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nonstructural proteins NS1, NS3, and NS5
of the New Guinea C strain of dengue virus type 2 (DEN-2)
were obtained by nucleotide and protein sequencing.
Clones were prepared containing cDNA of DEN-2 virus
in the plasmid pUC8. The nucleotide sequences of viral
cDNA inserts were determined and the cDNA of each clone
positioned on the flavivirus genomic map by comparison
of the deduced amino acid sequence with that of yellow
fever virus. Radiolabelled E, NS1, NS3 and NS5 were
purified by lectin affinity chromatography and preparative
gel electrophoresis. Purified proteins were subsequently
analysed by Edman degradation to establish the origins
of the amino termini of these proteins in the deduced
DEN-2 amino acid sequence. Thus the amino acid sequences
surrounding the likely proteolytic cleavage sites used
in the formation of these four proteins were determined.
Of particular interest was the sequence containing the
amino terminus of NS3, namely Lys-Lys-Gln-Arg-Ala-Gly
where Ala is the first amino acid of NS3. Cleavage following
one basic residue in the flavivirus polyprotein has
not been reported previously.
Bielefeldt Ohmann, H., D. W. Beasley,
et al. (1997). "Analysis of a recombinant dengue-2
virus-dengue-3 virus hybrid envelope protein expressed
in a secretory baculovirus system." J.Gen.Virol.
78(Pt 11): 2723-33.
In a step towards a tetravalent dengue virus subunit
vaccine which is economical to produce, highly immunogenic
and stable, a hybrid dengue virus envelope (E) protein
molecule has been constructed. It consists of 36 amino
acids from the membrane protein, the N-terminal 288
amino acids of the dengue-2 virus E protein plus amino
acids 289-424 of the dengue-3 virus E protein. It has
been engineered for secretory expression by fusion to
a mellitin secretory signal sequence and truncation
of the hydrophobic transmembrane segment. Using the
baculovirus expression system and serum-free conditions,
more than 95% of recombinant dengue-2 virus-dengue-3
virus hybrid E protein (rD2D3E) was secreted into the
cell culture supernatant in a stable form with multiple
features indicative of preserved conformation. The hybrid
molecule reacted with a panel of dengue virus- and flavivirus-specific
MAbs which recognize linear or conformational epitopes
on dengue virions. Human dengue virus-specific antisera
also reacted with the protein. The hybrid rD2D3E protein
was able to inhibit the in vitro binding of dengue-2
and dengue-3 viruses to human myelomonocytic cells,
suggesting that the receptor-binding epitope(s) was
preserved. Adjuvant-free immunization with the hybrid
protein induced an antibody response to both dengue-2
and dengue-3 virus in outbred mice, comparable in strength
to that of individual rD2E and rD3E proteins. Notably,
these antibody responses were primarily of the IgG2a
and IgG2b isotype. A strong dengue virus cross-reactive
T cell response was also induced in the mice, suggesting
that dengue virus hybrid E proteins could form the basis
of an efficacious multivalent dengue virus vaccine.
Bielefeldt Ohmann, H. (1997). "Pathogenesis
of dengue virus diseases: missing pieces in the jigsaw."
Trends Microbiol. 5(10): 409-13.
The mechanisms involved in the pathogenesis of dengue
hemorrhagic fever and dengue shock syndrome remain unresolved.
Antibody-dependent enhancement of infection has long
been thought to play a central role; however, this remains
unverified. The alternative hypothesis that virus variation,
virulence and dynamics may account for severe dengue
disease, particularly in children, should be considered.
 
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