Serological analysis of Ebola virus survivors and close contacts in Sierra Leone: A cross-sectional study

PLoS Negl Trop Dis. 2019 Aug 1;13(8):e0007654. doi: 10.1371/journal.pntd.0007654. eCollection 2019 Aug.

Abstract

The 2013-2016 Ebola virus outbreak in West Africa was the largest and deadliest outbreak to date. Here we conducted a serological study to examine the antibody levels in survivors and the seroconversion in close contacts who took care of Ebola-infected individuals, but did not develop symptoms of Ebola virus disease. In March 2017, we collected blood samples from 481 individuals in Makeni, Sierra Leone: 214 survivors and 267 close contacts. Using commercial, quantitative ELISAs, we tested the plasma for IgG-specific antibodies against three major viral antigens: GP, the only viral glycoprotein expressed on the virus surface; NP, the most abundant viral protein; and VP40, a major structural protein of Zaire ebolavirus. We also determined neutralizing antibody titers. In the cohort of Ebola survivors, 97.7% of samples (209/214) had measurable antibody levels against GP, NP, and/or VP40. Of these positive samples, all but one had measurable neutralizing antibody titers against Ebola virus. For the close contacts, up to 12.7% (34/267) may have experienced a subclinical virus infection as indicated by detectable antibodies against GP. Further investigation is warranted to determine whether these close contacts truly experienced subclinical infections and whether these asymptomatic infections played a role in the dynamics of transmission.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Neutralizing / blood
  • Antibodies, Viral / blood*
  • Cross-Sectional Studies
  • Ebolavirus / immunology*
  • Female
  • Hemorrhagic Fever, Ebola / immunology*
  • Humans
  • Immunoglobulin G / blood
  • Male
  • Plasma / immunology
  • Sierra Leone
  • Survivors*
  • Young Adult

Substances

  • Antibodies, Neutralizing
  • Antibodies, Viral
  • Immunoglobulin G

Grants and funding

YK was was supported for this work by the Japanese agencies of J-PRIDE for Global Epidemic from AMED (JP17fm0208101j0001), by RPERID from AMED (JP17fk018029h0001), by a Grant-in-Aid for Scientific Research on Innovative Areas from MEXT (no. 16H06429, 16K21723 and 16H06434), and by funds from the Promotion of Joint International Research (Fostering Joint International Research (B)) from JSPS and from the Global Health Institute at UW-Madison. The funders had no role in the study design data collection and analysis, decision to publish, or preparation of the manuscript.