Disease relevance of Junin Virus

• Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor [1].
• Ribavirin, a broad spectrum antiviral agent, is effective in the treatment of other viral hemorrhagic fevers, and the studies done with Junin virus infections to date indicate that this drug may also have a beneficial effect in Argentine hemorrhagic fever [2].
• When Vero cells infected with Junín virus are cultured in the presence of 16 mM glucosamine, no infectious virus is produced and no surface antigens or virions are detected [3].

High impact information on Junin Virus

• In addition, we demonstrate that the Junín virus GP-C signal peptide subunit is myristoylated at its N-terminal glycine [4].
• Polyacrylamide gel electrophoresis of purified Junin virus revealed six distinct structural polypeptides, two major and four minor ones [5].
• 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 [6].
• The induction of endogenous interferon (IFN) was studied in 28 cases of Argentine hemorrhagic fever (AHF), a severe systemic disease caused by Junin virus [7].
• The G2 fusion subunit of the Junín virus envelope glycoprotein GP-C contains two hydrophobic heptad-repeat regions that are postulated to form a six-helix bundle structure required for the membrane fusion activity of Class I viral fusion proteins [8].

Chemical compound and disease context of Junin Virus

• Four of seven glycoprotein-specific antibodies neutralized Junin virus to high titres [9].
• Morphologic changes in cyclophosphamide (CY)-suppressed vs. control non-suppressed new-born rats infected i.c. with XJC13 strain of Junin virus were compared and the cells involved in CNS lesions were identified by the PAP technique [10].
• Formalin inactivated Junin virus: immunogenicity and protection assays [11].
• The effects of two myristic acid analogs on Junin virus (JV) replication were investigated [12].
• Replication of Junin virus in the presence of tunicamycin [13].

Biological context of Junin Virus

• In this paper, we report the nucleotide sequence of the glycoprotein precursor gene (GPC) of the Junin virus vaccine strain (Candid #1) and its flanking untranslated regions [14].

Anatomical context of Junin Virus

• Glial fibrillary acidic protein (GFAP) immunochemical profile after junin virus infection of rat cultured astrocytes [15].

Gene context of Junin Virus

• Zinc-binding properties of Junín virus nucleocapsid protein [16].
• The glycoprotein precursor gene of the attenuated Junin virus vaccine strain (Candid #1) [14].
• Effect of inhibitors of the intracellular exocytic pathway on glycoprotein processing and maturation of Junin virus [17].
• The effects of cyclophosphamide (CY), anti-mouse thymocyte sera, oxisuran, and cytosine arabinoside were evaluated in adult and newborn mice infected with Junin virus [18].
• During four consecutive passages, 30-45% of the cells showed granular cytoplasmic antigen by indirect immunofluorescence, employing both Argentine hemorrhagic fever convalescent sera and sera from animals immunized with Junin virus [19].

Analytical, diagnostic and therapeutic context of Junin Virus

• Subcutaneous injections of ribavirin into guinea pigs infected intraperitoneally or intracerebrally with Junin virus significantly increased the mean time to death but did not enhance survival of the animals [20].
• Purified Junin virus was disrupted by nonionic detergent treatment (Triton X-100), and subviral components were separated by ultracentrifugation [21].

References