
Serological analysis of Ebola virus survivors and close contacts in Sierra Leone: A cross-sectional study
Author(s) -
Peter Halfmann,
Amie J. Eisfeld,
Tokiko Watanabe,
Tadashi Maemura,
Makoto Yamashita,
Satoru Fukuyama,
Tammy Armbrust,
Isaiah Rozich,
Alhaji U. N’jai,
Gabriele Neumann,
Yoshihiro Kawaoka,
Foday Sahr
Publication year - 2019
Publication title -
plos neglected tropical diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.99
H-Index - 135
eISSN - 1935-2735
pISSN - 1935-2727
DOI - 10.1371/journal.pntd.0007654
Subject(s) - ebola virus , virology , sierra leone , serology , subclinical infection , seroconversion , antibody , ebolavirus , vp40 , medicine , outbreak , virus , immunology , antibody titer , ebola hemorrhagic fever , titer , development economics , economics
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.