostly of the capsids of virus particles develop in the cytoplasm of gut cells infected with cytoplasmic-polyhedrosis virus. Cores of the virus particles are found on the outer surfaces of these masses or in material adjacent to them. The complete virus particle is assembled just before it is enveloped by protein and incorporated into a developing polyhedron.Granules, tentatively identified as lysosomes, increase in number and size during the early stages of infection. Other granules and bodies observed in the gut cells are described.


2015 ◽  
Vol 89 (22) ◽  
pp. 11473-11486 ◽  
Author(s):  
Aris Zografidis ◽  
Filip Van Nieuwerburgh ◽  
Anna Kolliopoulou ◽  
Konstantinos Apostolou-Karampelis ◽  
Steven R. Head ◽  
...  

ABSTRACTThe lepidopteran innate immune response against RNA viruses remains poorly understood, while in other insects several studies have highlighted an essential role for the exo-RNAi pathway in combating viral infection. Here, by using deep-sequencing technology for viral small-RNA (vsRNA) assessment, we provide evidence that exo-RNAi is operative in the silkwormBombyx moriagainst both persistent and pathogenic infection ofB. moricytoplasmic polyhedrosis virus (BmCPV) which is characterized by a segmented double-stranded RNA (dsRNA) genome. Further, we show that Dicer-2 predominantly targets viral dsRNA and produces 20-nucleotide (nt) vsRNAs, whereas an additional pathway is responsive to viral mRNA derived from segment 10. Importantly, vsRNA distributions, which define specific hot and cold spot profiles for each viral segment, to a considerable degree overlap between Dicer-2-related (19 to 21 nt) and Dicer-2-unrelated vsRNAs, suggesting a common origin for these profiles. We found a degenerate motif significantly enriched at the cut sites of vsRNAs of various lengths which link an unknown RNase to the origins of vsRNAs biogenesis and distribution. Accordingly, the indicated RNase activity may be an important early factor for the host's antiviral defense in Lepidoptera.IMPORTANCEThis work contributes to the elucidation of the lepidopteran antiviral response against infection of segmented double-stranded RNA (dsRNA) virus (CPV;Reoviridae) and highlights the importance of viral small-RNA (vsRNA) analysis for getting insights into host-pathogen interactions. Three vsRNA pathways are implicated in antiviral defense. For dsRNA, two pathways are proposed, either based on Dicer-2 cleavage to generate 20-nucleotide vsRNAs or based on the activity of an uncharacterized endo-RNase that cleaves the viral RNA substrate at a degenerate motif. The analysis also indicates the existence of a degradation pathway that targets the positive strand of segment 10.


1996 ◽  
Vol 77 (1) ◽  
pp. 147-153 ◽  
Author(s):  
H. Nakazawa ◽  
F. Kendirgi ◽  
S. Belloncik ◽  
R. Ito ◽  
S. Takagi ◽  
...  

1965 ◽  
Vol 11 (4) ◽  
pp. 703-707 ◽  
Author(s):  
W. A. Smirnoff

Hyalophora cecropia (Linnaeus) is susceptible to infection by a cytoplasmic polyhedrosis virus. Electron microscope studies showed spherical viral particles known as "cores" which remain in groups of 12 to 17 subunits. The virus particles were embedded in a protein mass located in craters of the polyhedra. Larvae of the first, second, and third instars were more susceptible to viral infection than later instars. However, up to 50% of the larvae of later instars sometimes survived. The larvae of subsequent instars and the pupa were very resistant and periodic injections of strong dosages of virus material produced no ill effect. In general, larvae infected by this cytoplasmic virus shrank to less than half normal size before death.


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