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Viral Infections and Outbreaks Research / Infection Control and Ventilation · Journal article
The Journal of Immunology · July 28, 2026
Raises a question worth testing. It does not answer one.
This is an in vitro systems serology study showing that fever temperatures (40°C) impair EBOV neutralization but enhance effector functions (complement and Fc receptor-mediated activation) in antibodies from survivors and zoonotic-exposed individuals. The findings suggest a mechanistic hypothesis that fever may shift antibody responses away from neutralization toward innate effector pathways, but do not establish causation or clinical benefit.
Observational cohort study with in vitro systems serology. 60 survivors of the 2013–16 Ebola epidemic in Guinea; 81 individuals of pygmy ancestry in the Republic of Congo with frequent zoonotic exposures but no documented EBOV infection.. Intervention: In vitro exposure of sera to EBOV antigens (full-length GP, soluble glycoprotein sGP) at fever temperature (40°C) and physiologic temperature (37°C). Compared with: Physiologic temperature (37°C) versus fever temperature (40°C). n = 141. Guinea and the Republic of Congo.
Neutralization of EBOV is impaired under fever temperatures (40°C) in both affinity-matured and non-specific antibody responses Effector-mediated functions, particularly against EBOV soluble glycoprotein (sGP), are enhanced at febrile temperatures Temperature-sensitive enhancement of effector function correlates with full length GP and sGP-directed IgG subclasses, IgA, FcγR-binding and FcαR-binding antibodies
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The findings suggest that fever may modulate the balance between neutralizing and effector antibody functions during acute EBOV infection; however, the in vitro nature of the assays and lack of clinical outcome data mean this remains mechanistic and does not yet guide treatment or prevention strategies. Long-term clinical protection correlates require prospective follow-up or challenge studies.
An exploratory systems serology study characterizing temperature-dependent antibody function in vitro; raises mechanistic questions about fever and EBOV immunity but does not test clinical protection or provide causal evidence.
As stated by the source record.
Quoted from the source exactly as published.
The findings suggest that fever may modulate the balance between neutralizing and effector antibody functions during acute EBOV infection; however, the in vitro nature of the assays and lack of clinical outcome data mean this remains mechanistic and does not yet guide treatment or prevention strategies. Long-term clinical protection correlates require prospective follow-up or challenge studies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Abstract Introduction In 2013-16, Western Africa experienced the largest known outbreak of the highly lethal virus, Ebolavirus (EBOV) and ongoing sporadic outbreaks have occurred since. EBOV is the causative agent of EBOV hemorrhagic fever, characterized by a high-grade fever. Antibody responses to EBOV have been correlated with protection against EBOV disease. However, it is unclear how antibody functions result in protection from repeat exposure. Understanding antibody-mediated mechanisms of protection against Ebola infection is critical to maximize long-term protection against infection. Methods We utilize a systems serology approach to analyze a cohort of 60 survivors of the 2013-16 Ebola epidemic in Guinea and 81 individuals of pygmy ancestry in the Republic of Congo who did not have documented EBOV infection, but do experience frequent zoonotic exposures to characterize the impact of fever conditions on affinity matured EBOV-directed antibody responses. Antibody binding and cellular activation were measured at both physiologic (37C) and high grade fever (40C) temperatures. Results We show that neutralization of EBOV is impaired under fever temperatures, both for affinity-matured and non-specific antibody responses. In contrast, effector-mediated functions, particularly against the EBOV soluble glycoprotein (sGP, a signature previously linked to enhanced protection in animal vaccine challenge models), are enhanced at febrile temperatures. This temperature-sensitive enhancement of effector function correlates with full length GP and sGP-directed IgG subclasses, IgA, FcγR-binding- and FcαR-binding antibodies, demonstrating a highly associated network of humoral features that are maintained during periods of febrile temperatures. Conclusion Collectively, our findings suggest that although neutralization plays a key role in surveillance in a non-fever state, fever modulates affinity-matured antibody responses to the hemorrhagic fever-inducing EBOV, moving antibody profiles to a pro-effector function phenotype. Funding Source NIH NIAID U19 AI135995 Topic Categories Viral Immunology (VIR)
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