Efficacy of Coxiella burnetii and its chloroform-methanol residue (CMR) fraction against Rift Valley fever virus infection in mice

Zvilich, Menachem; Williams, Jim C.; Waag, David M.; Rill, Wayne R.; Bell, Paul; Kende, Meir

doi:10.1016/0166-3542(95)00003-5

Cited by 4 publications

(1 citation statement)

References 28 publications

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“…In the late 1970s, a role for inflammatory cytokines in viral disease was already plausible, since BCG, Corynebacterium parvum, and Coxiella burnetii, which were among the macrophage activators that protected mice against malaria (81,85,93) and helped formulate our thinking about the possible role of TNF in disease pathogenesis, had also been shown to protect against viruses in vivo (68,218,379,450). Another observation that defied a traditional explanation, but suited one based on cytokines was that liver cells in which hepatitis B virus was replicating (as determined by immunohistochemistry and in situ hybridization) were not the ones that showed histological evidence of damage (43).…”

Section: Severe Viral Diseasesmentioning

confidence: 99%

Pathogenesis of Malaria and Clinically Similar Conditions

et al. 2004

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There is now wide acceptance of the concept that the similarity between many acute infectious diseases, be they viral, bacterial, or parasitic in origin, is caused by the overproduction of inflammatory cytokines initiated when the organism interacts with the innate immune system. This is also true of certain noninfectious states, such as the tissue injury syndromes. This review discusses the historical origins of these ideas, which began with tumor necrosis factor (TNF) and spread from their origins in malaria research to other fields. As well the more established proinflammatory mediators, such as TNF, interleukin-1, and lymphotoxin, the roles of nitric oxide and carbon monoxide, which are chiefly inhibitory, are discussed. The established and potential roles of two more recently recognized contributors, overactivity of the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) and the escape of high-mobility-group box 1 (HMGB1) protein from its normal location into the circulation, are also put in context. The pathogenesis of the disease caused by falciparum malaria is then considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself

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