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M C Weissenbacher

Publications and source records attributed to M C Weissenbacher.

At least 19 recordsLinked to original sources
PubMed2003

Long-lasting astrocyte reaction to persistent Junin virus infection of rat cortical neurons.

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 (+) neurons peaked during the acute period (27.7+/-6.8), dropped within the intermediate (4.8+/-4.0 to 1.4+/-1.1) and increased (7.6+/-4.3) at the onset of the late neurological syndrome. In infected vs. control rats, the number of GFAP (+) astrocytes maximized during the acute stage (19+/-4 vs. 11+/-5), and from the end of the intermediate (27+/-5 vs. 21+/-5) up to the late (37+/-7 vs. 26+/-6) periods. In turn, surface density of GFAP (+) material in infected samples peaked at 0.196+/-0.066, while it failed to exceed 0.090+/-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.

Animals↗
PubMed1996

Serological evidence of human Hantavirus infection in Argentina, Bolivia and Uruguay.

A serological survey was conducted in 1985-1987 to determine the presence of infection for Hantavirus in the general population in Argentina, Uruguay, Paraguay and Bolivia, as well as among rodent-exposed laboratory workers in Argentina. Out of 748 individuals tested by immunofluorescence 20 proved positive for Hantaan virus 76/118 strain of whom 16 also reacted against Seoul virus 80/39 strain and 2 against Puumala virus Sotkamo strain. Ten out of 72 Argentine laboratory workers were positive for the first 2 viruses by ELISA, immunofluorescence and/or plaque reduction neutralization test, in 4 of whom recent infection was demonstrated by IgM antibody presence. Inapparent Hantavirus infection was thus demonstrated for the first time in 2.7% of regional inhabitants, together with 13.9% among rodent-exposed laboratory workers. Our data established the existence of human Hantavirus infection nearly 10 years before the recognition of clinical cases of hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome in Argentina.

Adolescent↗
PubMed1996

Hantavirus pulmonary syndrome in Argentina. Possibility of person to person transmission.

In March 1995 the first case of a familiar outbreak of Hantavirus pulmonary syndrome (HPS) was notified in El Bolson, in the South of Argentina. Until December 15, 1996, a total of 77 cases of HPS had been notified with 48% mortality, distributed in three geographical areas of the country, South, North and Center. During 1996, of the 19 cases from El Bolsón, three were local physicians, one of whom -during the prodrome of her illness- travelled to Buenos Aires to be attended. In the hospital, two of the physicians who assisted her, developed HPS 27 and 28 days after the first contact. These data suggest for the first time the possibility of interhuman transmission of the Hantavirus responsible for the pulmonary syndrome.

Argentina↗
PubMed1990

A new genome type of adenovirus 3 associated with severe lower acute respiratory infection in children.

Adenovirus 3 was found associated with ten cases of infantile lower acute respiratory infection in patients aged 2-18 months. Of these, five had a fatal outcome, with severe lung damage. Restriction enzyme analysis with Bam HI, Bcl I, Bgl II, Bst E II, Hind III, Sal I, Sma I, Xba I, and Xho I revealed the presence of the same genome type in all ten specimens. The genomic variant was different from those previously reported for serotype 3 and therefore was tentatively denominated 3f.

Acute Disease↗
PubMed1990

Hantavirus infection in laboratory and wild rodents in Argentina.

Serum samples from urban and laboratory rats, laboratory mice and wild and laboratory cricetids in Argentina were tested by immunofluorescence and plaque reduction neutralization tests to investigate prevalence of anti-Hantavirus antibodies. A total of 102 sera were obtained from laboratory rodents in 4 different animal-rooms, 31 from harbor rats and 30 from wild cricetids in 1985-1987. Anti-Hantavirus antibodies were detected in 22.5% of Rattus norvegicus in 3 of the animal-rooms but harbor rats were found to be free of Hantavirus infection. Previously, the presence of anti-Hantavirus antibodies had been demonstrated in the sera obtained from laboratory workers in these same 3 animal-rooms; it can be concluded that the laboratory rats were the source of this human infection. On the contrary, laboratory mice and cricetids failed to show Hantavirus infection while the wild vesper mouse Calomys musculinus (the main Junin virus reservoir) showed a prevalence of 23.5%. The presence of Hantavirus infection is hereby reported for the first time in wild C. musculinus and in laboratory R. norvegicus in Argentina.

Animals↗
PubMed1990

[Human immunodeficiency virus infection associated with tuberculosis].

In order to detect an association between HIV infection and tuberculosis (TB), 130 TB inpatients were studied one of whom presented a pulmonary disease due to Mycobacterium avium intracellulare. All had advanced TB, 95.4%, with pulmonary localization. Serum anti-HIV antibodies were detected by ELISA and their presence confirmed by immunoblotting in 4 (3.1%) individuals, three males and one female, with different degrees of pulmonary TB. Of the males, 1 was bisexual, 2 were promiscuous, and the female was the sexual partner of a non symptomatic HIV-infected man. No immunological disturbances or other AIDS related alterations were observed. There was one case of miliary TB, but neither atypical X-ray abnormalities nor extrapulmonary involvement were found. Tuberculin reaction was positive in three of the four HIV infected patients. Clinical, radiological and bacteriological evolution were favorable. Adverse drug reaction occurred in two cases, one of them presenting serious toxidermia caused by isoniazid. Of the 130 individuals, 12 presented risk factors for HIV infection so that the prevalence of anti-HIV antibodies presented here, 4 cases out of 12, is consistent with data from previous reports for high risk populations.

AIDS Serodiagnosis↗
PubMed1989

Comparison of three techniques for detection of respiratory viruses in nasopharyngeal aspirates from children with lower acute respiratory infections.

A comparison of immunofluorescence (IF), enzyme-linked immunosorbent assay (ELISA), and isolation in tissue culture (TC) for detection of respiratory viruses was performed on 496 nasopharyngeal aspirates from children under 5 years of age with lower acute respiratory infections who were receiving attention at three hospitals in Buenos Aires, Argentina. All samples were tested by the three methods for respiratory syncytial virus (RSV), influenza A and B, adenovirus, and parainfluenza 1 and 3. Viral diagnosis was made in 167 samples (33.7%); of these, 124 (74.3%) were isolated in TC, whereas 120 (71.8%) were detected by ELISA and 127 (76%) by IF. RSV was detected in 121 samples, mainly by ELISA and IF. The sensitivity and specificity of each rapid technique as compared with isolation in TC were similar, reaching 98% and 92%, respectively. When ELISA was compared with IF, the sensitivity was 95%, and the specificity was 98%. Adenovirus was detected in 18 patients by TC. For this virus, rapid techniques sensitivity as compared with TC was low (almost 22%). Parainfluenza 3 was readily detected by IF and TC; influenza A, B and parainfluenza 1 were detected in few samples; and tissue culture proved more efficient than rapid techniques. The results indicate that both rapid techniques are good tools for the detection of most respiratory viruses except for adenovirus, for which TC cannot be omitted.

Adenoviridae Infections↗
PubMed1989

Astrocytic reaction predominance in chronic encephalitis of Junin virus-infected rats.

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.

Animals↗
PubMed1988

Long-term protection against Argentine hemorrhagic fever in Tacaribe virus infected marmosets: virologic and histopathologic findings.

Tacaribe virus may represent a better alternative than attenuated strains of Junin virus (JV) for immunization against Argentine hemorrhagic fever (AHF) because of possible risk of persistent infection of disease associated with live, attenuated strains. Callithrix jacchus marmosets, which suffer 100% mortality if inoculated with the pathogenic XJ strain of JV, were used to evaluate possible Tacaribe virus persistence, subclinical, or long-term disease and the duration of protection against challenge with JV. Histologic studies did not show pathogenic changes due to Tacaribe virus in primates sacrificed from 7 to 480 days postinoculation (pi). No virus was recovered in tissue samples after primary culture or cocultures with sensitive cells. The presence of anti-Tacaribe neutralizing serum antibodies and protection against pathogenic JV were detected up to 480 days after a single dose of Tacaribe virus. However, anti-Junin antibodies were detected only after challenge. In other experiments, protection against JV was evaluated histologically and virologically. Two primates were immunized with Tacaribe virus, challenged with JV, and sacrificed 18 or 21 days later. Subclinical histopathologic findings were associated with recovery of JV only by the sensitive primary culture-coculture techniques. The immunogenicity, degree of protection, and safety of Tacaribe virus indicate its potential as a vaccine against human AHF.

Animals↗
PubMed1988

Ribavirin effect on experimental Junin virus-induced encephalitis.

Junin virus, the etiological agent of Argentine hemorrhagic fever, produces in man a disease mainly characterized by hemorrhagic alterations, commonly accompanied by neurological symptoms, and leading to 10% mortality. Intracerebral inoculation in 10-day-old rats or intraperitoneal inoculation in 2-day-old rats leads to high mortality due to severe encephalitis. Here, the effect of Ribavirin on these experimental models was tested in order to evaluate the degree of protection achieved against neuropathological manifestations. In intracerebrally infected 10-day-old rats the drug was administered 2 hr before virus inoculation. Doses ranged from 30 to 90 mg/kg body weight. Protection reached 40% for the 60 and 90 mg doses. Intraperitoneally infected 2-day-old rats received the drug in five 30-mg daily doses, starting the same day as virus inoculation. Survival was 73%. Viral replication within peritoneal macrophages dropped markedly, leading to much lower CNS viral titres. Together with results reported in primates, our findings support further studies on Ribavirin, with a view to eventual trials in humans.

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↗
PubMed1988

Mortality induced by adoptive immunity in Junin virus-infected athymic mice.

The effect of normal or sensitized spleen cell transfer from syngeneic euthymic mice to Junin virus-infected suckling athymic mice was studied. Transfer was performed 1 or 7 days after infection. In both cases, an acute lethal disease developed 6-11 days after transfer. The mortality reached 100% in all infected groups receiving normal or sensitized splenocytes, while it was negligible for different control groups of athymic mice. Transfer of normal or sensitized splenocytes was unable to significantly modify brain viral titers, as compared with infected nontransferred athymic mice killed after a 25-day observation period. Brain lesions were demonstrated in about half of the infected athymic mice transferred with sensitized splenocytes and in all euthymic infected mice. These results show that splenocyte transfer from immunocompetent donors is able to change the normal course of persistent Junin virus infection in nude mice to a lethal acute disease, thus pointing to a main role for T cells in its pathogenesis.

Animals↗
PubMed1987

Protection of Junín virus-infected marmosets by passive administration of immune serum: association with late neurologic signs.

Argentine hemorrhagic fever (Junín virus) is a human viral disease for which immune therapy proves effective, though a late neurologic syndrome is occasionally associated with the treatment. We attempted to determine in the infected marmoset Callithrix jacchus whether immune therapy leads to protection and/or CNS damage. Fifteen C jacchus were inoculated with 10(3) tissue culture infectious dose 50% (TCID50) of the XJ strain of Junín virus. On day 6 post infection (pi), 12 primates were treated with homologous immune serum. Animals were observed daily; and hematologic, serologic, virologic, and histologic studies were performed. All primates, both treated and controls, presented leukopenia, thrombocytopenia, anemia, and weight loss from day 14 pi onward. The three control animals died on days 22, 25, and 32 pi. Among the 12 treated monkeys, 3 died on days 21, 22, and 29. Hematologic values returned to normal during the second month; initial weight was recovered by the fourth month. Three out of the nine survivors showed neurologic alterations of various degrees, with hind-limb paralysis in the most severe case. Among treated monkeys, viremia and viral titers in the lungs, kidney, and lymph nodes were lower than in controls. Neutralizing antibodies were present in high titers in all treated marmosets, except in the one presenting paralysis in which values were minimal and viral persistence was detected in CNS. In conclusion, immune serum treatment of Junín virus-infected marmosets was found to reduce mortality from 100% to 25%. Viremia and viral titers in organs were lowered, and late neurologic signs appeared in 30% of treated survivors.

Animals↗
PubMed1987

Tacaribe virus: a new alternative for Argentine hemorrhagic fever vaccine.

Tacaribe virus is know to protect guinea pigs and primates against lethal challenge with Junín virus. A long-term study on the effect of Tacaribe virus infection in the guinea pig was carried out to determine the extent of cross-protection and whether antigen and/or viral persistence and tissue damage could be detected in immune animals. Viral titers, antigen expression in organs, and histologic lesions were sequentially searched for up to 540 days postinfection (pi). Neutralizing antibodies (Abs) and cross-protection to Junín virus were evaluated up to 660 days pi. Tacaribe virus titers and antigen peaked at 7-10 days pi to become undetectable after 30 days pi, except for a transient viral recovery from salivary gland. Virus was undetectable by coculture at 365 and 540 days pi. No immunoglobulins or C3 deposits were detected by immunofluorescence in brain or kidney at any stage, and histologic lesions were absent throughout. Anti-Tacaribe and anti-Junín neutralizing Abs were detected up to 660 days and full protection against challenge was achieved at 365 and 540 days, declining to 33% at 660 days pi. The results warrant consideration of Tacaribe virus as potential heterologous vaccine against Argentine hemorrhagic fever.

Animals↗
PubMed1986

Chronic neurologic disease in Junín virus-infected rats.

The purpose of this study was to determine whether Junín virus persistence in CNS of rats was capable of inducing late neurologic disease. Following intracerebral inoculation of newborn animals with XJ strain, three distinct stages could be discerned: an early phase of acute disease, up to 30 days pi, with 5% mortality; an intermediate one, extending to 280 days pi, without clinical signs but with evident viral persistence; and a final period of chronic illness, featuring clinical neurologic syndrome, severe perivascular inflammatory reaction, PAP-labeled viral antigen in a few cerebral and cerebellar neurons, and virus recovery only by coculture. Late neurologic disease seems associated to the lack of effective clearance of brain virus, leading to viral persistence and long lasting immunologic stimulation. The importance of animal models for pathogenic studies on CNS persistent viral infections leading to late neurologic disease is stressed.

Animals↗
PubMed1986

Therapeutic effect of the antiviral agent ribavirin in Junín virus infection of primates.

In order to assess the effect of the antiviral Ribavirin on the course of Junín virus infection in Callithrix jacchus, seven inoculated monkeys were treated with 15 mg of the drug, twice a day, starting 6 days after infection when all animals were viremic. The three untreated controls showed typical signs of Junín virus infection at 14 days pi and their mean time of death was 18 days. In contrast, no signs of illness were detected in Ribavirin-treated animals until 24 days pi, when marmosets showed signs of neurological involvement: 5 of these animals died (mean day of death: 36) but the two remaining treated monkeys improved and survived infection without sequelae. The comparison of survival rates (0% vs 28%) and the delay of the mean day of death observed indicates that the Ribavirin treatment used has therapeutic effect on Junín virus infection in vivo.

Animals↗