Increased Tumor Necrosis Factor-  Levels in Argentine Hemorrhagic Fever

Heller, Michel; Saavedra, María C.; Falcoff, R.; Maiztegui, Julio I.; Molinas, Felisa C.

doi:10.1093/infdis/166.5.1203

Cited by 59 publications

(42 citation statements)

References 2 publications

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“…Consistent with published data, this group also had elevated serum levels of TNF-␣. 10 These data, together with the significant correlations found between the levels of the cytokines and TNF-␣, substantiate the activation of pro-inflammatory and anti-inflammatory cytokine pathways in these patients. In addition, levels of two acute-phase proteins, fibrinogen and von Willebrand factor, have also been reported to be increased in patients with AHF.…”

Section: Discussionsupporting

confidence: 60%

See 1 more Smart Citation

Proinflammatory cytokines and elastase-alpha-1-antitrypsin in Argentine hemorrhagic fever.

Marta

Montero²,

Hack³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Section: Discussionsupporting

confidence: 60%

“…8,9 We have previously shown that increased levels of tumor necrosis factor-␣ (TNF-␣) in AHF patients were related to disease severity. 10 In contrast, circulating levels of interleukin-1␤ (IL-1␤) were not detected in these patients.…”

mentioning

confidence: 90%

Proinflammatory cytokines and elastase-alpha-1-antitrypsin in Argentine hemorrhagic fever.

Marta

Montero²,

Hack³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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“…It has been reported that during JUNV infection, macrophages and dendritic cells are the initial sites of viral replication (9,27) and are involved in spreading the virus to other tissues (36). It has been suggested that this initial infection of macrophages might be responsible for the source of the elevated cytokine levels seen during Junín virus infection (30,37,39). Indeed, we showed here that Candid 1 induced production of IFN-␤ and TNF-␣ and that this induction was strongest between 2 and 4 hpi.…”

Section: Discussionsupporting

confidence: 57%

Junín Virus Infects Mouse Cells and Induces Innate Immune Responses

Cuevas

Lavanya

Wang

et al. 2011

J Virol

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Junín virus is the causative agent for Argentine hemorrhagic fever, and its natural host is the New World rodent Calomys musculinus. The virus is transmitted to humans by aerosolization, and it is believed that many of the clinical symptoms are caused by cytokines produced by sentinel cells of the immune system. Here we used the Junín virus vaccine strain Candid 1 to determine whether mouse cells could be used to study virus entry and antiviral innate immune responses. We show that Candid 1 can infect and propagate in different mousederived cell lines through a low-pH-dependent, transferrin receptor 1-independent mechanism, suggesting that there is a second entry receptor. In addition, Candid 1 induced expression of the antiviral cytokines tumor necrosis factor alpha and beta interferon in macrophages, and this induction was independent of viral replication. Using Candid 1, as well as virus-like particles bearing the viral glycoprotein, to infect different primary cells and established macrophage cell lines with deletions in the Toll-like receptor (TLR) pathway, we show that TLR2 is a cellular sensor of both the Parodi and Candid 1 viral glycoproteins. Because Junín virus is highly lethal in humans, the use of an experimentally tractable model system, such as the mouse, could provide a better understanding of the antiviral innate cellular responses to Junín virus and the role of these responses in pathogenesis.

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“…Elevated levels of mediators, including TNF-␣, were detected in the acute-phase sera of several EBOV-infected patients (35) and in infected animals (17). Increased TNF-␣ values were found to correlate with the severity of Junin virus infections causing Argentine hemorrhagic fever (16). Therefore, it seems reasonable to assume that massive cytokine release triggered by filovirus-induced activation of mononuclear phagocytic cells may induce a systemic inflammatory response syndrome, which can be provoked by cytokine treatment and can be observed during endotoxin-induced shock (1, 4).…”

Section: Discussionmentioning

confidence: 93%

Infection and Activation of Monocytes by Marburg and Ebola Viruses

Ströher

West

Bugany

et al. 2001

J Virol

217

211

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In this study we investigated the effects of Marburg virus and Ebola virus (species Zaire and Reston) infections on freshly isolated suspended monocytes in comparison to adherent macrophages under culture conditions. Our data showed that monocytes are permissive for both filoviruses. As is the case in macrophages, infection resulted in the activation of monocytes which was largely independent of virus replication. The activation was triggered similarly by Marburg and Ebola viruses, species Zaire and Reston, as indicated by the release of the proinflammatory cytokines interleukin-1␤ (IL-1␤), tumor necrosis factor ␣, and IL-6 as well as the chemokines IL-8 and gro-␣. Our data suggest that infected monocytes may play an important role in the spread of filoviruses and in the pathogenesis of filoviral hemorrhagic disease.

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Increased Tumor Necrosis Factor- Levels in Argentine Hemorrhagic Fever

Cited by 59 publications

References 2 publications

Proinflammatory cytokines and elastase-alpha-1-antitrypsin in Argentine hemorrhagic fever.

Proinflammatory cytokines and elastase-alpha-1-antitrypsin in Argentine hemorrhagic fever.

Junín Virus Infects Mouse Cells and Induces Innate Immune Responses

Infection and Activation of Monocytes by Marburg and Ebola Viruses

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