School of Medicine and Health Sciences Poster Presentations

Title

Evaluation of Longitudinal Antibody Responses in Zika-Infected Individuals from Colombia

Document Type

Poster

Abstract Category

Immunology/Infectious Diseases

Keywords

Zika, Antibody Response

Publication Date

Spring 5-1-2019

Abstract

Since the Zika epidemic in 2015, there have been striking associations between Zika virus (ZIKV) infection and neurological complications, sequelae which are most devastatingly seen in fetal development.1,2 As a result, there is an urgent need for a vaccine against Zika. However, in order to elicit protective, neutralizing antibodies there is a critical need-to-know of how pre-existing immunity to Dengue virus affects the antibody response to Zika infection. We have previously observed that people who developed Guillain-Barre syndrome (GBS) had higher titers of Dengue and Zika neutralizing antibodies than those who did not develop GBS during Zika infection.3 This study hypothesizes that in regions endemic for flavivirus infection, individuals who developed GBS and had high neutralizing antibody titers will have antibodies that target different viral epitopes from those who do not. To conduct this study, clinically diagnosed plasma samples taken from Zika-infected persons living in Colombia, South America were tested for the presence and strength of memory antibodies at two different time points after virus clearance. Sera were collected at 1-year (mean 1.3 years) and 2 years (mean 2.3 years) post-Zika infection and were tested against the ZIKV E (envelope) protein. As expected, all serum samples bound highly to ZIKV E monomer protein with detectable waning in titer over one year (Figure 1). In order to map the targeted viral epitopes, we ran competition ELISAs using known monoclonal antibodies, 4G2 and ZK67. These antibodies target the fusion loop (FL) and Domain III (DIII) of the E protein respectively. Interestingly, we found that the majority of sera contained antibodies targeting the FL but not DIII. Therefore, we investigated whether there were clinical differences in people who did or did not develop Guillain-Barre syndrome (GBS). We found that FL responses were significantly stronger in people who did not develop GBS, and that DIII responses were undetectable in all patients (Figure 2). Our future direction is to expand this dataset to map epitopes found on the ZIKV E dimer, which will better reflect the natural conformation of ZIKV E protein.

Open Access

1

Comments

Presented at Research Days 2019.

This document is currently not available here.

Share

COinS
 

Evaluation of Longitudinal Antibody Responses in Zika-Infected Individuals from Colombia

Since the Zika epidemic in 2015, there have been striking associations between Zika virus (ZIKV) infection and neurological complications, sequelae which are most devastatingly seen in fetal development.1,2 As a result, there is an urgent need for a vaccine against Zika. However, in order to elicit protective, neutralizing antibodies there is a critical need-to-know of how pre-existing immunity to Dengue virus affects the antibody response to Zika infection. We have previously observed that people who developed Guillain-Barre syndrome (GBS) had higher titers of Dengue and Zika neutralizing antibodies than those who did not develop GBS during Zika infection.3 This study hypothesizes that in regions endemic for flavivirus infection, individuals who developed GBS and had high neutralizing antibody titers will have antibodies that target different viral epitopes from those who do not. To conduct this study, clinically diagnosed plasma samples taken from Zika-infected persons living in Colombia, South America were tested for the presence and strength of memory antibodies at two different time points after virus clearance. Sera were collected at 1-year (mean 1.3 years) and 2 years (mean 2.3 years) post-Zika infection and were tested against the ZIKV E (envelope) protein. As expected, all serum samples bound highly to ZIKV E monomer protein with detectable waning in titer over one year (Figure 1). In order to map the targeted viral epitopes, we ran competition ELISAs using known monoclonal antibodies, 4G2 and ZK67. These antibodies target the fusion loop (FL) and Domain III (DIII) of the E protein respectively. Interestingly, we found that the majority of sera contained antibodies targeting the FL but not DIII. Therefore, we investigated whether there were clinical differences in people who did or did not develop Guillain-Barre syndrome (GBS). We found that FL responses were significantly stronger in people who did not develop GBS, and that DIII responses were undetectable in all patients (Figure 2). Our future direction is to expand this dataset to map epitopes found on the ZIKV E dimer, which will better reflect the natural conformation of ZIKV E protein.