Ebola virus infection in guinea pigs: presumable role of granulomatous inflammation in pathogenesis

Ryabchikova, E. I.; Колесникова, Л. И.; Smolina, M.; Ткачев, В. В.; Pereboeva, Larisa; Баранова, С Г; Гражданцева, А. А.; Rassadkin, Yu. N.

doi:10.1007/bf01718165

Cited by 97 publications

(108 citation statements)

References 15 publications

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“…This evidence suggests that hepatocyte apoptosis occurs during EBOV infection. Necrotic hepatocytes were also observed (data not shown), confirming earlier reports (6,(23)(24)(25).…”

Section: Indication Of Ebov-induced Hepatocyte Apoptosissupporting

confidence: 91%

“…Severe liver dysfunction is a hallmark of lethal EBOVinfection, as evidenced by hepatocyte death and accumulation of the liver enzymes ASTand ALTin theblood (15)(16)(17). Hepatocyte necrosis has been described in EBOV infection and may be a direct consequence of extensive viral replication in these cells (6,(23)(24)(25). However, apoptotic cell death of hepatocytes in EBOVinfected mice has not been reported.…”

Section: Indication Of Ebov-induced Hepatocyte Apoptosismentioning

confidence: 99%

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Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Bradfute

Swanson

Smith

et al. 2009

The Journal of Immunology

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Ebolavirus (EBOV) is a member of the filovirus family and causes severe hemorrhagic fever, resulting in death in up to 90% of infected humans. EBOV infection induces massive bystander lymphocyte apoptosis; however, neither the cellular apoptotic pathway(s) nor the systemic implications of lymphocyte apoptosis in EBOV infection are known. In this study, we show data suggesting that EBOV-induced lymphocyte apoptosis in vivo occurs via both the death receptor (extrinsic) and mitochondrial (intrinsic) pathways, as both Fas-associated death domain dominant negative transgenic mice and mice overexpressing bcl-2 were resistant to EBOV-induced lymphocyte apoptosis. Surprisingly, inhibiting lymphocyte apoptosis during EBOV infection did not result in improved animal survival. Furthermore, we show for the first time that hepatocyte apoptosis likely occurs in EBOV infection, and that mice lacking the proapoptotic genes Bim and Bid had reduced hepatocyte apoptosis and liver enzyme levels postinfection. Collectively, these data suggest that EBOV induces multiple proapoptotic stimuli and that blocking lymphocyte apoptosis is not sufficient to improve survival in EBOV infection. These data suggest that hepatocyte apoptosis may play a role in the pathogenesis of EBOV infection, whereas lymphocyte apoptosis appears to be nonessential for EBOV disease progression.

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“…This evidence suggests that hepatocyte apoptosis occurs during EBOV infection. Necrotic hepatocytes were also observed (data not shown), confirming earlier reports (6,(23)(24)(25).…”

Section: Indication Of Ebov-induced Hepatocyte Apoptosissupporting

confidence: 91%

Section: Indication Of Ebov-induced Hepatocyte Apoptosismentioning

confidence: 99%

Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Bradfute

Swanson

Smith

et al. 2009

The Journal of Immunology

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“…Guinea pigs inoculated with wild-type EBOV develop only a short-lived, nonlethal febrile illness Bowen et al, 1980;Ryabchikova et al, 1996). A lethal guinea pig model for EBOV infection was developed eventually by infecting inbred and outbred guinea pig strains with ZEBOV, followed by sequential passages (4-8 times) of virus in naïve guinea pigs Bowen et al, 1980;Conolly et al, 1999;Ryabchikova et al, 1996) (Table 1).…”

Section: Guinea Pig Modelsmentioning

confidence: 99%

Disease modeling for Ebola and Marburg viruses

Bente

Gren

Strong

et al. 2009

Disease Models &Amp; Mechanisms

158

143

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The filoviruses Ebola and Marburg are zoonotic agents that are classified as both biosafety level 4 and category A list pathogens. These viruses are pathogenic in humans and cause isolated infections or epidemics of viral hemorrhagic fever, mainly in Central Africa. Their natural reservoir has not been definitely identified, but certain species of African bat have been associated with Ebola and Marburg infections. Currently, there are no licensed options available for either treatment or prophylaxis. Different animal models have been developed for filoviruses including mouse, guinea pig and nonhuman primates. The ‘gold standard’ animal models for pathogenesis, treatment and vaccine studies are rhesus and cynomolgus macaques. This article provides a brief overview of the clinical picture and the pathology/pathogenesis of human filovirus infections. The current animal model options are discussed and compared with regard to their value in different applications. In general, the small animal models, in particular the mouse, are the most feasible for high biocontainment facilities and they offer the most options for research owing to the greater availability of immunologic and genetic tools. However, their mimicry of the human diseases as well as their predictive value for therapeutic efficacy in primates is limited, thereby making them, at best, valuable initial screening tools for pathophysiology, treatment and vaccine studies.

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“…While rodents clearly have utility as models of filoviral disease, we recently showed that rodent models of EBOV HF are not ideal for studying human EBOV HF ; others have suggested that guinea pigs are inadequate for analyzing the pathogenesis of human EBOV HF (Ryabchikova et al, 1996). More specifically, neither mice nor guinea pigs exhibit the hemorrhagic manifestations that characterize primate EBOV infections.…”

Section: Introductionmentioning

confidence: 99%

Filovirus Pathogenesis in Nonhuman Primates

Geisbert¹,

Jahrling²,

Larsen³

et al. 2002

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information including suggestionsfor reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway Suile1204 Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Project (0704-0188), Washington, DC 20503.

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Ebola virus infection in guinea pigs: presumable role of granulomatous inflammation in pathogenesis

Cited by 97 publications

References 15 publications

Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Mechanisms and Consequences of Ebolavirus-Induced Lymphocyte Apoptosis

Disease modeling for Ebola and Marburg viruses

Filovirus Pathogenesis in Nonhuman Primates

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