Antibody‐dependent enhancement of viral infection: molecular mechanisms and <i>in vivo</i> implications

Takada, Ayato; Kawaoka, Yoshihiro

doi:10.1002/rmv.405

Cited by 297 publications

(255 citation statements)

References 105 publications

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“…[17][18][19]. None of these mechanisms seemed to be involved in the enhancement of HCVpp infectivity, because the infectivity of pp was enhanced with chimpanzee serum but not with derivative IgG and, furthermore, heat-treated human serum (30 min at 65°C) still enhanced, suggesting that complement also was not involved.…”

Section: Resultsmentioning

confidence: 99%

Evidence for cross-genotype neutralization of hepatitis C virus pseudo-particles and enhancement of infectivity by apolipoprotein C1

Meunier

Engle

Faulk

et al. 2005

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

231

249

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The lack of a cell culture system to support hepatitis C virus (HCV) replication has hampered studies of this frequent cause of chronic liver disease. However, pseudotyped retroviral particles (pp) bearing the HCV envelope glycoproteins have provided a different approach to HCV studies. We used genotype 1a pp to detect neutralizing antibodies (NtAb) in eight chimpanzees and four humans infected with 1a strains, and developed pp of genotypes 2a, 3a, 4a, 5a, and 6a to study cross-reactivity. NtAb was detected in one of four chimpanzees and none of three humans with acute resolving infection, suggesting that NtAb is not required for HCV clearance. NtAb were detected at high titer in two of four chimpanzees and, in Patient H, all with persistent infection; responses paralleled humoral responses to envelope 1 and 2 proteins and, in some cases, correlate also with antibodies to the hypervariable region 1, previously thought to be the primary site of neutralization. NtAb raised during 1a infections could neutralize HCVpp of genotypes 4a, 5a, and 6a but had only limited reactivity against 2a and 3a. The detection of high-titer NtAb with cross-genotype reactivity has important implications for the development of active and passive immune-prophylaxis strategies against HCV. Finally, we found that HCVpp infectivity was enhanced by human or chimpanzee sera; apolipoprotein C1 alone or as a component of high-density lipoproteins caused this enhancement. Future studies of the in vivo role of apolipoprotein C1 might provide additional insights into the infection process of HCV.neutralizing antibodies ͉ high-density lipoproteins

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Section: Resultsmentioning

confidence: 99%

Evidence for cross-genotype neutralization of hepatitis C virus pseudo-particles and enhancement of infectivity by apolipoprotein C1

Meunier

Engle

Faulk

et al. 2005

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

231

249

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“…Indeed, heterologous challenge of mice with CV-B3 after an initial infection with CV-B2 resulted in enhanced pathology 15,16 which especially can be due to the phenomenon of antibody-dependent enhancement. 15,17,18,19,9 Moreover it has been shown that in adult mice homologous challenge with CVB4-E2 resulted in hyperglycaemia, 20 and that challenge of pups of dams infected during pregnancy resulted in enhanced pathology in the offspring through possibly immune-mediated mechanisms due to pre-existing immunity. 21 In conclusion, in vitro assays displayed that serum samples of mice inoculated with CV-B4 E2 had an enhancing effect able to increase, on the one hand, the CV-B4 E2-induced production of antiviral mediators by spleen cells cultures and, on the other hand, the infection of these cells with CV-B4 E2.…”

Section: Discussionmentioning

confidence: 99%

Immunoglobulin G-dependent enhancement of the infection with Coxsackievirus B4 in a murine system

et al. 2016

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It was demonstrated that specific IgG can enhance the infection with CV-B4, in vitro, in the human system. This enhancement could be involved in the pathophysiology of CV-B4 induced diseases. To investigate further the role of enhancing IgG in the infection with CV-B4 E2 in vivo, animal models are needed. Therefore, it was decided to assess whether inoculation of CV-B4 E2 to mice results in the appearance of IgG able to enhance the infection with this virus. Swiss albino mice were inoculated with CV-B4 E2 intraperitoneally. Serum samples were obtained from tail vein blood collected from day 0 to day 80 p.i. IgG were isolated by Protein G affinity chromatography. Seroneutralisation assays were carried out. In total murine spleen cells cultures inoculated with CV-B4 E2 mixed with various dilutions of serum or IgG samples, the enhancing activity was assayed through i) the antiviral activity titer of supernatants ii) the detection of intracellular viral RNA by RT-PCR iii) the level of infectious particles in supernatants.In most serum samples (76/105), neutralizing and enhancing activities were detected peaking between days 14 and 30 p.i and were higher in sera from mice inoculated with 2.10 6 TCID50 units than with lower doses. The enhancing activity was due to the IgG-enriched fraction of serum from CV-B4 E2 infected animals but not from control animals.These data show that IgG from immune mice can enhance the infection of splenocytes with CV-B4 E2 in vitro and open the way to explore whether such an enhancing activity can play a role in vivo.

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“…A popular hypothesis is that DHF͞DSS results from antibody-dependent enhancement, whereby antibodies from a previous infection facilitate subsequent infection with a heterogeneous serotype (3). However, the exact mechanisms of pathogenesis remain contentious, and the potential for enhancement also may depend on the particular strain type (genotype) within the serotype and immunological differences within the host (4)(5)(6)(7). Theoretical studies of the potential impact of antibody-dependent enhancement on the epidemiology of dengue have shown that enhancement of transmission may generate cycles or chaotic oscillations in infection numbers (8), leading to an optimum degree of enhancement to prevent extinction (9), whereas enhancement of mortality may prevent immunologically similar serotypes from coexisting (10).…”

mentioning

confidence: 99%

Cross-protective immunity can account for the alternating epidemic pattern of dengue virus serotypes circulating in Bangkok

Adams

Holmes

Zhang

et al. 2006

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

253

225

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Dengue virus, the causative agent of dengue fever and its more serious manifestation dengue hemorrhagic fever, is widespread throughout tropical and subtropical regions. The virus exists as four distinct serotypes, all of which have cocirculated in Bangkok for several decades with epidemic outbreaks occurring every 8 -10 years. We analyze time-series data of monthly infection incidence, revealing a distinctive pattern with epidemics of serotypes 1, 2, and 3 occurring at approximately the same time and an isolated epidemic of serotype 4 occurring in the intervening years. Phylogenetic analysis of virus samples collected over the same period shows that clade replacement events are linked to the epidemic cycle and indicates that there is an interserotypic immune reaction. Using an epidemic model with stochastic seasonal forcing showing 8-to 10-year epidemic oscillations, we demonstrate that moderate cross-protective immunity gives rise to persistent out-of-phase oscillations similar to those observed in the data, but that strong or weak cross-protection or cross-enhancement only produces in-phase patterns. This behavior suggests that the epidemic pattern observed in Bangkok is the result of cross-protective immunity and may be significantly altered by changes in the interserotypic immune reaction.cross-immunity ͉ mathematical model ͉ phylogenetics ͉ rsv ͉ phase pattern

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Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications

Cited by 297 publications

References 105 publications

Evidence for cross-genotype neutralization of hepatitis C virus pseudo-particles and enhancement of infectivity by apolipoprotein C1

Evidence for cross-genotype neutralization of hepatitis C virus pseudo-particles and enhancement of infectivity by apolipoprotein C1

Immunoglobulin G-dependent enhancement of the infection with Coxsackievirus B4 in a murine system

Cross-protective immunity can account for the alternating epidemic pattern of dengue virus serotypes circulating in Bangkok

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