Susceptible adult murine model for Junin virus (original) (raw)
Related papers
Neurovirulence of wild and laboratory Junin virus strains in animal hosts
Journal of Medical Virology, 1990
The neurovirulence of Candid #1 and XJCL3 laboratory strains and CbalV4454 and Cba-FHA5069 wild strains of Junin virus was studied in albino mice, guinea pigs, and a South American wild rodent, Calomys musculinus, of different ages inoculated by the intracerebral route. Infectivity in brain and organs, lethality, and neuropathological lesions were determined. The laboratory and wild strains showed similar neurovirulence only in 2-day-old mice. The neurovirulence of laboratory strains decreased with the age of the animal, and the Candid #1 strain affected only 2-day-old mice.
Junin virus-induced delayed-type hypersensitivity suppression in adult mice
Journal of Medical Virology, 1988
Junin virus (JV) infection of suckling mice leads to lethal meningoencephalitis consistent with a delayed-type hypersensitivity (DTH)-like immune response. In contrast, there are no central nervous system (CNS) alterations, and high antibody titers are induced in resistant adult mice. As a possible explanation, JV infection in adult mice may provoke DTH depression. Thus in this work we study the alterations induced by JV in the immune response of adult mice by using sheep red blood cells (SRBC) as an unrelated indicator antigen. JV infection was found to abrogate DTH significantly, regardless of SRBC priming time, virus strain attenuation, and viral route of inoculation. The effect proved viral dose-dependent and required live and infectious virus. However, the humoral response to SRBC, as determined by splenic "plaque-forming cell" count was found higher than controls. These results are consistent with adult mouse response to JV infection. In contrast to the guinea pig model, there is no destruction of immunocompetent cells. T-cell percentage in the spleen was high, suggesting involvement with DTHsuppressive action. We suggest that the immune response to SRBC in adult infected mice may be used for understanding the mechanisms involved in resistance.
Long-lasting astrocyte reaction to persistent Junin virus infection of rat cortical neurons
Journal of Neural Transmission, 2003
Immunoperoxidase labeling was performed in histological sections from rat brain harvested during acute (10-30 days), clinically inapparent (90-270 days) and late (450-540 days) stages of Junin virus-induced neurological disease. In frontoparietal cortex, count of viral antigen (þ) neurons peaked during the acute period (27.7 AE 6.8), dropped within the intermediate (4.8 AE 4.0 to 1.4 AE 1.1) and increased (7.6 AE 4.3) at the onset of the late neurological syndrome. In infected vs. control rats, the number of GFAP (þ) astrocytes maximized during the acute stage (19 AE 4 vs. 11 AE 5), and from the end of the intermediate (27 AE 5 vs. 21 AE 5) up to the late (37 AE 7 vs. 26 AE 6) periods. In turn, surface density of GFAP (þ) material in infected samples peaked at 0.196 AE 0.066, while it failed to exceed 0.090 AE 0.043 in controls. Both astrocyte hypertrophy relapsing into chronicity, as depicted by surface density, and astrocyte hyperplasia preceding the onset of the late neurological syndrome, support their pathogenic contribution to disease expression.
Junín Virus Infects Mouse Cells and Induces Innate Immune Responses
Journal of Virology, 2011
ABSTRACTJunín virus is the causative agent for Argentine hemorrhagic fever, and its natural host is the New World rodentCalomys 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 mouse-derived 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 ...
Astrocytic reaction predominance in chronic encephalitis of junin virus-infected rats
Journal of Medical Virology, 1989
Junin virus antigen distribution and astrocytic reaction to prolonged infection were characterized in rat brain by the PAP technique. During the acute stage of neurologic disease following intracerebral inoculation, Junin antigen was detected in 100% of animals, strongly in most neurons but also to a much lesser degree in scattered astrocytes, dropping to 20% of rats at 540 days postinfection. Initially labeled in all brain areas, viral antigen gradually disappeared from hippocampus but persisted irregularly in cerebral cortex, basal ganglia, Purkinje cells, pons, and medulla oblongata. Such a pattern suggests that specific neuronal subpopulations, in spite of apparently unaltered cell morphology, may persistently harbor the virus, leading on occasion to a delayed neurologic syndrome. During both the acute and chronic stages of disease, a mild inflammatory exudate was observed, characterized by the presence of T and B lymphocytes, as well as macrophages and unidentified round cells. GFAP immunostaining showed increased astrocytic reaction as infection lapsed into chronicity. Corpus callosum, hippocampus, and cerebellum exhibited the sharpest reactive astrocytosis, followed by basal ganglia, pons, and medulla oblongata, whereas in cerebral cortex it was considerably less. Astrocyte activation, which failed to correlate with viral antigen presence in neurons, seems to result from a generalized condition, possibly including diffusible brain factors triggered by viral infection. Such widespread astroglial reaction may thus contribute to the outcome of the late neurologic syndrome.
Formalin inactivated junin virus: Immunogenicity and protection assays
Journal of Medical Virology, 1989
The aim of this study was to determine if Junin virus inactivated with formalin (FA) was immunogenic and able to elicit a protective response in the guinea pig. The XJ-Clone 3 strain of Junin virus grown in Vero cells was exposed to FA a t 0°C. The following inactivated antigens were prepared: A,, 0.1% FA for 50 hr; A*, 0.1% FA for 50 hr followed by concentration with polyethylene glycol (PEG); B,, 0.05% FA for 70 hr; B2, 0.05% FA for 70 hr plus PEG concentration; C, 0.1% FA for 50 hr followed by ultracentrifugation and purification by sucrose gradient. No residual infectivity was detected in any inactivated antigen either after two passages in newborn mice or by coculture with Vero cells.
Infection and Immunity, 1983
Lymphatic tissue is one of the main sites for replication of Junin virus. To characterize which cells are involved in that replication, the presence of Junin virus in purified populations of macrophages and dendritic cells from the spleens of guinea pigs infected with pathogenic and attenuated strains was investigated by immunofluorescence and intracerebral inoculation into newborn mice. The pathogenic strain was present both in macrophages and in dendritic cells, but the attenuated strain selectively infected dendritic cells. These observations suggest that the pathogenic behavior and replication efficiency of these two strains of Junin virus may be related to a difference in cell targets.
Archives of Virology, 2005
SummaryOtherwise resistant adult mice were rendered susceptible to intracerebral Junin virus (JV) infection only when a staggered cyclophosphamide (CY) schedule was used.Forty-five-day old Balb/c mice, intracerebrally JV-infected and immunosuppressed with four 50 mg/kg body weight CY doses at days −1, +1, +4, +6 (day 0: viral infection) developed a lethal disease (86.6 per cent mortality) with high CNS viral titers and brain lesions. Neutralizing antibodies were absent throughout, while immunofluorescent antibody levels were considerably diminished.The transfer of hyperimmune serum conferred partial though significant protection on CY-treated animals but no correlation was found between CNS viral titers and mortality since in both infected CY-treated and untreated mice similar brain viral content was found.This was also confirmed by immune spleen cell transfer at day 0 where the clearance achieved was unable to modify the time course of the disease.Feasible mechanisms explaining rec...