Ebola virus antibody decay–stimulation in a high proportion of survivors

Charlene Adaken, Janet T. Scott, Raman Sharma, Robin Gopal, Steven Dicks, Saidia Niazi, Samreen Ijaz, Tansy Edwards, Catherine C. Smith, Christine P. Cole, Philip Kamara, Osman Kargbo, Heidi A. Doughty, Johan Griensven, Peter W. Horby, Sahr M. Gevao, Foday Sahr, Richard J. Dimelow, Richard S. Tedder, Malcolm G. Semple, William A. Paxton and Georgios Pollakis ()
Additional contact information
Charlene Adaken: University of Liverpool
Janet T. Scott: University of Liverpool
Raman Sharma: Liverpool School of Tropical Medicine
Robin Gopal: National Infections Service, Public Health England
Steven Dicks: Public Health England
Saidia Niazi: Public Health England
Samreen Ijaz: Public Health England
Tansy Edwards: London School of Hygiene and Tropical Medicine
Catherine C. Smith: University of Liverpool
Christine P. Cole: College of Medicine and Allied Health Sciences
Philip Kamara: National Safe Blood Service, Ministry of Health and Sanitation
Osman Kargbo: National Safe Blood Service, Ministry of Health and Sanitation
Heidi A. Doughty: National Health Service Blood and Transplant
Johan Griensven: Institute of Tropical Medicine
Peter W. Horby: University of Oxford
Sahr M. Gevao: National Safe Blood Service, Ministry of Health and Sanitation
Foday Sahr: University of Sierra Leone
Richard J. Dimelow: GlaxoSmithKline
Richard S. Tedder: University of Liverpool
Malcolm G. Semple: University of Liverpool
William A. Paxton: University of Liverpool
Georgios Pollakis: University of Liverpool

Nature, 2021, vol. 590, issue 7846, 468-472

Abstract: Abstract Neutralizing antibody function provides a foundation for the efficacy of vaccines and therapies1–3. Here, using a robust in vitro Ebola virus (EBOV) pseudo-particle infection assay and a well-defined set of solid-phase assays, we describe a wide spectrum of antibody responses in a cohort of healthy survivors of the Sierra Leone EBOV outbreak of 2013–2016. Pseudo-particle virus-neutralizing antibodies correlated with total anti-EBOV reactivity and neutralizing antibodies against live EBOV. Variant EBOV glycoproteins (1995 and 2014 strains) were similarly neutralized. During longitudinal follow-up, antibody responses fluctuated in a ‘decay–stimulation–decay’ pattern that suggests de novo restimulation by EBOV antigens after recovery. A pharmacodynamic model of antibody reactivity identified a decay half-life of 77–100 days and a doubling time of 46–86 days in a high proportion of survivors. The highest antibody reactivity was observed around 200 days after an individual had recovered. The model suggests that EBOV antibody reactivity declines over 0.5–2 years after recovery. In a high proportion of healthy survivors, antibody responses undergo rapid restimulation. Vigilant follow-up of survivors and possible elective de novo antigenic stimulation by vaccine immunization should be considered in order to prevent EBOV viral recrudescence in recovering individuals and thereby to mitigate the potential risk of reseeding an outbreak.

Date: 2021
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DOI: 10.1038/s41586-020-03146-y

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