Antibody neutralization of picornaviruses: can fever help?

Boeyé, Albert; Delaet, Ingrid; Brioen, Paul

doi:10.1016/0966-842x(94)90631-9

Cited by 6 publications

(4 citation statements)

References 26 publications

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“…At higher than physiologic temperatures, binding of bivalent antibody can neutralize picornaviruses by irreversibly neutralizing the virus through disruption of the virion, which leads to ejection of RNA. Fever enhances this process in vivo, confirming the popular belief in the virtues of fever [140].…”

Section: Some Immunological Aspectssupporting

confidence: 62%

Fever, Cancer Incidence and Spontaneous Remissions

Kleef

Jonas

Knogler³

et al. 2001

Neuroimmunomodulation

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Objective: Accumulating evidence exists for (1) an inverse correlation between the incidence of infectious diseases and cancer risk and (2) an inverse correlation between febrile infections and remissions of malignancies. This review is part of an effort of the Office of Alternative Medicine at the National Institutes of Health to examine this evidence. Methods: A review of the literature to a key word search was undertaken, using the following key words: fever, infectious diseases, neoplasm, cancer incidence and spontaneous remission. Results: The data reviewed in this article support earlier observations on the topic, i.e. that the occurrence of fever in childhood or adulthood may protect against the later onset of malignant disease and that spontaneous remissions are often preceded by feverish infections. Conclusion: Pyrogenic substances and the more recent use of whole-body hyperthermia to mimic the physiologic response to fever have successfully been administered in palliative and curative treatment protocols for metastatic cancer. Further research in this area is warranted.

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Section: Some Immunological Aspectssupporting

confidence: 62%

Fever, Cancer Incidence and Spontaneous Remissions

Kleef

Jonas

Knogler³

et al. 2001

Neuroimmunomodulation

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“…Additionally, heat stimulates T cell helper function, resulting in enhanced antibody synthesis by murine B cells (Jampel et al, 1983). Thermal stress enables some antibodies to irreversibly neutralize specific viruses (i.e., to have viricidal activity) (Boeye et al, 1994;Delaet and Boeye, 1993). Exposure of lymphocytes to fever-range thermal stress alters the intracellular organization, expression, or activation status of cytoskeletal proteins (i.e., spectrin), heat shock proteins (hsp70 family), and signal M.…”

Section: Fever-range Thermal Effects On Immune Activationmentioning

confidence: 97%

Impact of Fever-Range Thermal Stress on Lymphocyte-Endothelial Adhesion and Lymphocyte Trafficking

Appenheimer

Chen

Girard

et al. 2005

Immunological Investigations

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The evolutionarily conserved febrile response has been associated with improved survival during infection in endothermic and ectothermic species although its protective mechanism of action is not fully understood. Temperatures within the range of physiologic fever influence multiple parameters of the immune response including lymphocyte proliferation and cytotoxic activity, neutrophil and dendritic cell migration, and production or bioactivity of proinflammatory cytokines. This review focuses on the emerging role of fever-range thermal stress in promoting lymphocyte trafficking to secondary lymphoid organs that are major sites for launching effective immune responses during infection or inflammation. Specific emphasis will be on the molecular basis of thermal control of lymphocyte-endothelial adhesion, a critical checkpoint controlling lymphocyte extravasation, as well as the contribution of interleukin-6 (IL-6) trans-signaling to thermal activities. New results are presented indicating that thermal stimulation of lymphocyte homing potential is evident in evolutionarily distant endothermic vertebrate species. These observations support the view that the evolutionarily conserved febrile response contributes to immune protection and host survival by amplifying lymphocyte access to peripheral lymphoid organs.

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“…Fig. 24 shows that similar doses of human and mouse IL-1f3 competitively inhibited the binding of human 125I-IL-1 3 higher affinity for the mouse cytokine ( Fig. 2A).…”

Section: Imentioning

confidence: 99%

“…Temperature elevation during fever constitutes a component of host defense that increases host survival and enhances different arms of the inflammatory and immune responses, such as T-cell proliferation and differentiation, secretion of interferons (IFNs), neutrophil migration, and the neutralizing capacity of antibodies (1)(2)(3). Fever may also have detrimental effects in some circumstances (1,2).…”

mentioning

confidence: 99%

A mechanism for the inhibition of fever by a virus.

Alcamı́

Smith

1996

Proc. Natl. Acad. Sci. U.S.A.

140

107

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Poxviruses encode proteins that block the activity of cytokines. Here we show that the study of such virulence factors can contribute to our understanding of not only virus pathogenesis but also the physiological role of cytokines. Fever is a nonspecific response to infection that contributes to host defense. Several cytokines induce an elevation of body temperature when injected into animals, but in naturally occurring fever it has been difficult to show that any cytokine has a critical role. We describe the first example of the suppression of fever by a virus and the molecular mechanism leading to it. Several vaccinia virus strains including smallpox vaccines express soluble interleukin 1 (IL-1) receptors, which bind IL-1p but not IL-la. These viruses prevent the febrile response in infected mice, whereas strains that naturally or through genetic engineering lack the receptor induce fever. Repair of the defective IL-18 inhibitor in the smallpox vaccine Copenhagen, a more virulent virus than the widely used vaccine strains Wyeth and Lister, suppresses fever and attenuates the disease. The vaccinia-induced fever was inhibited with antibodies to IL-lp. These findings provide strong evidence that IL-118, and not other cytokines, is the major endogenous pyrogen in a poxvirus infection. cies of postvaccinial complications, but the reasons are unknown (6).Poxviruses encode many proteins that interfere with host immune functions (7,8), such as soluble cytokine receptors that blockade cytokines and modulate virus virulence (9). The VV IL-1,B receptor (vIL-103R) is encoded by gene B15R in the Western Reserve (WR) strain (10), and binds IL-1l3 with high affinity, but not IL-la or IL-1 receptor antagonist (11). Inactivation of the B15R gene from VV WR decreases virus virulence in mice after intracranial injection (12) but enhances virus virulence when administered intranasally (11). These contradictory results might be explained by either deletion mutant virus having additional mutations affecting virus virulence or, alternatively, may reflect the properties of IL-ll3, a cytokine that induces beneficial effects but is detrimental when produced in large amounts (13). Since a natural route of poxvirus infections is the respiratory tract (4), the vIL-lf3R may function to prevent the adverse effects of excessive IL-1,B.Here we report that the WR vIL-lf3R prevents the febrile response in intranasally infected mice. In this model, smallpox vaccine strains lacking the vIL-lf3R induced fever, and repair of the nonfunctional vIL-l,BR in strain Copenhagen prevented fever and attenuated virus virulence.Fever is an ancient nonspecific systemic response to infection, which is conserved in both invertebrates and vertebrates (1). Temperature elevation during fever constitutes a component of host defense that increases host survival and enhances different arms of the inflammatory and immune responses, such as T-cell proliferation and differentiation, secretion of interferons (IFNs), neutrophil migration, and the neutralizing capa...

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Antibody neutralization of picornaviruses: can fever help?

Cited by 6 publications

References 26 publications

Fever, Cancer Incidence and Spontaneous Remissions

Fever, Cancer Incidence and Spontaneous Remissions

Impact of Fever-Range Thermal Stress on Lymphocyte-Endothelial Adhesion and Lymphocyte Trafficking

A mechanism for the inhibition of fever by a virus.

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