Human Infection with Arenaviruses in the Americas

Peters, C. J.

doi:10.1007/978-3-642-56029-3_3

Cited by 135 publications

(152 citation statements)

References 42 publications

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“…Arenaviruses are attractive pathogens to investigate the mechanisms and possible application of lethal mutagenesis because of the very limited number of effective antiviral inhibitors available and the impact of arenavirus diseases on human health (Buchmeier et al, 2007;Macher & Wolfe, 2006;Peters, 2002). Administration of FU to mice impeded the establishment of a persistent infection with LCMV, an observation that constituted a proof-of-principle of the feasibility of a lethal mutagenesis approach in vivo (RuizJarabo et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

An interfering activity against lymphocytic choriomeningitis virus replication associated with enhanced mutagenesis

Martı́n

Abia

Domingo

et al. 2009

Journal of General Virology

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Previous studies have documented that, in the presence of the mutagenic base analogue 5-fluorouracil (FU), lymphocytic choriomeningitis virus (LCMV) that persisted in BHK-21 cells decreased its infectivity to a larger extent than intracellular viral RNA levels, prior to virus extinction. This observation, together with in silico simulations, led to the proposal of the lethal defection model of virus extinction. This model suggests the participation of defective-interfering genomes in the loss of infectivity by increased mutagenesis. Since LCMV naturally produces defective-interfering particles, it was important to show that a capacity to interfere is produced in association with FU treatment. Here, we document that BHK-21 cells persistently infected with LCMV grown in the presence of FU, but not in its absence, generated an interfering activity that suppressed LCMV infectivity. Interference was specific for LCMV and was sensitive to UV irradiation and its activity was dose-and time-dependent. The interfering preparations produced positive LCMV immunofluorescence and viral particles seen by electron microscopy when used to infect cells, despite some preparations being devoid of detectable infectivity. Interference did not involve significant increases of mutant spectrum complexity, as predicted by the lethal defection model. The results provide support for a specific interference associated with LCMV when the virus replicates in the presence of FU. The excess of interference relative to that observed in the absence of FU is necessary for LCMV extinction.

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Section: Introductionmentioning

confidence: 99%

An interfering activity against lymphocytic choriomeningitis virus replication associated with enhanced mutagenesis

Martı́n

Abia

Domingo

et al. 2009

Journal of General Virology

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“…First isolated during an outbreak in the San Joaquin region of northeast Bolivia, MACV is one of five reported South American arenaviruses capable of causing hemorrhagic disease in humans (8)(9)(10)(11)(12)(13). The other viruses include Junin virus (JUNV), Sabia virus (SABV), Guanarito virus (GTOV), and Chapare virus (CHPV).…”

mentioning

confidence: 99%

“…The other viruses include Junin virus (JUNV), Sabia virus (SABV), Guanarito virus (GTOV), and Chapare virus (CHPV). Machupo virus is the etiologic agent of Bolivian hemorrhagic fever (BHF), a disease clinically similar to Argentine hemorrhagic fever caused by JUNV (10,(13)(14)(15)(16)(17)(18)(19). The primary route of MACV exposure is believed to be through contact with aerosolized excretions and secretions from the rodent reservoir, Calomys callosus (9,20,21).…”

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confidence: 99%

Rescue of a Recombinant Machupo Virus from Cloned cDNAs and In Vivo Characterization in Interferon (αβ/γ) Receptor Double Knockout Mice

Patterson

Seregin

Huang

et al. 2014

J Virol

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Machupo virus (MACV) is the etiological agent of Bolivian hemorrhagic fever (BHF), a reemerging and neglected tropical disease associated with high mortality. The prototypical strain of MACV, Carvallo, was isolated from a human patient in 1963, but minimal in vitro and in vivo characterization has been reported. To this end, we utilized reverse genetics to rescue a pathogenic MACV from cloned cDNAs. The recombinant MACV (rMACV) had in vitro growth properties similar to those of the parental MACV. Both viruses caused similar disease development in alpha/beta and gamma interferon receptor knockout mice, including neurological disease development and high mortality. In addition, we have identified a novel murine model with mortality and neurological disease similar to BHF disease reported in humans and nonhuman primates.

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“…Arenaviruses are endemic to rodent populations, and zoonotic infection of humans can result in severe acute hemorrhagic fevers (43,49). Up to 300,000 infections by Lassa fever virus occur annually in Africa (44), and cases of Argentine, Bolivian, and Venezuelan hemorrhagic fevers are regularly reported in South America (49).…”

mentioning

confidence: 99%

“…Up to 300,000 infections by Lassa fever virus occur annually in Africa (44), and cases of Argentine, Bolivian, and Venezuelan hemorrhagic fevers are regularly reported in South America (49). Genetic diversification and worldwide dissemination of arenaviruses with their rodent hosts (51) provide opportunities for the continued emergence of new pathogenic strains (10).…”

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confidence: 99%

A Novel Zinc-Binding Domain Is Essential for Formation of the Functional Junín Virus Envelope Glycoprotein Complex

York

Nunberg

2007

J Virol

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The envelope glycoprotein of the Junín arenavirus (GP-C) mediates entry into target cells through a pHdependent membrane fusion mechanism. Unlike other class I viral fusion proteins, the mature GP-C complex retains a cleaved, 58-amino-acid signal peptide (SSP) as an essential subunit, required both for trafficking of GP-C to the cell surface and for the activation of membrane fusion. SSP has been shown to associate noncovalently in GP-C via the cytoplasmic domain (CTD) of the transmembrane fusion subunit G2. In this report we investigate the molecular basis for this intersubunit interaction. We identify an invariant series of six cysteine and histidine residues in the CTD of G2 that is essential for incorporation of SSP in the GP-C complex. Moreover, we show that a CTD peptide fragment containing His-447, His-449, and Cys-455 specifically binds Zn 2؉ at subnanomolar concentrations. Together, these results suggest a zinc finger-like domain structure in the CTD of G2. We propose that the remaining residues in the series (His-459, Cys-467, and Cys-469) form an intersubunit zinc-binding center that incorporates Cys-57 of SSP. This unusual motif may act to retain SSP in the GP-C complex and position the ectodomain loop of SSP for its role in modulating membrane fusion activity. The unique tripartite organization of GP-C could provide novel molecular targets for therapeutic intervention in arenaviral disease.

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Human Infection with Arenaviruses in the Americas

Cited by 135 publications

References 42 publications

An interfering activity against lymphocytic choriomeningitis virus replication associated with enhanced mutagenesis

An interfering activity against lymphocytic choriomeningitis virus replication associated with enhanced mutagenesis

Rescue of a Recombinant Machupo Virus from Cloned cDNAs and In Vivo Characterization in Interferon (αβ/γ) Receptor Double Knockout Mice

A Novel Zinc-Binding Domain Is Essential for Formation of the Functional Junín Virus Envelope Glycoprotein Complex

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