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At least 19 recordsLinked to original sources
PubMed1993

Replication and physical parameters important for preparing purified Junin virus.

Junin virus (JV) is an Arenavirus and the causative agent of Argentine hemorrhagic fever (AHF), an often fatal human disease. The attenuated strain XJ-clone 3 (XJC13) of JV, after being tested in humans, has been considered a promising vaccine. We found that synthesis of JV XJC13 reaches a peak 2 days after infection and the kinetics of synthesis are little affected by the multiplicity of infection (MOI) in a range from 0.125 to 1.00. Virus synthesis is sensitive to actinomycin D, indicating that cellular biosynthesis is required for viral replication. Combined precipitation and ultracentrifugation of supernatant from virus-infected cells yielded large amounts of concentrated and purified virion that banded in sucrose as a single peak with average density 1.177 +/- 0.015 g/ml. Purified virions have an average diameter of 203 +/- 23 nm by electron microscopy and an average sedimentation coefficient of 454 +/- 27 S. The results from the present study should assist in the preparation of large amounts of attenuated Junin virus which are required for vaccination against and diagnosis of Argentine hemorrhagic fever.

Animals↗
PubMed1996

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

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.

Animals↗
PubMed1976

RNA composition of Junin virus.

Junin virus grown in BHK-21 cells was labeled with [3H]uridine and highly purified by differential and isopycnic centrifugation. The RNAs extracted with phenol and analyzed by polyacrylamide gel electrophoresis were shown to be composed of four large species (33, 28, and 18S) and three small ones (4, 5, and 5.5S). This pattern was similar to ones already reported for other arenaviruses. However, there was a striking difference when the virus labeling was performed in the presence of actinomycin D. Labeling of viral rRNA was as much as 60% of the levels obtained in the absence of the drug under conditions in which cellular rRNA's were inhibited by 95% or more.

Arboviruses↗
PubMed1980

Protection of guinea pigs inoculated with Tacaribe virus against lethal doses of Junin virus.

Guinea pigs were protected against lethal doses of Junin virus by a previous inoculation with Tacaribe virus. Fourteen guinea pigs were infected with 10(6) 50% lethal doses (LD50) of Tacaribe virus and superinfected 45 days later with 10(3) LD50 of Junin virus. Appropriate control groups for both infections were also studied. The replication of Junin virus was impaired, as no virus was isolated from blood and organs of animals killed on days 9 and 11 after infection. High levels of neutralizing antibodies to Tacaribe virus were present by day 45, and no cross-reacting neutralizing antibodies to Junin virus were detected. However, three days after challenge with Junin virus, a typical secondary immune response to this virus was established. From these results it was concluded that the protection observed was mainly due to a specific immune response that was triggered by the Junin virus but primed by Tacaribe virus, which is antigenically similar to Junin virus.

Animals↗
PubMed2002

Evaluation of an enzyme-linked immunosorbent assay for detection of antibodies to Junin virus in rodents.

Junin virus is the etiological agent of Argentine hemorrhagic fever, a serious rodent-borne disease. An enzyme-linked immunosorbent assay (ELISA) to detect Junin virus IgG antibodies in rodents was evaluated using sera from 27 Calomys musculinus and five Calomys laucha, inoculated experimentally with a live attenuated strain of this arenavirus. The test performance was compared against an indirect immunofluorescence assay (IFA). The ELISA had a sensitivity and specificity of 100% and a reproducibility of 87.9% for samples with titers above the selected cut-off value. IFA had lower sensitivity (53%) with the same specificity. The ELISA results were similar, whether carried out on whole blood or serum samples, thus eliminating the need for serum separation. A high correlation (K=0.86) between ELISA and IFA results was obtained from 1011 wild sigmodontine and murine rodents collected within and outside of the Argentine hemorrhagic fever endemic area. These results indicate that Junin virus IgG ELISA is the most suitable assay for detection of Junin virus antibodies in rodent samples.

Animals↗
PubMed1997

Molecular characterization of attenuated Junin virus strains.

The Junin virus strain Candid #1 was developed as a live attenuated vaccine for Argentine haemorrhagic fever. In this paper we report the nucleotide sequences of S RNA of Candid #1 and its more virulent ancestors XJ#44 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 #1 and its progenitor strains revealed some changes that are unique to the vaccine strain. These changes could be provisionally associated with the attenuated phenotype.

Amino Acid Sequence↗
PubMedDate not supplied

Cross-protection between Tacaribe complex viruses. Presence of neutralizing antibodies against Junin virus (Argentine hemorrhagic fever) in guinea pigs infected with Tacaribe virus.

Cross-protection between Junin virus and five other Tacaribe complex viruses and the serological response of guinea pigs inoculated with Tacaribe virus are reported here. Previous infection with Tamiami or Pichinde viruses significantly delayed guinea pig deaths. A 58% survival rate was found among animals immunized with three doses of Amapari virus, while guinea pigs inoculated with one dose of Machupo or Tacaribe virus were fully protected against Junin virus. Neutralization tests performed in serum samples of guinea pigs immunized with five doses of Tacaribe virus showed that they developed monologous and heterologous neutralizing antibodies.

Animals↗
PubMed1983

Congenital and perinatal infection with Junin virus in guinea pigs.

Junin virus infection in guinea pigs is known to be similar to human Argentine hemorrhagic fever (AHF). The guinea pig was chosen as a model for transplacental transmission of Junin virus, as both guinea pig and man have a similar placental structure. Pregnant guinea pigs were infected with the pathogenic XJ strain of Junin virus intramuscularly route at different stages of pregnancy. The group infected during the last third of pregnancy produced 16 newborn, but mortality reached 100%: 18% were born with typical AHF hemorrhagic signs, 54% without signs, and the remainder were stillborn. Virus was recovered from organs of newborns, as well as placental tissues. A second group, infected in the second third of pregnancy, died with intrauterine fetuses, all of which showed hemorrhagic signs and virus present. In a last group, infected in the first third of pregnancy, fetuses were free from macroscopic lesions. In order to determine whether lactation may be an alternative infection route in guinea pigs, mother guinea pigs were infected with Junin virus at different times postparturition. The 84% noninfected newborn housed together with their infected mothers died during the suckling period, half with typical AHF signs. Junin virus transmission from mother to fetus was thus proved, and lactation may be considered as an alternative perinatal infection route.

Animals↗
PubMed1985

[Association of the infection of the thymus and bone marrow with the establishment of persistent infection with Junin virus in 2 genera of rodents].

Junin virus infection of immune system organs was correlated with persistence establishment in the mouse and rat. Rockland mice under 24 or at 72 and 120 h of age received 10(4) pfu of Junin virus XJ strain by ic route. Separately, two groups of mice under 24 h old were infected with the same dose of XJ or XJCl3 strain by the same route respectively. Results showed that higher thymus virus titer correlated with greater survival. In turn, the former also seemed to correlate with decreasing age at inoculation time, although there was considerable strain dependence. In order to correlate replication levels in thymus with clinical progress in mice, animals under 24 h of age were inoculated with XJ. At 14 days pi apparently healthy mice from this batch were separated from those presenting severe neurologic sings. In the asymptomatic mice, thymus titers ranged from 1.7 to 3.2 log, while no virus was found in thymus harvested from obviously ill animals. However brain virus titers in the two groups proved similar. To confirm these findings, 72 h old Wistar rats were inoculated in with 10(4) pfu of either Junin virus strain: with XJ strain (90% survival) virus could be readily isolated from thymus and bone marrow at day 7 pi, whereas with XJCl3 (5% survival) no virus could be rescued from any organ tested. Therefore, our results strongly suggest a close correlation between productive thymic infection and Junin virus persistence establishment in these rodents, depending on immune response regulation rather than on viral variation.

Animals↗
PubMed1988

Mouse splenocyte transfer effect depends on donor's Junin virus infection stage.

Splenocytes from Junin-virus-persistently-infected euthymic mice taken at 45 days postinfection seemed unable to induce overt signs of disease, to cause death, or to modify brain viral levels when transferred to athymic Junin-virus-infected mice. Findings differed sharply when the same recipients were transferred with splenocytes taken at 6 or 30 days postinfection from immunocompetent mice infected in adult life, since mortality reached 80 or 50%, respectively, and brain viral titers were significantly lowered. Furthermore, splenocytes taken at 6 days postinfection from whole adult mice proved harmless to persistently infected euthymic mice. These findings strongly suggest the existence of an immune system alteration in the immunocompetent mouse, attributable to Junin virus persistence. This premise is based on the fact that splenocytes from persistently infected mice were unable to recognize viral antigen expressed on recipient-infected cells. The absence or impairment of a specific cytotoxic T cell population is hereby postulated.

Animals↗
PubMed1995

The role of mononuclear blood cells in experimental Junin virus spread to the central nervous system.

The neuroinvasiveness of Junin virus depends on the viral strain, animal species, and age. The role of infected blood cells in hematogenous Junin virus spread to the central nervous system (CNS) was studied by determining the growth in pheripheral mononuclear cells and brain tissue of Candid 1 and XJCL3 laboratory strains, in Calomys musculinus and guinea pigs. The present study demonstrated that Junin virus replicates in circulating peripheral lymphocytes and macrophages of 11-day-old guinea pigs and 6 +/- 1-day-old Calomys musculinus. Moreover, the observation that mononuclear phagocyte depletion did block Junin virus neuroinvasion firmly indicates that the cellular viremia (circulating monocytes) is one of the mechanisms of Junin virus attenuated strains spread to the CNS in animal hosts.

Animals↗
PubMed1986

Role of Calomys musculinus peritoneal macrophages in age-related resistance to Junin virus infection.

In nature, the cricetid Calomys musculinus is the principal host of Junin virus, the etiological agent of Argentine hemorrhagic fever. In the experimental infection, adult C. musculinus survived whereas newborns died after intraperitoneal inoculation with the XJ.Cl3 strain of Junin virus. The role of peritoneal macrophages in this age-related resistance was studied. Junin virus multiplied in cultivated macrophages from either neonatal or adult animals and, therefore, it was not possible to correlate the susceptibility of peritoneal macrophages to Junin virus infection with the age-dependent resistance. When adult and neonatal animals were treated with silica prior to Junin virus infection, deaths occurred in the adults, while a delay and decrease in the mortality rate were observed in neonatals. These results suggest that in neonatal C. musculinus macrophages could be permissive cells for Junin virus multiplication, whereas in adult cricetids, these cells would act as a barrier against viral infection by means of an extrinsic antiviral activity.

Aging↗
PubMed1975

Experimental biology and pathogenesis of Junin virus infection in animals and man.

A fatal disease resembling Argentine haemorrhagic fever of man has been produced in guinea-pigs and mice by inoculation with Junin virus. Infected guinea-pigs show macroscopic and microscopic haemorrhagic lesions, marked bone marrow changes, decreased leukocytes and platelets in the peripheral blood, and impairment of immunological response. This response permits differentiation between pathogenic (XJ) and attenuated (XJ Cl(3)) strains. Guinea-pigs inoculated with the XJ Cl(3) strain develop an inapparent infection accompanied by slight haematological changes, the appearance of antibody, and protection against challenge with the pathogenic strain. The attenuated strain has been used successfully as an immunizing antigen in 636 human volunteers. Guinea-pigs infected with Tacaribe virus show cross-protection against Junin virus, with the presence of heterologous neutralizing antibodies. Suckling mice infected with Junin virus develop a typical viral encephalitis; the pathogenicity of the virus decreases with increasing age of the mice. Experiments with thymectomized mice and with mice treated with antithymocyte serum suggest that the pathogenicity of Junin virus in this host is related to the integrity of the thymus-dependent immune system. There is evidence that humoral antibodies do not play any role in the development of the encephalitic lesions but rather protect mice against Junin virus infection. A recent serological survey among laboratory workers and inhabitants of the endemic area has demonstrated the presence of inapparent infection with Junin virus.

Animals↗
PubMed1990

Method for improving accuracy of virus titration: standardization of plaque assay for Junin virus.

Titrating infective virus is one of the most important and common techniques in virology. However, after many years of widespread use, the parameters governing the accuracy of titration values are still not well understood. It was found that under conditions currently used for virus titration, only a small percentage of virus in the inoculum is adsorbed onto the cells and thereby detected in the titration assay. The objective of our work was to establish the conditions for a plaque assay which could estimate more accurately the titer of Junin virus. Two different stain methods were compared and several parameters governing plaque formation were studied. The volume of the inoculum appeared as the most important factor affecting observed titer. A linear relationship between the volume of inoculum and the reciprocal apparent titer allowed us to estimate an absolute titer by extrapolation. The approach described here is likely to be applicable to the more accurate estimation of the titer of a wide range of virus.

Adsorption↗
PubMed1990

Contrasuppressor cells induced by Junin virus.

Intracerebral inoculation of Junin virus (JV) in all susceptible mouse models available induces a lethal meningoencephalitis compatible with a delayed-type hypersensitivity (DTH) immune response. In contrast, adult BALB/c mice prove resistant to infection and no DTH response is seen. JV inoculation in adult BALB/c mice induces DTH suppression to unrelated antigens such as sheep red blood cells. (SRBC). This suppression is mediated by JV-induced T cells (Tsv), which are operative from 1 to 24 days post-infection (p.i.), and seems to be related to adult mouse survival. The presence of JV-induced contrasuppressor cells (CS) bearing the Thy-1+, Ly 1+2- phenotype, able to abrogate Tsv cells-mediated suppression, is described here. Thus, CS cells may be involved in the mechanism by which mice avoid over-exposure to Tsv-mediated DTH suppression. Such CS cells were found in the spleen of inoculated animals and may also be induced by transferring JV-free Tsv cells to 'naive' recipients, in which JV inoculation then induces morbidity.

Animals↗
PubMed2005

Polarized entry and release of Junin virus, a New World arenavirus.

Junin virus (JUNV), the causative agent of Argentine haemorrhagic fever, is a human pathogen that naturally enters the body through the epithelial cells of the respiratory and digestive tracts. The interaction of JUNV with two types of polarized epithelial cultures, Vero C1008 and A549, was investigated. Radioactive virus-binding assays showed that JUNV infects polarized lines preferentially through the apical surface. High-level expression of viral nucleoprotein was detected in polarized cell lines infected through the apical domain. Virus production from apical media was about 100-fold higher than that found into the basolateral medium. Confocal-immunofluorescence analysis revealed high-level expression of glycoprotein at the apical-membrane surface. Disruption of the microtubule network by colchicine impaired JUNV vectorial release. This is the first study to analyse the interaction between a member of the virus family Arenaviridae and polarized epithelial cells, showing preferential entry and release from the apical plasma membrane.

Animals↗