Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 222, Issue 9, Pages 1488-1497Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiaa268
Keywords
Ebola virus; post-Ebola sequelae; T-cell response
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Funding
- National Institute of Allergy and Infectious Diseases [HHSN272201400048C, BAA-NIAID-DAITNIHAI2013167]
- National Institutes of Health [1R01AI123535]
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Background. Ebola virus (EBOV) disease has killed thousands of West and Central Africans over the past several decades. Many who survive the acute disease later experience post-Ebola syndrome, a constellation of symptoms whose causative pathogenesis is unclear. Methods. We investigated EBOV-specific CD8(+) and CD4(+) T-cell responses in 37 Sierra Leonean EBOV disease survivors with (n = 19) or without (n = 18) sequelae of arthralgia and ocular symptoms. Peripheral blood mononuclear cells were infected with recombinant vesicular stomatitis virus encoding EBOV antigens. We also studied the presence of EBOV-specific immunoglobulin G, antinuclear antibodies, anti-cyclic citrullinated peptide antibodies, rheumatoid factor, complement levels, and cytokine levels in these 2 groups. Results. Survivors with sequelae had a significantly higher EBOV-specific CD8(+) and CD4(+) T-cell response. No differences in EBOV-specific immunoglobulin G, antinuclear antibody, or anti-cyclic citrullinated peptide antibody levels were found. Survivors with sequelae showed significantly higher rheumatoid factor levels. Conclusion. EBOV-specific CD8(+) and CD4(+) T-cell responses were significantly higher in Ebola survivors with post- Ebola syndrome. These findings suggest that pathogenesis may occur as an immune-mediated disease via virus-specific T-cell immune response or that persistent antigen exposure leads to increased and sustained T-cell responses.
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