Systemic toxicity of polyinosinic acid: Polycytidylic acid in rodents and dogs

Phillips, Barrie M.; Hartnagel, Ralph E.; Kraus, P.; Tamayo, Ruy Pérez; Fonseca, Emma H.; Kowalski, Robert L.

doi:10.1016/0041-008x(71)90330-9

Cited by 18 publications

(3 citation statements)

References 3 publications

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“…Because of this immunomodulation, Poly I:C has long been considered as a potential adjuvant to therapeutic strategies, including those for cancer. However, dissociation of its toxicity from therapeutic efficacy has been a challenge for its clinical application [ 182 ]. In recent years, it has been investigated against CHIKV and shown to inhibit CHIKV-induced CPE in human bronchial epithelial cells, as well as virus titers in infected cells.…”

Section: Host-targeting Antiviralsmentioning

confidence: 99%

Current Strategies for Inhibition of Chikungunya Infection

Subudhi

Chattopadhyay

Mishra

et al. 2018

Viruses

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Increasing incidences of Chikungunya virus (CHIKV) infection and co-infections with Dengue/Zika virus have highlighted the urgency for CHIKV management. Failure in developing effective vaccines or specific antivirals has fuelled further research. This review discusses updated strategies of CHIKV inhibition and provides possible future directions. In addition, it analyzes advances in CHIKV lifecycle, drug-target development, and potential hits obtained by in silico and experimental methods. Molecules identified with anti-CHIKV properties using traditional/rational drug design and their potential to succeed in subsequent stages of drug development have also been discussed. Possibilities of repurposing existing drugs based on their in vitro findings have also been elucidated. Probable modes of interference of these compounds at various stages of infection, including entry and replication, have been highlighted. The use of host factors as targets to identify antivirals against CHIKV has been addressed. While most of the earlier antivirals were effective in the early phases of the CHIKV life cycle, this review is also focused on drug candidates that are effective at multiple stages of its life cycle. Since most of these antivirals require validation in preclinical and clinical models, the challenges regarding this have been discussed and will provide critical information for further research.

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Section: Host-targeting Antiviralsmentioning

confidence: 99%

Current Strategies for Inhibition of Chikungunya Infection

Subudhi

Chattopadhyay

Mishra

et al. 2018

Viruses

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“…rC] or its stabilized analogs that dsRNA induce flu-like sym ptom s (4,14,18,(37)(38)(39)(40)(41) and num erous elements of the APR characteristic of a viral infection. (42) Fever, chills, nausea, vomiting, and myalgias are seen even at doses of poly[rI?…”

Section: Systemic Toxicity Of and Cytokine Induction By Dsrnamentioning

confidence: 99%

Viral Double-Stranded RNA, Cytokines, and the Flu

Majde¹

2000

Journal of Interferon & Cytokine Research

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The symptoms of the flu, such as fever, drowsiness, and malaise, are the sole means by which this common clinical syndrome is defined. The syndrome is usually the first clinical manifestation of both acute bacterial and viral infections. In the case of acute bacterial infections, several proinflammatory cytokines induced by bacterial products have been implicated as the causative agents of the flu syndrome. Viruses induce similar cytokines to bacteria, plus substantial amounts of interferon-alpha (IFN-alpha), although the direct association of these cytokines with the viral flu syndrome is less clear. Furthermore, the viral inducer(s) of cytokines has not been defined. The best candidate cytokine inducer associated with a majority of viral infections is virus-associated double-stranded RNA (dsRNA). This review examines the essential physical properties of toxic dsRNA, the cytokines induced by it, its viral and cellular sources, evidence for its presence in infected cells, its quantities in normal and infected cells, its cytotoxic mechanisms, and its cell-penetration properties. Toxic effects of viruses and dsRNA are compared. Energetics and extraction artifact issues are also discussed. Whereas most research on dsRNA toxicity has employed synthetic dsRNA, studies with virus-associated dsRNA are featured when available. Finally, a model for how viral dsRNA might initiate systemic disease is presented.

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“…However, its high to)~ieity appears to preclude the e~tensive use of this substance in man (6,10,11,12).…”

Section: Introductionmentioning

confidence: 99%

The protective effect of the interferon inducers tilorone hydrochloride and poly I?C on experimental tick-borne encephalitis in mice

Hofmann

Kunz

1972

Archiv f Virusforschung

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SummaryTilorone HC1 induced interferon in the serum of mice thus affording protection against fatal TBE when given 24 hours prior to infection and in a dose of 200 rag/ kg mouse. After application of a lower dose (50 mg/kg mouse) mice succumbed to the infection but had a slightly longer survivM time than untreated controls.Tilorone HC1 was also used in combination with Poly I : C. The latter was given 3 hours after infection i. e. at a time, when the Tilorone HCl-induced serum interferon already decreased. Thus, a second peak of interferon was demonstrated, which was only slightly higher than that in non-Tilorone HC1 treated control mice. However, the combined application of low doses of both interferon inducers did not show any advantage over the single application as far as rates and time of survival of mice were concerned.

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Systemic toxicity of polyinosinic acid: Polycytidylic acid in rodents and dogs

Cited by 18 publications

References 3 publications

Current Strategies for Inhibition of Chikungunya Infection

Current Strategies for Inhibition of Chikungunya Infection

Viral Double-Stranded RNA, Cytokines, and the Flu

The protective effect of the interferon inducers tilorone hydrochloride and poly I?C on experimental tick-borne encephalitis in mice

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