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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 289 records · Page 16Linked to original sources
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↗
PubMed1977

Antibody-dependent cellular cytotoxicity against murine leukemia viral antigens: studies with human lymphoblastoid cell lines and human peripheral lymphocytes as effector cells comparing rabbit, goat, and mouse antisera.

A thymic lymphoblastoid cell line derived from a New Zealand Black mouse produces murine leukemia virus (MuLV) and was used as a target in model systems for the in vitro study of antibody-dependent cellular cytotoxicity (ADCC). Several human lymphoblastoid cell lines were investigated as potential effector cells. The most promising (Raji cells) bound to antibody-coated target cells but caused only modest levels of ADCC at 25:1 effector-to-target cell ratio with substantial lysis in the absence of antiserum. Human peripheral lymphocytes were active as effector cells in ADCC at a 5:1 ratio and produced no lysis in the absence of antibody. These cells were used to demonstrate that high dilutions of rabbit antisera to MuLV antigens p30, p15, p12, and p10 were capable of mediating lysis of MuLV-producing target cells but not of a virus-negative murine cell line. A murine antiserum to Thy 1.2 and three caprine antisera to MuLV antigens that were active in complement-mediated cytotoxicity functioned poorly in inducing ADCC; however, rabbit antisera to similar antigens were 16- to 512-fold more efficient in cell-mediated than in complement lysis. The inefficiency of goat antisera was not due to shedding of cell surface antigens or generation of blocking factors but rather to lack of lytic interaction of antibody-coated targets with the effector cells.

Animals↗
PubMed1976

The seroepidemiology of reovirus, coxsackievirus infections among Panamanian Indian children.

Rates of hepatitis B virus infection varied significantly among Panamanian Indian tribes. Chocó and Mainland Cuna Indians had a greater prevalence of antibody to hepatitis B surface antigen than Guaymi and Island Cuna Indians. The village water supply appeared to be the major environmental difference that distinguished the tribes from one another. Since contaminated water plays a role in the transmission of enterovirus, an attempt was made to assess relative exposure to contaminated water by determination of the prevalence of antibodies to reovirus and coxsackievirus B in children 10 years old or younger. Infection with coxsackievirus B occurred more frequently in Chocó and Mainland Cuna Indians than in Guaymi or Island Cuna Indians. Although essentially all children tested were exposed to reoviruses, Mainland Cuna Indians had the highest geometric mean titers of antibody, followed by Chocó, Guaymi, and Island Cuna Indians in descending order. This parallel in rates of hepatitis B and enterovirus infection supports the hypothesis that fecal-oral transmission of hepatitis B virus is important in certain populations.

Antibodies, Viral↗
PubMed1976

Radioimmunoassay for antibody to hepatitis B surface antigen shows transmission of hepatitis B virus among household contacts.

The epidemiology of infections with hepatitis B virus was studied by measurement of serum antibodies to hepatitis B surface antigen (HBS Ag) with the radioimmuno-precipitation test. Prospective studies of household contacts of HBS Ag-positive patients with acute hepatitis demonstrated that four of 41 children and one of 60 adults experienced anicteric seroconversions. Two of the 60 adults also had mild icteric hepatitis and became chronically antigenemic. Neither HBS Ag nor antibody to HBS Ag was detected in follow-up blood samples from 85 seronegative contacts of HBS Ag-negative patients with hepatitis, although seven icteric secondary cases were identified. Household contacts of HBS Ag carriers frequently had serologic evidence of exposure to hepatitis B virus (44% of adults), but the remainder had neither detectable antigen nor antibody.

Adolescent↗
PubMed1976

IgM levels and IgM-mediated immune responses in patients with acute hepatitis A, acute hepatitis B and chronic HB antigenaemia.

Immunoglobulin M (IgM) levels and their relationship to isohaemagglutinins, febrile agglutinins, sheep cell agglutinins, and rheumatoid factor were measured in patients with acute hepatitis A, acute hepatitis B, chronic hepatitis B antigenaemia, and normal control populations. Significant IgM elevations were observed in both types of acute hepatitis, but not in chronic hepatitis B antigenaemia. There was no correlation of the IgM level with either the prevalence or titre of any IgM-mediated immune response studied. These data suggest that the IgM elevations in both types of hepatitis may reflect virus-specific IgM synthesis.

Agglutinins↗
PubMed1975

Familial clustering of hepatitis B surface antigen among Panamanian Indians.

Several authors have suggested that the host genome determines the occurrence of chronic HBS Ag (hepatitis B surface antigen). In attempts to evaluate this possibility, total infection rate and the combined frequencies of HBS Ag and antibody to HBS Ag and radioimmunoprecipitation to measure antibody to HBS Ag, we tested sera from 255 Panamanian Guaymi Indians. They represented 48 families and 32 living units. Clusters of chronically antigenemic individuals were found in families. Clusters of infection were not found in families or living units. Differences in family composition (age and sex) did not explain the increased occurrence of HGS Ag. These findings support the hypothesis that some humans have an inherited susceptibility to chronic infection with hepatitis B virus after exposure.

Adolescent↗
PubMed1975

The epidemiology of hepatitis B antigen and antibody among Panamanian Cuna Indians.

Previous studies of hepatitis B antigen (HBsAg) and antibody to it (anti-HBs) showed widely differing exposures between Panamanian Indian tribes. Cuna Indians living on islands appeared infrequently exposed to HBsAg; we found no one antigenemic and low age specific anti-HBs rates. In contrast, mainland dwelling Guaymi and Chocó Indians had a high prevalence of anti-HBs. We have now measured HBsAg by counterelectrophoresis and anti-HBs by radioimmunoassay in two Cuna Indian groups who live in the Darien forest. The prevalence of HBsAg among Darien Cuna was low, 3 positive of 239 tested, but 106 (44%) had anti-HBs. Darien Cuna thus evidenced greater exposure to HBsAg than island Cuna (8% had anti-HBs) and had an anti-HBs prevalence similar to the neighboring Chocó Indians (42%). The Guaymi Indians of western Panama had a lower frequency of anti-HBs (29%) than either Chocó or mainland Cuna but their frequency of chronic antigenemia was significantly greater. These data suggest that while exposure may be a function of village habitat, chronic antigenemia may reflect differences in host responses.

Adolescent↗
PubMed1970

Serological relationship of the Tacaribe complex of viruses to lymphocytic choriomeningitis virus.

By means of the indirect fluorescent-antibody test, cross serological reactivity was demonstrated between lymphocytic choriomeningitis (LCM) virus and the viruses of the Tacaribe complex. Antisera to all members of the Tacaribe complex reacted with LCM virus; LCM antisera gave significant staining of Amapari virus, but minimal or inconsistent reactions with Tacaribe virus, and no reaction with two other viruses of the Tacaribe complex. A low level cross-reaction was observed in complement fixation tests of Machupo and Pichinde antisera against LCM antigen. Immunization with Tacaribe and Amapari viruses did not protect mice against challenge with LCM virus. Because of the identical appearance of the virions, the sharing of antigens, and the many biological similarities between LCM and the Tacaribe complex viruses, it is proposed that they be considered as constituting a new taxonomic group of viruses.

Animals↗
PubMedDate not supplied

Differential effects of propranolol on lymphocyte rosette formation and response to plant mitogens.

The effects of propranolol on various lymphocyte functions were studied to gain a better understanding of the recently demonstrated suppressive effect of propranolol on rheumatoid factor production. D- and L-propranolol at a concentration of 1 X 10(-4)M inhibited the formation of human EA rosettes. The inhibition occurred within one minute of adding the compounds, was reversible, and did not affect cell viability. Addtion of propranolol to preformed EA rosettes failed to disaggregate them. Patching and capping of SIg by an Fab'2 anti-IgG were inhibited at 2.5 X 10(-5)M and above. Propranolol at 2.5 X 10(-5)M also inhibited lymphocyte response to phytohemagglutinin and pokeweed mitogen without evidence of cell toxicity by trypan blue staining or absolute numbers of surviving cells. Congeners of propranolol with mainly beta adrenergic blocking properties did not show inhibitory effects. The inhibitory activities of propranolol are interpreted in terms of propranolol's membrane stablizing effects and ability to interfere with membrane receptor movement.

Animals↗