The Production of Fever by Influenzal Viruses

Wagner, Robert R.; Bennett, Ivan L.; LeQuire, Virgil S.

doi:10.1084/jem.90.4.321

Cited by 47 publications

(15 citation statements)

References 12 publications

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“…Limited heating destroyed infectivity without affecting pyrogenicity (Wagner et al, 1949) indicating, as in our studies, that virion components are involved. Physical and chemical treatments of myxo-and paramyxoviruses have suggested that the HA (Kanoh & Kawasaki, 1966), lipid (Siegert & Braune, 1964 and carbohydrate (Atkins & Bodel, 1974) and other host- derived components of the virion (Brand & Liew, 1983) may be involved in pyrogenicity.…”

Section: Discussionsupporting

confidence: 84%

Influenza virus pyrogenicity: central role of structural orientation of virion components and involvement of viral lipid and glycoproteins

Pickering¹,

Smith

Sweet³

1992

Journal of General Virology

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Ultraviolet light-inactivated, non-infectious influenza virus is pyrogenic; virion components are probably responsible for this pyrogenicity. To try to identify the pyrogenic component, influenza virions were disrupted with either bromelain or sodium deoxycholate (DOC). Treatment of infectious virions with bromelain, under conditions that removed the surface glycoproteins (spikes), destroyed their pyrogenicity. The supernatant, containing non-aggregated and modified glycoproteins, was also non-pyrogenic. Disruption ofvirions with DOC considerably reduced pyrogenicity; however, some was retained by the sub-viral cores. Viral nucleoprotein and matrix protein, purified from the supernatant, were non-pyrogenic. Aggregated stellate clusters of surface glycoproteins separated on sucrose gradients were pyrogenic in half of numerous tests performed with different batches of material. Treatment of virus with ether resulted in complete loss of pyrogenicity. Liposomes made from extracted viral lipid were non-pyrogenic. In contrast, virosomes made from the viral lipid and the aggregated stellate clusters of surface glycoproteins were pyrogenic. Hence, optimum pyrogenicity depends upon the integrity of the virus particle, but haemagglutinin and/or neuraminidase appear essential, and lipid may be involved.

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Section: Discussionsupporting

confidence: 84%

Influenza virus pyrogenicity: central role of structural orientation of virion components and involvement of viral lipid and glycoproteins

Pickering¹,

Smith

Sweet³

1992

Journal of General Virology

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“…The complete inhibition of the pyrogenic effect of the virus by in vitro incubation with homologous immune sera was confirmed (16). However, neither the normal nor the tolerant sera modified the pyrogenicity of the virus (see Fig.…”

Section: 0-mentioning

confidence: 84%

Studies on the Pathogenesis of Fever With Influenzal Viruses

Atkins

Huang

1958

The Journal of Experimental Medicine

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Tolerance to the pyrogenic action of intravenously injected virus has been studied in rabbits given either PR8 strain of influenza A virus or Newcastle disease virus (NDV). The following findings suggest that the capacity of the animal to release an endogenous pyrogen is a critical factor. (a) Viruses produce fever by the release of endogenous pyrogen. (b) Tolerance to the pyrogenic effect of reinjected virus is associated with a decrease or absence of endogenous pyrogen production. (c) Tolerance to virus fever may be induced by the prior injection of endogenous pyrogen. (d) Cross-tolerance has been demonstrated between virus and bacterial endotoxin (typhoid vaccine), both of which cause the release of endogenous pyrogen. A difference has been noted in the mechanism of tolerance to successive injections of virus and of bacterial endotoxin. Repeated injections of endotoxins bring about an accelerated clearance of these substances from the blood stream with the result that there is a diminished stimulus to endogenous pyrogen production. Tolerance to virus, on the other hand, is unaccompanied by changes in the rate at which virus disappears from the circulation. It is postulated that circulating endogenous pyrogen, induced by the injection of a number of pyrogenic agents including viruses, temporarily suppresses the further release of endogenous pyrogen and thereby contributes to virus tolerance.

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“…There are important biochemical differences in the pyrogenic agents themselves and also in the fevers resulting from an injection of virus and bacterial endotoxin (9,10). Similarly, the rapid, transient fall in circulating polymorphonuclear leukocytes after injection of endotoxin (1, 2) is unlike the slower but more sustained lymphopenia which is produced by virus (9,17). The significance of changes in circulating cells in the pathogenesis of fever with either of these agents has not, however, been established with certainty.…”

Section: Discussionmentioning

confidence: 99%

“…The development of lymphopenia coincides closely with the rise in temperature, both being maximal at about 4 hours after inoculation of the virus. There is no consistent change in the number of polymorphonuclear leukocytes (9,17).…”

Section: Attempt To Produce Endogeneou~ P Yrogen By In Vitro Teckniqumentioning

confidence: 98%

“…Tolerance to the pyrogenic effect of the virus is much more rapidly acquired, appearing with some viruses after a single inoculation. These features of the febrile response as well as certain distinctive properties of virus as a pyrogenic agent have led previous investigators to conclude that there is a fundamental difference in the pathogenesis of fever following the injection of viruses and bacterial endotoxins (9,10).…”

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confidence: 99%

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Studies on the Pathogenesis of Fever With Influenzal Viruses

Atkins

Huang

1958

The Journal of Experimental Medicine

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A substance with pyrogenic properties appears in the blood streams of rabbits made febrile by the intravenous inoculation of the PR8 strain of influenza A and Newcastle disease viruses (NDV). By means of a technique involving passive transfer of sera from animals given virus to recipient rabbits, the titer of circulating pyrogen was found to be closely correlated with the course of fever produced by virus. Certain properties of the pyrogen are described which differentiate it from the originally injected virus and suggest that the induced pyrogen is of endogenous origin. These properties resemble those of endogenous pyrogens occurring in other forms of experimental fever. The source of virus-induced pyrogen is unknown. In vitro incubation of virus with various constituents of the circulation did not result in the appearance of endogenous pyrogen. Granulocytopenia induced by HN2 failed to influence either fever or the production of endogenous pyrogen in rabbits injected with NDV. Similarly, the intraperitoneal inoculation of NDV into prepared exudates did not modify the febrile response. These findings do not lend support to the possibility that the polymorphonuclear leukocyte is a significant source of endogenous pyrogen in virus-induced fever. It is concluded that the liberation of an endogenous pyrogen from some as yet undefined source is an essential step in the pathogenesis of fever caused by the influenza group of viruses.

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The Production of Fever by Influenzal Viruses

Cited by 47 publications

References 12 publications

Influenza virus pyrogenicity: central role of structural orientation of virion components and involvement of viral lipid and glycoproteins

Influenza virus pyrogenicity: central role of structural orientation of virion components and involvement of viral lipid and glycoproteins

Studies on the Pathogenesis of Fever With Influenzal Viruses

Studies on the Pathogenesis of Fever With Influenzal Viruses

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