Genetic Organization of Junin Virus, the Etiological Agent of Argentine Hemorrhagic Fever

Romanowski, Vı́ctor

doi:10.1007/978-1-4615-3028-2_4

Cited by 12 publications

(13 citation statements)

References 71 publications

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“…Our laboratory is conducting a study to evaluate the significance of these differences at the protein-RNA interaction level. At this point it might be recalled that N has been proposed to be the transcription anti-terminator and, therefore changes in its interaction with RNA might affect regulation of the transcription\replication process (Romanowski, 1993).…”

Section: G Albarin4 O and Others C G Albarin4 O And Othersmentioning

confidence: 99%

Molecular characterization of attenuated Junin virus strains.

Romanowski

Ghiringhelli²,

Albariño

et al. 1997

Journal of General Virology

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The Junin virus strain Candid F1 was developed as a live attenuated vaccine for Argentine haemorrhagic fever. In this paper we report the nucleotide sequences of S RNA of Candid F1 and its more virulent ancestors XJF44 and XJ (prototype). Their relationship to Junin virus wild-type MC2 strain and other closely and distantly related arenaviruses was also examined. Comparisons of the nucleotide and amino acid sequences of N and GPC genes from Candid F1 and its progenitor strains revealed some changes that are unique to the vaccine strain. These changes could be provisionally associated with the attenuated phenotype.

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Section: G Albarin4 O and Others C G Albarin4 O And Othersmentioning

confidence: 99%

Molecular characterization of attenuated Junin virus strains.

Romanowski

Ghiringhelli²,

Albariño

et al. 1997

Journal of General Virology

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“…Junin virus (JV), a member of the family Arenaviridae, is an enveloped RNA virus with a fragmented helicoidal nucleocapsid. The virion contains two major proteins: a nucleocapsid associated protein NP (MW 60 64 KD), an external glycoprotein GP38 (MW 38 KD, G1) and a minor glycoprotein GP50 (MW 45 50 KD, G2) [19,22]. GP38, which has been claimed to induce neutralizing antibodies, seems to be the only glycoprotein exposed on the virion surface as it was shown by in vitro iodination of intact purified virions [19].…”

Section: Introductionmentioning

confidence: 99%

Low-pH-induced fusion of Vero cells infected with Junin virus

Castilla

Mersich

1996

Archives of Virology

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Junin virus (JV) infected Vero cells were used to investigate virus capacity to induce cell-cell fusion. Polykaryocyte formation due to JV was found to be pH and temperature-dependent. A reduced fusion activity was detected on BHK-21 cells. Different JV-strains exhibited a similar extent and pH dependence of their fusion activity. Neutralizing antibodies against the main viral glycoprotein (GP38) inhibited syncytium production and GP38 conformational changes in response to acid treatment were detected by an immunoprecipitation assay.

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“…Junin virus (JV) is a member of the Arenaviridae family of enveloped RNA viruses. Virions contain a genome composed of two segments of single-stranded RNA and two major structural proteins, the nucleocapsid protein (NP, MW 60-64 kDa) and an external glycoprotein (GP38, MW 38 kDa) [20]. Other minor proteins have also been described in purified virions or in infected cells [5,6,10].…”

Section: Introductionmentioning

confidence: 99%

The entry of Junin virus into Vero cells

Castilla

Mersich

Candurra

et al. 1994

Archives of Virology

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The entry mechanism of Junin virus (JV) into Vero cells was studied analyzing the effect of lysosomotropic compounds and acid pH on JV infection. Ammonium chloride, amantadine, chlorpheniramine and procaine inhibited JV production. The action of ammonium chloride was exerted at early times of infection. Virus internalization was inhibited and viral protein expression was not detected. When the extracellular medium was buffered at low pH, the ammonium chloride induced block on JV infection was overcome. Furthermore, JV was able to induce fusion of infected cells at pH 5.5 leading to polykaryocyte formation. Taken together, these results demonstrate that JV entry occurs through an endocytic mechanism requiring a low pH dependent membrane fusion.

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Genetic Organization of Junin Virus, the Etiological Agent of Argentine Hemorrhagic Fever

Cited by 12 publications

References 71 publications

Molecular characterization of attenuated Junin virus strains.

Molecular characterization of attenuated Junin virus strains.

Low-pH-induced fusion of Vero cells infected with Junin virus

The entry of Junin virus into Vero cells

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