scholarly journals Sulfated Polysaccharide, Curdlan Sulfate, Efficiently Prevents Entry/Fusion and Restricts Antibody-Dependent Enhancement of Dengue Virus Infection In Vitro: A Possible Candidate for Clinical Application

2013 ◽  
Vol 7 (4) ◽  
pp. e2188 ◽  
Author(s):  
Koji Ichiyama ◽  
Sindhoora Bhargavi Gopala Reddy ◽  
Li Feng Zhang ◽  
Wei Xin Chin ◽  
Tegshi Muschin ◽  
...  
2010 ◽  
Vol 155 (10) ◽  
pp. 1617-1624 ◽  
Author(s):  
Mikako Ito ◽  
Ryo-zabro Mukai ◽  
Tomohiko Takasaki ◽  
Akira Kotaki ◽  
Ichiro Kurane

Author(s):  
Puneet Bhatt ◽  
Sasidharan Pillai Sabeena ◽  
Muralidhar Varma ◽  
Govindakarnavar Arunkumar

AbstractThe pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.


2016 ◽  
Vol 90 (24) ◽  
pp. 11122-11131 ◽  
Author(s):  
Meihui Xu ◽  
Roland Züst ◽  
Ying Xiu Toh ◽  
Jennifer M. Pfaff ◽  
Kristen M. Kahle ◽  
...  

ABSTRACT Half of the world's population is exposed to the risk of dengue virus infection. Although a vaccine for dengue virus is now available in a few countries, its reported overall efficacy of about 60% is not ideal. Protective immune correlates following natural dengue virus infection remain undefined, which makes it difficult to predict the efficacy of new vaccines. In this study, we address the protective capacity of dengue virus-specific antibodies that are produced by plasmablasts a few days after natural secondary infection. Among a panel of 18 dengue virus-reactive human monoclonal antibodies, four groups of antibodies were identified based on their binding properties. While antibodies targeting the fusion loop of the glycoprotein of dengue virus dominated the antibody response, two smaller groups of antibodies bound to previously undescribed epitopes in domain II of the E protein. The latter, largely serotype-cross-reactive antibodies, demonstrated increased stability of binding at pH 5. These antibodies possessed weak to moderate neutralization capacity in vitro but were the most efficacious in promoting the survival of infected mice. Our data suggest that the cross-reactive anamnestic antibody response has a protective capacity despite moderate neutralization in vitro and a moderate decrease of viremia in vivo . IMPORTANCE Antibodies can protect from symptomatic dengue virus infection. However, it is not easy to assess which classes of antibodies provide protection because in vitro assays are not always predictive of in vivo protection. During a repeat infection, dengue virus-specific immune memory cells are reactivated and large amounts of antibodies are produced. By studying antibodies cloned from patients with heterologous secondary infection, we tested the protective value of the serotype-cross-reactive “recall” or “anamnestic” response. We found that results from in vitro neutralization assays did not always correlate with the ability of the antibodies to reduce viremia in a mouse model. In addition, a decrease of viremia in mice did not necessarily improve survival. The most protective antibodies were stable at pH 5, suggesting that antibody binding in the endosomes, after the antibody-virus complex is internalized, might be important to block virus spread in the organism.


2013 ◽  
Vol 100 (1) ◽  
pp. 238-245 ◽  
Author(s):  
Nilda V. Ayala-Nuñez ◽  
Patsaporn Jarupathirun ◽  
Suzanne J.F. Kaptein ◽  
Johan Neyts ◽  
Jolanda M. Smit

2010 ◽  
Vol 85 (4) ◽  
pp. 1671-1683 ◽  
Author(s):  
K. Boonnak ◽  
K. M. Dambach ◽  
G. C. Donofrio ◽  
B. Tassaneetrithep ◽  
M. A. Marovich

2018 ◽  
Vol 12 (1) ◽  
pp. e0006154 ◽  
Author(s):  
Dominic Paquin-Proulx ◽  
Vivian I. Avelino-Silva ◽  
Bianca A. N. Santos ◽  
Nathália Silveira Barsotti ◽  
Fabiana Siroma ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document