Antibody-enhanced dengue virus infection in primate leukocytes

Halstead, Scott B.; OʼRourke, Edward J.

doi:10.1038/265739a0

Cited by 503 publications

(342 citation statements)

References 12 publications

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“…Because the antibody is heterologous, however, the virus is not neutralized and is free to replicate once inside the macrophage. Thus, it is hypothesized that prior infection, through a process known as antibody-dependent enhancement (ADE), enhances the infection and replication of dengue virus in cells of the mononuclear cell lineage (15,62,66,67,106). It is thought that these cells produce and secrete vasoactive mediators in response to dengue infection, which causes increased vascular permeability leading to hypovolemia and shock (see below).…”

Section: Pathogenesismentioning

confidence: 99%

Dengue and Dengue Hemorrhagic Fever

Gubler¹

1997

Tropical Infectious Diseases

633

756

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Section: Pathogenesismentioning

confidence: 99%

Dengue and Dengue Hemorrhagic Fever

Gubler¹

1997

Tropical Infectious Diseases

633

756

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“…After the period of transient crossprotection, a second episode of infection with a heterotypic dengue virus may then lead to a process known as antibodydependent enhancement (ADE; refs. [15][16][17]. ADE occurs when cross-reactive antibodies stimulated by a prior infection wane to levels that no longer neutralize the heterotypic virus.…”

Section: Alternative Hypothesesmentioning

confidence: 99%

Ecological and immunological determinants of dengue epidemics

Wearing¹,

Rohani

2006

Proc. Natl. Acad. Sci. U.S.A.

289

286

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The management of infectious diseases is an increasingly important public health issue, the effective implementation of which is often complicated by difficulties in teasing apart the relative roles of extrinsic and intrinsic factors influencing transmission. Dengue, a vector-borne strain polymorphic disease, is one such infection where transmission dynamics are affected by environmental variables as well as immune-mediated serotype interactions. To understand how alternative hypotheses concerning dengue infection and transmission may explain observed multiannual cycles in disease incidence, we adopt a theoretical approach that combines both ecological and immunological mechanisms. We demonstrate that, contrary to perceived wisdom, patterns generated solely by antibody-dependent enhancement or heterogeneity in virus virulence are not consistent with serotype-specific notification data in important ways. Furthermore, to generate epidemics with the characteristic signatures observed in data, we find that a combination of seasonal variation in vector demography and, crucially, a short-lived period of cross-immunity is sufficient. We then show how understanding the persistence and eradication of dengue serotypes critically depends on the alternative assumed mechanisms.antibody-dependent enhancement ͉ multistrain dynamics ͉ transient cross-immunity ͉ vector-transmitted disease

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“…The cellular receptors have now been isolated for both poliovirus (Mendelsohn et al, 1986(Mendelsohn et al, , 1989Shepley et al, 1988) and the major group rhinoviruses (Greve et al, 1989;Staunton et al, 1989); however, the attachment of HAV has not been characterized extensively (Seganti et al, 1987(Seganti et al, , 1989. Viruses can interact with cells in a variety of ways (Dimmock, 1982;Hsu et al, 1988;Marsh & Helenius, 1989;Reagan et al, 1984); in addition to attaching to specific receptors, it has been shown that viruses can bind by indirect mechanisms, for example the attachment of dengue virus to cells bearing Fc receptors is enhanced by antibody raised to the virus (Halstead & O'Rourke, 1977), whereas cytomegalovirus exploits flz-microglobulin in its interaction with cells (Grundy et al, 1987). t Present address: Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, U.K.…”

Section: Introductionmentioning

confidence: 99%

Parameters influencing the attachment of hepatitis A virus to a variety of continuous cell lines

Zajac

Amphlett²,

Rowlands³

et al. 1991

Journal of General Virology

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We have investigated the interactions of purified radiolabelled hepatitis A virus (HAV) with a variety of continuous cell lines. Virus labelled either in vitro with radiolabelled iodine or in vivo with radiolabelled uridine bound to cells with similar efficiency. Attachment to BS-C-1 cells was calcium ion-dependent and this correlated with infectivity assay results. The cell tropism of HAV attachment was examined using cell suspensions and confluent cell monolayers at both 4 °C and 37 °C. The maximum level of attachment was observed at 4 *C with cells in suspension, but was severely inhibited by 2 % foetal calf serum; these results again correlated with infectivity assays. The components of serum which inhibit attachment have been characterized by gel filtration chromatography, sucrose density gradient analysis, immunoprecipitation and Western blotting. The data show that such components are of high Mr and that the serum glycoprotein, ct2-macroglobulin, can partly mimic the inhibitory effect of whole serum.

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Antibody-enhanced dengue virus infection in primate leukocytes

Cited by 503 publications

References 12 publications

Dengue and Dengue Hemorrhagic Fever

Dengue and Dengue Hemorrhagic Fever

Ecological and immunological determinants of dengue epidemics

Parameters influencing the attachment of hepatitis A virus to a variety of continuous cell lines

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