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At least 19 recordsLinked to original sources
PubMed1978

Interrelationships among arenaviruses measured by indirect immunofluorescence.

An evaluation of reciprocal indirect immunofluorescent antibody titers for at least one representative of each known arenavirus serotype leads to the conclusion that the Old World aranaviruses are more closely related to each other than to other members of the group. These relationships are particularly evident in evaluations of human convalescent sera. New World arenaviruses cross-react strongly with each other in most instances but only weakly with with Old World arenaviruses.

Animals↗
PubMed1979

Argentine hemorrhagic fever: a primate model.

Experimental Junin virus infection of a New World primate, Callithrix jacchus, was evaluated. The virus produced anorexia, loss of weight, thrombocytopenia, leukopenia, and hemorrhagic and neurological symptoms and terminated in death. Virus was recovered from urine, blood samples and all tissues taken at autopsy. These preliminary observations show that several aspects of the experimental disease in C. jacchus are quite similar to severe natural Argentine hemorrhagic fever of man.

Animals↗
PubMed1975

International arbovirus research.

International cooperation in arbovirus research became increasingly prominent shortly after it was found in the early 1940's, that antigenic relationships existed among certain viruses isolated in different areas of thw world. The interest of a number of scientists and of a private organization led to the establishment of an international information exchange and to the preparation of an international catalogue of arboviruses including certain other viruses of vertebrates. International cooperation was fostered by the interest taken in these agents by the World Health Organization and the creation by this agency of an international net of collaborating laboratories with assigned areas of the world. A number of recent problems have been revealed and solved, or partly solved by this international effort, among which are questions relating to: the Marburg agent disease, the existence of an antigenic relationship between rabies virus and some arboviruses, aspects of the ecology or viruses in the California, Uukuniemi and Kemerovo groups, as well as several unanticipated antigenic relationships among viruses. Numerous questions still remain the solution of which might be expedited by continued and increased cooperative international effort such as overwintering or survival of viruses under unfavorable circumstances, pathogenic potential for man and domestic animals of certain viruses, role on chronic illnesses, establishment of the etiology of certain diseases and investigations of the basic properties of viruses, particularly of the Bunyaviridae.

Animals↗
PubMed1975

Ultrastructural and immunohistochemical study of the human kidney in Argentine haemorrhagic fever.

In six lethal cases of Argentine Haemorrhagic Fever (AHF) a disease caused by Junin virus, kidney samples were studied by means of immunofluorescent and electron microscopic techniques.--The ultrastructural studies showed that the distal and collecting tubes presented a large number of virus like intracytoplasmic particles. Those particles were present in the lumen of the endoplasmic reticulum cisternae and showed two distinct morphological aspects. Some of them were of high electron density and contained a few granules. The others were larger in size, electron lucid, and contained a variable number of ribosome like granules. Both types of particles originated from the endoplasmic reticulum wall by a process of budding. The presence of these particles was coincident with a severe cell damage which lead to necrosis and desquamation; and with large quantities of Junin virus antigen as demonstrated by immunofluorescence.--On the basis of these observations it is assumed that in AHF the cell damage is due to direct viral replication within the affected cells.

Antigens, Viral↗
PubMed1978

Argentine hemorrhagic fever. Alterations of the complement system and anti-Junin-virus humoral response.

We investigated immunologic mechanisms and the role of complement in the pathogenesis of Argentine hemorrhagic fever, a disease caused by the Junin virus, a member of the arenavirus group. Total serum complement activity was reduced to 68 per cent of control values in patients with severe or moderate disease (P less than 0.001). C2, C3 and C5 values were also low (12 to 60 per cent) during the early acute period of the disease. However, serum C4 content was increased to 160 per cent of the control values in the same patients. Total complement activity returned to normal with clinical and laboratory recovery, at the time of detection of antibodies against Junin virus. C1q reactive material was found in four of 19 cases and no relation to the evolution of the disease could be established. These results suggest that immune complexes are not important in the pathogenesis of Argentine hemorrhagic fever, but that activation of the complement system has a role.

Antibodies, Viral↗
PubMed1975

Ultrastructural and immunohistochemical studies in five cases of Argentine hemorrhagic fever.

Ultrastructural and immunohistochemical studies on tissues from five patients with Argentine hemorrhagic fever revealed previously undetected lesions caused by the viral infection. Two types of particle were seen in the cells of all organs examined. The particles had some characteristics similar to those described for arenaviruses. However, the virus-like particles were intracellular, had a single membrane, and apparently originated by a process of budding into the endoplasmic reticulum cisternae. Intranuclear bodies and three types of cytopolasmic change were observed in conjunction with the virus-like particles; Antigenic determinants of Junin virus were demonstrated in cells of all organs examined. Immunohistochemical experiments also indicated alterations in the cellular mechanisms of protein synthesis. Until now the pathogenesis of human diseases produced by arenaviruses has not been established. The results of this study suggest that in Argentine hemorrhagic fever the virus is responsible for a direct pathogenic action.

Adult↗
PubMed1976

A rhesus monkey model for the study of Bolivian hemorrhagic fever.

Two groups of rhesus monkeys were inoculated with either 10(5) (group 1) or 10(3) (group 2) plaque-forming units of Machupo virus, the etiologic virus of Bolivian hemorrhagic fever. The monkeys were observed for clinical signs; body temperatures, viremias, hematologic changes, and virus-neutralizing antibody were measured. The onset of clinical signs for groups 1 and 2 occurred on days 4-6 and 7-10, respectively, with fever, anorexia, and depression. These and other signs became more severe, and all of the monkeys died; the respective mean times to death for groups 1 and 2 were 14.3 and 19.5 days. Hematocrit, neutrophil, and lymphocyte values decreased in both groups until a few days before death and then increased slightly. Viremias in the two groups peaked on days 13 and 16, respectively, and persisted until death; the sole exception was one monkey in group 2 that developed neutralizing antibody by day 21. The response of the rhesus monkey to Machupo virus thus provides a useful model for the study of Bolivian hemorrhagic fever.

Animals↗
PubMed1976

Prophylactic control of simian hemorrhagic fever in monkeys by an interferon inducer, polyriboinosinic-polyribocytidylic acid-poly-L-lysine.

A nuclease-resistant complex of polyriboinosinic-polyribocytidylic acid containing poly-L-lysine and carboxymethylcellulose was used as prophylactic treatment of simian hemorrhagic fever in rhesus monkeys. This infection has proven uniformly fatal to more than 50 monkeys. Treatment 8 hr before infection and repeatedly thereafter completely prevented the development of viremia and death. Untreated animals died before development of antibodies to the virus. None of the treated animals developed antibody to the virus, a fact which suggested that viral growth was essentially completely blocked by the compound.

Animals↗
PubMed1977

Junín virus infection of guinea pigs: electron microscopic studies of peripheral blood and bone marrow.

Thin sections of peripheral white blood cells and samples of bone marrow from guinea pigs infected with Junín virus were examined by electron microscopy. In peripheral blood cells, 40% of the granulocytes showed cytoplasmic lysis seven days after viral infection. After day 11 up to 80% of these cells showed morphological alterations. However, no intra- or extracellular viral particles were detected in these samples. Microscopy of bone marrow preparations revealed that 10% of the cells were altered five days after infection, and approximately 50% were affected after nine days. At this stage the megakaryocyte channels were seen to contain pleomorphic particles with a mean diameter of 80-100 nm. These particles had a unit membrane envelope and internal dense granules similar to those observed during other arenavirus infections. Therefore, it is suggested that the effect of Junín virus upon megakaryocytes may be a factor responsible for the acute thrombocytopenia observed in Argentine hemorrhagic fever.

Animals↗
PubMed1977

The circular, segmented nucleocapsid of an arenavirus-Tacaribe virus.

The nucleocapsid structures of Tacaribe virus, a member of the Arenaviridae, were purified from detergent-treated virus particles by equilibrium density gradient centrifugation. Negative-contrast electron microscopy indicated that they were coiled, circular filaments. They had a mean diam. of 5 to 10 nm and two predominant length classes of 640 nm and 1300 nm were found.

Arenaviridae↗
PubMed1978

Structural polypeptides of Machupo virus.

The structural proteins of an arenavirus pathogen, Machupo virus, were compared to the structural proteins of two previously characterized non-pathogenic arenaviruses, Pichinde and Tacaribe, in SDS-polyacrylamide gels. Similarities in mol. wt. of the major structural proteins from both pathogenic and non-pathogenic viruses were apparent; however, some differences in the number of glycosylation properties of minor proteins were observed. Machupo virions contain two major protein species. The most prominent is a non-glycosylated protein with a mol. wt. of 68000, while the other was glycosylated protein with a mol. wt. of 41000. Minor amounts of other proteins (mol. wt. 84000, 74000, 50000 and 15000) and a glycolipid were also observed.

Arenaviridae↗
PubMed1979

Pseudotypes of vesicular stomatitis virus and Pichinde virus.

Super-infection of Pichinde virus-infected cells with vesicular stomatitis virus (VSV) resulted in the production of pseudotype virus which was not neutralized by antiserum to VSV but which was neutralized by antiserum to Pichinde virus. Analysis of pseudotype virus production in relation to the kinetics of replication of Pichinde virus demonstrated that pseudotype virus production occurred when super-infection with VSV was initiated 8 h or more after infecting the cells with Pichinde virus. The quantities of pseudotype virus produced correlated with the quantities of Pichinde virus antigen detected on the surface of the cells both during acute infection and in cells chronically infected with Pichinde virus. The observations indicate that pseudotype of VSV and Pichinde virus are readily formed and that the formation of pseudotype virus may be used to examine the Pichinde virus antigens expressed on the surface of infected cells.

Antigens, Viral↗
PubMed1977

Arenavirus concentration by molecular filtration.

Liter volumes of a human arenavirus pathogen (Machupo) and a nonpathogen (Tacaribe) were concentrated 30 to 100 times in less than 90 min without significant loss of particle infectivity.

Arenaviridae↗
PubMed1977

Variation between strains of hamsters in the lethality of Pichinde virus infections.

Infection by Pichinde virus, a member of the arenavirus group, was studied in Golden Syrian hamsters (Mesocricetus auratus) with regard to possible mechanisms of resistance to virus infection in adult hamsters. Two hamster strains were found to differ in their susceptibility to lethal Pichinde virus infection. LVG/Lak randomly bred hamsters were found to be 100% susceptible to low doses of Pichinde virus during the first 6 days of life, but after 8 days of life, mortality was uncommon. Peak virus titers in the serum of animals infected at 3 days of life were 4 logs greater than in animals infected at 12 days. MHA/Lak inbred hamsters, in contrast, were found to be susceptible to lethal virus infection both as newborns and as adults. Peak virus titers of greater than 10(8) plaque-forming units/ml were observed in serum 8 days after infection of adult MHA hamsters as compared with less than 10(3) plaque-forming units/ml in the serum of adult LVG hamsters. Cultured primary kidney cells and peritoneal macrophages from either hamster strain supported Pichinde virus replication equally well in vitro. Antibodies to the complement-fixing antigens and to antigens at the surface of virus-infected cells were produced by both strains of hamsters. Cyclophosphamide immunosuppression rendered adult LVG animals susceptible to lethal infections, and virus grew to high titers in the treated animals. These findings suggest that immunological factors that appear early in life in LVG hamsters and are deficient in MHA hamsters limit Pichinde virus infection. Unlike previously reported arenavirus diseases, the observations suggest that death is produced by a direct viral effect and not through immunopathological mechanisms.

Animals↗
PubMed1978

Enhanced resistance against Junin virus infection induced by Corynebacterium parvum.

The effects of intraperitoneal administration of Corynebacterium parvum on the course of Junin virus infection in mice were investigated. This treatment produced enhanced resistance to the virus infection, evidenced by an increase in both survival times and the proportion of survivors. The protective effect was dependent upon the dose of C. parvum, and 280 mug/g of body weight was found to be the optimal dose. In various experiments, about 80% of the infected animals receiving this dose survived, whereas survival ranged between 0 and 20% among untreated infected mice. Maximal protection was afforded by C. parvum when administered simultaneously with the virus. A smaller but significant degree of resistance was induced by C. parvum given 3 or 6 days after infection. C. parvum injected before infection was ineffective. Viral titers measured in the brains of C. parvum-treated and untreated mice at various times after infection were found to be comparable. In addition, there were no significant differences between circulating-antibody titers measured either by neutralization tests or by complement fixation. Depression of the reticuloendothelial system by treatment with silica particles also resulted in enhanced resistance to Junin virus infection, suggesting that the protective effect of C. parvum is not likely to be due merely to its capacity to stimulate macrophages. The present data, highlighting that the presence of high titers of Junin virus and disease do not necessarily correlated, suggest that in mice this disease is not the consequence of cell damage caused directly by the virus but of a still undefined indirect mechanism induced by the virus, not necessarily mediated by macrophages.

Animals↗
PubMed1978

Replication of dengue and junin viruses in cultured rabbit and human endothelial cells.

The flavivirus dengue and the arenavirus Junin are both associated with a hemorrhagic shock syndrome in man. We have demonstrated the replication of these viruses in vitro in both rabbit and human endothelial cells by viral titers and immunofluorescent antibody studies. Rabbit endothelium established in continuous culture was derived from vena cava, while human cells in primary culture were derived from umbilical veins. In rabbit endothelium, dengue-2 virus passaged through monkey kidney monolayer cells (LLC-MK2) or human lymphoblastoid cells (raji) produced significantly more virus than the seed obtained from suckling mouse brain (MB). Inoculation of actively dividing, subconfluent human endothelial cells with the LLC-MK2 degue virus produced higher viral titers than inoculation of confluent cells. The appearance of Junin virus was delayed beyond that of dengue virus in rabbit endothelial cells although equivalent titers of virus were produced. In human cells, Junin virus was less productive than dengue virus and produced characteristic cycles of virus release. This is the first direct evidence for replication of human hemorrhagic fever viruses in endothelial cells.

Animals↗