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Biomedical subjects

J L Blejer

Publications and source records attributed to J L Blejer.

At least 19 recordsLinked to original sources
PubMed2001

Antibodies to Trypanosoma cruzi among blood donors in Buenos Aires, Argentina.

OBJECTIVES: The aim of this work was to study the prevalence of anti-Trypanosoma cruzi in the blood donor population in Buenos Aires, to compare the relative sensitivity and specificity of the two screening tests used and to confirm the results with a third assay. MATERIAL AND METHODS: Between May 1995 and July 1999, 64,887 blood donor consecutive samples were screened with the following commercial tests: indirect hemagglutination (IHA) (Polychaco, Buenos Aires, Argentina) and enzyme-linked immunosorbent assay (ELISA) (40,222 with Chagatek, Organon Teknika, Buenos Aires, Argentina, and 24,665 with Chagas EIA, Abbott, São Paulo, Brazil). Repeatedly reactive samples in one or both tests were analyzed with a third method: dot blot (Bio Chagas, Gador, Buenos Aires, Argentina) or particle agglutination (Serodia, Fujirebio, Tokyo, Japan). Sera that reacted in at least two tests were considered positive. RESULTS: The seroprevalence was 2.66% (1744 samples were reactive for one or both screening tests), and 1.46% (949 samples) were confirmed positive. The ELISAs proved to be more sensitive (relative sensitivity: 99.67-99.71%) whereas 192 samples (0.47%) were IHA false-negatives (relative sensitivity: 79.77%). Relative specificity for EIA was 98.47--99.23% and for IHA 99.85%. CONCLUSIONS: Results suggest the need of performing two screening tests for Chagas disease in blood banks from endemic areas and the importance of a third confirmatory assay to avoid unnecessary medical counseling.

Animals↗
PubMed2000

[Is TT virus (TTV) a true hepatitis virus cause?].

TT virus (TTV) was first detected in the blood of three patients with elevated serum alanine aminotransferase following transfusion who were negative for all known hepatitis viruses. This virus exhibited hepatotropism, and its titers correlated with elevation in serum aminotransferase concentration suggesting that it was a true hepatitis virus. Moreover, it was demonstrated that the presence of TTV DNA is not associated with biochemical or histologic evidence of liver injury. The virus has been found worldwide with a high prevalence in the general population and there is evidence that it may be transmitted by parenteral exposure to blood, enterally and transmitted from mother to child. An association between TTV infection and acute or chronic hepatitis or other diseases has not been consistently observed.

Blood Donors↗
PubMed1999

[Prevalence of Trypanosoma cruzi antibodies in blood donors].

Blood transfusion is the second most common transmission route of Chagas' disease in endemic areas. Discrepancies between the available diagnostic kits are common, which indicates that a single test is not satisfactory. The aim of this work was to study the seroprevalence of anti-Trypanosoma cruzi markers, to compare sensitivity and specificity of the two screening assays currently in use and to confirm the results with a third test. A total of 20,860 volunteer blood donors were studied. Donations were screened with indirect hemagglutination assay (IHA) and enzyme immunoassay (EIA). Repeatedly reactive samples were assayed with an EIA carried out on strips, to which a mixture of T. cruzi antigens was applied as an horizontal line (DB). Sera that reacted in at least two tests were considered positive. A total of 576 samples were reactive for one or both screening tests (2.76%) and 391 of them (1.87%) were confirmed positive. EIA proved to be more sensitive, with no false negative results (100% sensibility), whereas 98 samples (0.47%) were IHA false negative (74.93% sensibility). Specificity for EIA was 99.3% and for IHA 99.8%. In our case, almost 0.9% of donated blood is discarded because of false reactive anti-T. cruzi results; two thirds correspond to false positive EIA and one third to false positive IHA. It is important to note that in our population we have not registered false negative results for EIA but there were false negative IHA. This fact implies that although the first method is less specific, it is much more sensitive. It is important to confirm the screening results in order to avoid unnecessary donor counselling and permit future donations. The DB test employed in our study results a useful alternative for this purpose.

Animals↗
PubMed1995

Evaluation of HTLV-I/II infection in blood donors in Buenos Aires.

HTLV-I and HTLV-II are two related retroviruses that are transmitted by sexual contact, breast feeding, blood transfusion and needle sharing. In this study the prevalence of HTLV-I and HTLV-II was evaluated in voluntary blood donors as a measure of the infection in the general population. Samples were tested by a gelatine particle agglutination test and repeatedly reactive samples were confirmed by Western blot tests (WBT), enriched with recombinant rgp21, rgp461 y rgp4611 proteins, which differentiates HTLV-I and HTLV-II antibodies. Of 19,426 samples, 40 were repeatedly reactive by particle agglutination (0.21%). When analyzed by WBT, 6 met the criteria for HTLV-I (0.036%), 2 for HTLV-II (0.01%) and 1 for HTLV-I/II, 13 samples were indeterminate and 18 were negative. The prevalence is low and comparable to that from non endemic countries. Screening for anti HTLV-I/II antibodies is necessary to prevent transmission through blood transfusions.

Adolescent↗
PubMed1995

[Determination of anti-HTLV-I/II antibodies: Experience in 28,897 blood donations in Buenos Aires].

PURPOSE: The first human retrovirus, HTLV-I, was isolated in 1980; HTLV-II was described later. The former is endemic in southwestern Japan, the Caribbean and equatorial Africa; whereas the latter prevails in intravenous drug addicts, being also endemic in American indian populations. Both viruses are either sexually transmitted, from mother to child mainly by breast-feeding, by blood transfusion or by sharing contaminated needles. With regard to transmission, since they are intracellular viruses, it occurs only when whole blood or cellular components are transfused; this is not the case when either plasma or plasma derivatives are used. The likelihood of transmission decreases as the storage time increases. HTLV-I is associated, at least, with two diseases: adult T-cell leukaemia/lymphoma (ATLL), and the tropical spastic paraparesis (TSP) or HTLV-I-associated myelopathy (HAM). ATLL occurs after a latency period of 20 to 30 years; whereas the incubation period ranges from 3 to 5 years in the case of the neurological disease. Most individuals infected with the virus remain healthy; the risk of developing the hematological complication is 2-4% whereas it is below 1% in the case of TSP. No clear association of HTLV-II with any known disease has been reported as yet. In this study, we have assessed the prevalence of HTLV-I and HTLV-II in the sera of the blood donors who have come to our Division, with the aim of avoiding the spreading of this oncogenic virus by transfusion. This study could serve as a measure of the infection in the general population. MATERIAL AND METHODS: A total of 28,897 samples were analyzed from May 1993 to January 1995. Anti-HTLV-I/II antibodies were analyzed by the method of passive agglutination of gelatin participles (PA). Samples which reacted were tested again by the same method, and those reacting for the second time were further confirmed by Western blot (WBT), a method with the ability to differentiate between antibodies anti-HTLV-I and anti-HTLV-II. RESULTS: Of the 28,897 samples, 47 were repeatedly reactive by PA (0.16%). Analysis by WBT resulted in 10 reactive results with HTLV-I (0.035%), 2 reactive results with HTLV-II (0.007%); in one sample it could not be determined whether the anti-HTLV-I or anti-HTLV-II antibody was present. Of the remaining samples, 21 were non-reacting, whereas 13 were indeterminated. CONCLUSION: Prevalence of HTLV-I and HTLV-II seropositive blood donors is low and similar to that found in other non-endemic countries. We believe that routine evaluation of anti-HTLV-I and HTLV-II antibodies in blood donors would be warranted in our country, since transmission of the viruses by transfusion of blood components has been clearly shown. It is possible that the recipients of the reactive units do not develop the disease. Nevertheless, these individuals constitute an important source of virus dissemination, both during the perinatal period and by sexual intercourse. In fact, advise to seropositive donors would prevent transmission by these routes. Lastly, it should be noticed that investigation of anti-HTLV-I/II antibodies could result in a surrogate method for detecting other viral infections transmitted by these routes.

Adolescent↗
PubMed1994

Neural spread of Junin virus in intraperitoneally inoculated rats.

On the basis of an already demonstrated Junín virus (JV) neural route after peripheral footpad infection of newborn rats, here we attempted to determine the viral pathway following intraperitoneal inoculation. As from the 2nd week post-infection, neurological disease developed reaching 84% mortality at 30 days. Immunoperoxidase labeling of viral antigen, concomitantly with infectivity assays and histological examination, was carried out in serially harvested samples. Whenever infectivity was detected, whether by viral rescue from coculture or by conventional isolation, viral antigen staining was achieved. Infective JV was present at threshold levels in spleen and liver from days 2 to 10, and in blood from days 5 to 15. In neural tissues, viral antigen was initially disclosed at day 5 in thoracic rachideal ganglia and related spinal cord segments. From day 7 thereafter, the entire spinal cord was involved; at this stage, first evidence of viral infection was found in brain stem, with subsequent spread to other encephalon structures at day 10. According to harvested samples, no significant differences were found in labeled cell percentages at thoracic vs cervical or lumbar levels of spinal cord. In contrasts, greater involvement of cerebral cortex versus brain stem, hippocampus or cerebellum was demonstrated shortly before death. Although JV antigen was overwhelmingly predominant in neurons, no morphological changes were apparent in such cells. Since rachideal spinal ganglia and spinal cord infection invariably preceded viral spread to encephalon, concomitantly with viral clearance from lymphoreticular organs and blood, a neural pathway seems warranted.

Animals↗
PubMed1992

Immunoperoxidase tracing of Junin virus neural route after footpad inoculation.

To determine the pathway adopted by peripherally inoculated Junin virus (JV) to reach the CNS, rat tissues were serially harvested to trace the sequence of viral progression from right hind footpad to brain. Immunoperoxidase (PAP) labeling of viral antigen, concomitantly with infectivity assays and histological examination of each selected sample, were carried out. As from the 2nd week post-infection (pi), neurological disease inducing 100% mortality at 1 month was evident. At day 5 pi, viral antigen was first detected at footpad level in epidermic and dermic cells, as well as in neighbouring myocytes; labeled macrophages infiltrating small nerve branches were also disclosed. As from 10-15 days pi, viral antigen became apparent along ipsilateral sciatic nerve structures and within lumbar spinal ganglion neurons, followed by a fast viral spread throughout CNS neurons that involved spinal cord and brain. Concurrent histopathology featured minimal inflammatory reaction together with generalized astrocytic activation. Hematogenous viral transport was negligible, since JV was isolated much earlier and in higher infectivity titers in neural tissues than in blood. It may be concluded that after viral replication in footpad, JV neural route was demonstrated by its PAP labeling from peripheral nerves to cerebral cortex.

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↗
PubMed1987

Macrophages are involved in age-dependent resistance of rats to Junin virus infection.

We attempted to correlate rat age with resistance to intraperitoneal infection with the XJ strain of Junin virus. Accordingly, mortality, viral replication in macrophages and brain, as well as neutralizing antibody (NA) levels were recorded in animals inoculated at 2, 5, 10 and 26 days of life. Two-day-old animals demonstrated both the greatest mortality (86%) and viral replication in macrophages, allowing virus to reach the brain where high titers were detected. This age group also had the highest NA titers. Mortality, viral multiplication and NA titers diminished with increasing age of the animals. The ability of peritoneal macrophages to support viral replication, therefore, seems to determine rat susceptibility to intraperitoneal infection with Junin virus.

Aging↗
PubMed1986

Junin virus access to CNS by extraneural rat inoculation.

This study was carried out to determine the pathways along which two strains of Junin virus (JV), the pathogenic XJV and the attenuated XJC13V, reach the CNS following IP inoculation of 2-day-old rats. A sequential study of infectivity and antigen distribution in peritoneal macrophages, spleen, and brain was performed. Mortality was 85% with the former strain, but only 15% with the latter. At 4-7 days PI, XJV-infected animals had viral antigen in 10% of peritoneal macrophages. Viremia and spleen virus lasted for 10-15 days. Low brain titers were detected at day 7, with a peak at day 15. Brain antigen correlated with virus titers. In contrast, XJC13V-infected rats, macrophage antigen appeared later and to a lesser degree (1% of cells). Viremia and spleen virus were transient, while both the titer of brain virus and the viral antigen proved lower. Antibody titers were over twofold higher for XJ-infected animals. It is suggested that the different replication rate at the inoculation site could account for the greater ability of the XJV strain to reach the CNS. A greater antigen mass and/or more numerous antigenic determinants presented by the macrophage could explain the higher antibody titers found in XJ-injected rats, which were unable, however, to prevent viral spread.

Animals↗
PubMed1986

Brain inflammatory exudate in Junin virus-infected rats: its characterization by the immunoperoxidase (PAP) technique.

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. Fifty per cent of the control rats exhibited widespread cerebral necrosis vs. only 15% of the immunosuppressed animals. The first cells to reach Junin virus-infected CNS in controls were T lymphocytes, which destroyed viral antigen-laden target neurons and astrocytes. B lymphocytes and macrophages, presumably attracted by viral antigen and/or by lymphokines, made their appearance a day or two later. Activated macrophages phagocytosed necrotic cells and perhaps exerted a cytotoxic effect upon target neural cells, whereas the actual role of B lymphocytes requires further explanation. In CY-treated rats, cerebral lesions were smaller and the cellular exudate, though similar, proved much scantier than in controls. A similar extent of cerebellar necrosis was observed in both groups.

Animals↗
PubMed1986

Macrophage maturity and modulation of response to Junín virus in infected rats.

Replication of Junín virus in peritoneal macrophages from newborn rats was greater for prototype strain XJ than for strain XJC13, whereas in cells from adult animals viral multiplication proved minimal. Transfer of peritoneal adherent cells from normal adult to strain XJ-infected newborn rats lowered mortality significantly. Silica blockade of macrophages protected two-day-old strain XJ-infected animals and depressed brain titers of virus significantly, whereas treatment had no effect on strain XJC13-infected rats. Macrophages from infected two-day-old rats caused illness and death in recipient animals. Silica blockade rendered macrophage-mature 11-day-old rats partially susceptible to infection with Junín virus. Thus pathogenicity of strain XJ in the two-day-old rat by the intraperitoneal route depends on the ability to replicate in peritoneal macrophages, whereas strain XJC13 is nonlethal because it fails to multiply efficiently in these cells. Macrophage maturity seems essential to inhibit viral replication and thus confer protection on the adult host.

Age Factors↗
PubMed1985

[Role of macrophages in the dissemination of the Junin virus in the rat].

The 2-day-old rat is known to be susceptible to infection by ip route with the XJ strain of Junin virus but resists inoculation with XJC13 strain (85% vs 15% mortality). In order to determine whether peritoneal macrophages play a role in modulating the course of infection, viral replication in adherent peritoneal cells infected with either strain was studied. XJ was found to replicate 30-fold as regards XJC13 at day 3 pi. Besides, silica blockage of peritoneal macrophages was also evaluated. Following silica treatment, 60% survival was recorded for XJ-infected animals vs 15% for untreated infected controls. No significant differences were recorded for silica-treated XJC13-infected rats vs untreated infected controls. These preliminary findings indicate that, upon replication within the host's macrophages at the peritoneal inoculation site, virus spreads readily to reach the target organs. Effective silica blockage lends support to this pathway, as shown by significantly greater survival in XJ-infected rats.

Animals↗
PubMed1985

Attenuation parameters for Junin virus in the newborn rat.

To characterize a virus strain as attenuated, both biologic and biochemical criteria are necessary. In the case of Junin virus, the 2-day-old rat has proved to be a biologic attenuation marker as regards mortality. Here we studied the behaviour of the prototype XJ vs the attenuated XJC13 strain inoculated by either ic or ip route to determine differential hematologic and splenic parameters. Humoral immune response against SRBC was also investigated. By either route XJ caused significant leucocytosis, while the other hematologic parameters remained unchanged. No alterations were found following XJC13 infection. XJ produced significant splenomegaly whereas XJC13 had no effect. Similarly PFC anti-SRBC count was decreased during XJ infection but not after XJC13 infection. These differences between the pathogenic XJ and the attenuated XJC13 strain may be attributed to the former's greater spread. The drop in PFC could be due to spleen dysfunction and/or viral effects on the cell subpopulation involved.

Animals↗
PubMed1984

Protection conferred against Junin virus infection in rats.

2-day-old Wistar rats intracerebrally infected with the XJC13 strain of virus exhibited a 5% survival rate which rose to 71% after immune serum treatment. Brain viral titers were relatively unaffected by this treatment. Histologic studies showed necrosis in the cerebellum and brain cortex with mononuclear cell infiltration in both treated and nontreated groups. Beginning on day 16 postinfection, however, intracerebral perivascular gliosis foci and mild meningeal congestion were minimal in the treated animals. These findings imply that passively transferred humoral immunity leads to prompt recovery in this experimental model.

Animals↗
PubMed1984

[Differentiation among strains of Junín virus by intraperitoneal infection in the rat].

The 2-day-old rat is known to resist intracerebral infection with the XJ prototype strain of Junin virus, but 95-100% mortality results when infected with the attenuated XJC13 strain. When this animal was inoculated by intraperitoneal route, behaviour was diametrically opposite: the XJ strain proved lethal, while de XJC13 led to low mortality. Studies on mortality, virus titer in different organs, and anti-viral humoral response in 2-day-old rats infected with Junin virus strains were carried out in order to use this system as a new attenuation marker. Mortality rates recorded for rats inoculated with either strain, were markedly different, being 84% in the XJ-infected group and barely reaching 17% in the XJC13 group. Brain viral titers were higher in the former group than the latter (10(5.26) PFU/ml vs. 10(3) PFU/ml at day 17 pi). For this reason, viral replication may be used as a virulence marker in this experimental model. Antibody levels were also higher in the XJ group most likely due to greater viral replication. The above findings support the use of the 2-day-old rat as a biologic attenuation marker since susceptibility to infection is strain-dependent.

Animals↗