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C Videla

Publications and source records attributed to C Videla.

27 records · Page 2Linked to original sources
PubMed1987

Intracerebral infection of Cebus apella with the XJ-Clone 3 strain of Junín virus.

To assess the usefulness of the South American primate Cebus apella as a model for neurovirulence of Junín virus, eight monkeys were inoculated with 10(5) LD50 of the attenuated XJ-Clone 3 Junín virus strain by the intrathalamic route. After the second week, weight loss and polyadenopathies were observed in most animals, one-half of which had a transient leukothrombocytopenia. Moderate clinical central nervous system (CNS) involvement was present in four of eight monkeys, while the rest had only mild neurologic signs. All recovered except one, which developed a deep coma and was killed in a pre-mortem stage at 18 days post-infection (pi). Junín virus was isolated from the throat from five, from the blood from three, and from the brain from two monkeys. In the most severely ill animal, virus titers higher than viremia were detected in both inoculated and contralateral brain hemispheres, as well as in lung, lymph node, and small intestine. Junín antigens and "in vivo" bound immunoglobulins were detected by immunofluorescence (IF) in the brain of four animals at 18, 21, 40, and 155 days pi. Moderate lymphocytic parenchymal and meningeal infiltration were observed in the brain of four animals, and gliosis was also present in the most affected monkey. Although the clinical response to infection was not uniform, all infected monkeys developed high IF antibodies. Cebus apella cannot be used as a highly sensitive model for Argentine hemorrhagic fever (AHF). However, the results obtained show that the XJ-Clone 3 strain can replicate in the primate CNS and to induce lesions and immunoglobulin deposition. In addition, viral persistence is suggested by the late detection of viral antigens in brain at 40 and 155 days pi.

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PubMed1986

Experimental infection of Akodon molinae (Rodentia, Cricetidae) with Junín virus.

Experimental infection with the XJ-Clone 3 strain of Junín virus in laboratory bred Akodon molinae, a cricetid rodent inhabiting the borders of endemic Argentine hemorrhagic fever areas, was studied. Suckling animals inoculated intracerebrally proved sensitive and became chronically infected. Sixty percent of the rodents showed neurologic involvement, with mortality reaching 60%. Virus was recovered from the brain at 7, 15, 21, 37, and 57 days postinfection (pi). By immunofluorescence (IF), viral antigens were observed up to 182 days pi in cells of the central nervous system (CNS). Concurrently, immunoglobulin deposits were detected in infected CNS cells from 21 up to 182 days pi. These deposits increased with the progression of the immune response as measured by IF antibodies. The detection of immune complexes in brain cells of apparently healthy animals suggests that neither viral replication nor the development of a humoral immune response are necessary requisites for neurovirulence in this host. Infection of adult rodents by different routes failed to induce disease or mortality and virus could not be recovered from oral swabs, blood, or organs. Our data suggest that Akodon molinae could play a role in nature as an alternative reservoir of Junín virus in addition to the main reservoir, Calomys musculinus.

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PubMed1985

Junin virus-induced chromosomal aberrations in the guinea pig. Synergism between the attenuated strain XJ-clone 3 and caffeine.

The frequency of chromosomal aberrations in bone marrow cells of guinea pigs inoculated with the pathogenic XJ strain of Junin virus increased significantly at 6, 9, and 11 days postinoculation (p.i.). Animals inoculated with the attenuated XJ-clone 3 strain only showed significant increments of achromatic lesions (gaps) at 9 days p.i. Guinea pigs inoculated with the XJ-clone 3 strain and then treated with two doses of caffeine 24 and 12 h before killing at 9 days p.i. exhibited a significant increase of chromatid breaks and a parallel decrease of gaps. Because caffeine acts as an inhibitor of repair mechanisms of genetic damage, these results suggest a mutagenic effect of the attenuated strain.

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PubMedDate not supplied

[Intracerebral infection of athymic mice with an attenuated strain of Junín virus].

Infection of newborn immunocompetent (nu/+) mice with the XJ prototype strain of Junin virus, etiological agent of Argentine Hemorrhagic Fever, produces a lethal meningo-encephalitis due to cellular immune response. The same strain inoculated into athymic (nu/nu) mice produces an asymptomatic persistent infection. The purpose of this work was to determine the nu/nu mice response when infected with XJCl3, an attenuated Junin virus strain, since this strain behaves differently to the pathogenic prototype in various experimental hosts and humans. Fifty five suckling nu/nu mice and 45 nu/+ were inoculated intracerebrally with 10(3) PFU of the XJCl3 strain. Twenty nu/nu and 20 nu/+ were kept as uninoculated controls. Similar percentages of mortality were recorded for nu/nu and nu/+ infected animals (86 and 87%). In contrast, no morbi-mortality was detected in control animals which were kept in the same animal room. High virus titers were detected in brains and lungs of infected nu/nu at 7, 14, 21 and 70 days post-infection(pi). Virus titers in blood were 1 log lower than those found in organs. Immunohistochemical studies of brains showed viral antigen in the cytoplasm of cortical neurons at 21 and 70 days pi. An interstitial pneumonitis was detected in lungs of infected nu/nu at 7 and 21 days pi, while no lesions were observed in brains and spleens. Results show that the XJl3 strain behaves in a very different way in newborn nu/nu mice as the XJ prototype strain. Further studies are necessary to determine the pathogenic mechanisms involved.

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PubMedDate not supplied

[Rapid serologic diagnosis of Argentinian hemorrhagic fever in whole blood].

The usefulness of a method for detection of antibodies against Junin virus in whole blood was tested. N: NIH adult mice were inoculated with 10(3) PFU of attenuated XJ-Clon 3 Junin virus strain by intraperitoneal route and blood was obtained by retro-orbital puncture at 21 days post-infection. One blood aliquot (50 microliters) was collected in tubes containing a stabilizer solution for whole blood and another was processed for serum obtention. Immunofluorescent antibodies were tested on spot slides of a BHK/21 cell line persistently infected with Junin virus. High antibody titers (1/64 to 1/256) were detected in both whole blood and serum, with 66% coincidence between both procedures. These results show that the method of detection of antibodies in whole blood would be useful to test quickly for anti-Junin virus antibodies in seroepidemiologic studies, in endemic areas.

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