Argentine Hemorrhagic Fever: A Primate Model

Weissenbacher, Mercedes; Calello, Miguel A.; Colillas, O. J.; Rondinone, S N; Frigerio, M. J.

doi:10.1159/000149059

Cited by 51 publications

(28 citation statements)

References 4 publications

(4 reference statements)

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“…Mortality is 100% and animals exhibit anemia, leukopenia and thrombocytopenia, multiple hemorrhages and marked meningoencephalitis with extensive brain necrosis and demyelinization. Virus can be isolated in high titers from blood, brain and hemopoietic tissue, and JV antigens can be shown in those organs (91).…”

Section: Studies With the Xj Prototype Strain In Guinea Figs And Primmentioning

confidence: 99%

Epidemiology of argentine hemorrhagic fever

1988

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Present knowledge points to horizontal transmission as the most significant mechanism for Junín virus maintenance in the main natural reservoirs, namely Calomys musculinus and Calomys laucha. The existence of naturally infected Akodon azarae, both within and outside the endemic area, as well as the finding that other species, ecologically and phylogenetically related to the main reservoirs, such as Akodon molinae and Calomys callidus, can experimentally develop persistent infections with virus shedding through fauces, suggest a potential role for these cricetids as alternative reservoirs. Furthermore, since those rodents inhabit the borders of the area in which Argentine Hemorrhagic fever is endemic, the risk of spread of this area is to be expected. Whether the establishment of Junín virus persistence in Calomys musculinus and other reservoirs depends on viral or host factors, such as a selective defect in L3T4+ lymphocytes as recently shown for mice, remains to be explored.

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Section: Studies With the Xj Prototype Strain In Guinea Figs And Primmentioning

confidence: 99%

Epidemiology of argentine hemorrhagic fever

1988

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“…Guinea pigs (7,17,25), marmosets (5,22), and rhesus macaques (6,15,16) have been shown to be useful models for studying issues related to the pathogenesis of AHF. Recently, ribavirin (1--D-ribofuranosyl-1,2,4-triazole-3-carboxyamide), a broad-spectrum antiviral compound with significant activity in vitro and in vivo against a variety of viruses that cause hemorrhagic fever syndromes in humans, was evaluated for its therapeutic efficacy in guinea pigs infected with Junin virus (12).…”

mentioning

confidence: 99%

Ribavirin prophylaxis and therapy for experimental argentine hemorrhagic fever

McKee

Huggins

Trahan

et al. 1988

Antimicrob Agents Chemother

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Junin virus-infected rhesus macaques received prophylactic and therapeutic ribavirin to assess the potential of this drug for treating humans with Argentine hemorrhagic fever. When ribavirin was administered intramuscularly at the time of experimental infection with the lethal P3790 strain of Junin virus, all animals were protected from clinical disease. A delay in the initiation of therapy until after the onset of illness resulted in improvement and resolution of systemic signs of disease; however, survivors subsequently developed a late-onset central nervous system infection which was fatal in two of three animals. Side effects of ribavirin included thrombocytosis and severe anemia, both of which resolved promptly on withdrawal of drug therapy. Results of this study suggest that ribavirin may prove useful in treating humans with Argentine hemorrhagic fever.

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“…As a result, there have been models developed using a range of NHPs and viruses, for example, models based on wild-type Ebola virus or Marburg virus infection of the common marmoset or Simian hemorrhagic fever virus infection of rhesus macaques [16,17]. Junin infection of NHPs also results in a fatal disease which imitates natural infection in humans [18]. Therefore NHPs can be successfully used to create appropriate VHF models for filoviruses and arenaviruses.…”

Section: Host Cytokine Response To Vhfsmentioning

confidence: 99%

Cytokines and Viral Hemorrhagic Fever: Potential for Therapeutic Intervention

2015

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The recent Ebola outbreak in West Africa highlights the need to improve our understanding of why viral hemorrhagic fevers (VHFs) are so devastating. There is a requirement to generate effective prophylactics, such as vaccines, and therapies, especially those that are effective postsymptomatically. For a range of pathogens, it appears that overstimulation of pro-inflammatory cytokines, the 'cytokine storm', causes serious immunopathology in patients. In this review, we will focus on the cytokine response following infection by representatives of the viruses which can cause VHF: Ebola virus and Marburg virus, Crimean-Congo hemorrhagic fever virus, Dengue virus, Junin and Lassa virus. Specifically, the role of the cytokine storm in causing VHF and the use of therapeutic immunomodulatory compounds to help treat these fatal and debilitating diseases will be explored.

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Argentine Hemorrhagic Fever: A Primate Model

Cited by 51 publications

References 4 publications

Epidemiology of argentine hemorrhagic fever

Epidemiology of argentine hemorrhagic fever

Ribavirin prophylaxis and therapy for experimental argentine hemorrhagic fever

Cytokines and Viral Hemorrhagic Fever: Potential for Therapeutic Intervention

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