PubMed Health⌕ Search

Biomedical subjects

L R Overby

Publications and source records attributed to L R Overby.

At least 37 records · Page 2Linked to original sources
PubMed1979

Cryptic association of e antigen with different morphologic forms of hepatitis B surface antigen.

When highly purified HBsAg particles, separated by rate zonal centrifugation into populations differing in predominant size, were tested for HBeAg, the e1 specificity was detected preferentially in association with particle fractions containing large filaments and Dane particles. These results were obtained both by agar gel diffusion and by radioimmunoassay for e antigen. The e antigen activity present in these fractions was potentiated by prior treatment of particles with Tween 80, suggesting cryptic localization of e1 specificity within or under the outer membrane. The HBeAg released by detergent treatment from a purified preparation composed predominantly of small-particle forms of HBsAg was separated by electrofocusing into a peak of nonparticulate e antigen in the pH range of 5.7--6.0. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed three major polypeptides in this preparation with approximate molecular weights of 25,000, 55,000, and 70,000. Furthermore, two additional peaks of e antigen activity were detected which migrated in association with HBsAg particles at isoelectric points of 4.4 and 5.5--5.6. The major portion of e antigen remained in association with particles after further purification by rate zonal centrifugation.

Animals↗
PubMed1979

Serologic studies of transmission of hepatitis A in humans.

In 1968, studies of infectious hepatitis in volunteers were reported. Immunologic procedures for serologic study of the hepatitis A virus were not available at that time, and only the clinical and biochemical parameters of the disease were reported. Serial serum specimens from the participants in the study were retained; these specimens had been taken before inoculation and up to more than 100 days after inoculation. When a radioimmune assay for antibody to hepatitis A virus was developed, the series of sera was analyzed retrospectively. Forty-four male volunteers were involved in a series of three studies. Twenty (46%) of the volunteers were found to be initially immune to hepatitis A virus. Eighteen susceptible volunteers (with no preexisting antibody) were challenged with infectious virus. Eight of these volunteers developed clinical hepatitis and seroconverted; one seroconverted without evidence of clinical disease; and nine neither seroconverted nor had evidence of clinical disease. The radioimmune assay provided a method for diagnosis of immune status and of the acute disease caused by hepatitis A virus.

Antibodies, Viral↗
PubMed1979

Hepatitis B e-antigen and its correlation with other serological markers in chimpanzees.

Three chimpanzees experimentally infected with hepatitis B virus, and another three chimpanzees that were hepatitis surface antigen carriers, were studied for the presence of viral antigens and humoral immune responses. Quantitative analyses of hepatitis B surface and e-antigens in sequential serum samples at early acute stages revealed cyclic oscillations of these two antigens following a synchronous pattern. Similar analyses of anti-e-antigen and anti-hepatitis B core antigen antibodies from the three experimentally infected primates indicated that peak titers of these two antibodies occurred as surface antigen decreased to undetectable levels. Of the three surface-antigen carriers, two were positive for e-antigen and one was positive for e-antigen antibody for the entire course of surveillance (8, 9, and 22 months, respectively).

Animals↗
PubMed1979

Serodiagnosis of viral hepatitis A by a modified competitive binding radioimmunoassay for immunoglobulin M anti-hepatitis A virus.

A competitive binding radioimmunoassay (CBA) for antibody to hepatitis A virus (HAV) was evaluated and compared with a standard solid-phase radioimmunoassay for anti-HAV, CBA was found to be sensitive and specific for the detection of anti-HAV, as demonstrated by the 98% concordance of CBA and solid-phase radioimmunoassay test results. The standard CBA test was modified for the differential detection of acute (immunoglobulin M) and convalescent (immunoglobulin G) anti-HAV by incorporation of a step in which immunoglobulin G anti-HAV was preferentially absorbed with S. aureus cells (protein A). The modified CBA test was shown to be capable of differentiating between acute- and convalescent-phase sera. The modified CBAM test was able to detect immunoglobulin M anti-HAV up to approximately 4 weeks after the onset of illness.

Acute Disease↗
PubMed1978

Prevalence of hepatitis B e antigen and its antibody as detected by radioimmunoassays.

A solid-phase radioimmunoassay (RIA) for the detection of hepatitis B e antigen (HBeAg) and antibody (anti-HBe) was developed. The RIA was approximately 1,000-fold more sensitive than rheophoresis for HBeAg, and approximately 6,000-fold more sensitive than rheophoresis for anti-HBe. Generally, less than one-fifth of hepatitis B antigen (HBsAg)-positive sera from blood donors were positive for either HBeAg or anti-HBe by rheophoresis; in contrast, more than 90% of the samples were positive by the RIA method. The ratio of HBeAg to anti-HBe among HBsAg carriers varied in different geographic localities. Also, the presence of HBeAg correlated directly with the titer of HBsAg and the presence of Dane core particles. Anti-HBe was associated with lower titers of serum HBsAg.

Antibodies, Viral↗
PubMed1978

Detection of HBeAg and anti-HBe in acute hepatitis B by a sensitive radioimmunoassay.

A solid-phase radioimmunoassay using anti-HBe-coated polysterence beads and iodine-125-labeled anti-HBe of human origin was developed for the detection of HBeAg. Anti-HBe could be determined by a blocking test. Both assays were about 500-fold more sensitive than immunodiffusion. Few nonspecific positive results for HBeAg could be recognized in the anti-HBe test by increase in cpm over that of the negative control. HBeAg was not found in acute hepatitis A and non A-non B hepatitis or in a control group of accident patients. On admission to the hospital 12 of 48 (25%) acute hepatitis B patients from Greece and 17 of 20 (85%) acute hepatitis B patients from Germany were HBeAg-positive. All 39 initially HBeAg negative sera were already anti-HBe positive. Tests of the acute stage and follow-up sera of the 20 German patients indicated that HBeAg is regularly present in the incubation period and early acute phase of hepatitis B. After onset of disease the antigen is cleared from the serum very rapidly in uncomplicated cases and is usually followed by the appearance of anti-HBe. Like anti-HBc, anti-HBe can serve as a tool for the diagnosis of hepatitis B after the disappearance of HBsAg.

Acute Disease↗
PubMed1978

Characteristics of herpes simplex virus resistance to disodium phosphonoacetate.

Herpes simplex virus (HSV), which was partially resistant to the inhibitory effect of disodium phosphonoacetate (PAA), could be recovered following four virus passages in the presence of 100 microgram/ml PAA. Resistant strains were isolated from both HSV type 1 and HSV type 2. Virus resistance to PAA was not complete, and in most isolations a significant proportion of the virus stock remained susceptible to the drug. Resistance was shown to be heritable and persisted through virus passage and cloning experiments. PAA inhibited the replication of virus-specific DNA in sensitive strains of HSV but not in resistant strains of HSV. In vitro experiments directly demonstrated that PAA inhibited the activity of the virus-specific DNA polymerase 10 times more effectively in PAA-susceptible HSV than in PAA-resistant HSV. The treatment of HSV-infected mice with high levels of PAA did not induce the formation of resistant virus strains.

DNA Replication↗
PubMed1977

Antiviral potential of phosphonoacetic acid.

Phosphonoacetate has been found to inhibit specifically the replication of herpes-viruses. A partial inhibition of vaccinia virus represents the only activity outside the herpesvirus class. The drug was found to be a specific inhibitor of the virus-induced DNA polymerases. Normal cellular polymerases were relatively insensitive to phosphonoacetate, resulting in low cellular toxicity. Our working hypothesis is that the drug binds to the enzyme and that initiation of polynucleotide synthesis occurs in the presence of the drug and the required template, substrates, and cations. However, addition of deoxynucleosides to the elongating nascent chain is prevented by the enzyme-bound drug. Kinetic analyses indicated that phosphonoacetate did not interfere with the binding of DNA template to polymerase; and it did not compete with nucleotide substrate binding. The highly specific inhibitory effects of phosphonoacetate allowed for the selection of partially resistant strains of HSV. Resistance of virus to the drug in cell culture was directly correlated with the same relative resistance of the corresponding cell-free DNA polymerases. Phosphonoacetate was also effective therapeutically in herpesvirus skin and ocular infections in animals. Intraperitoneal administration of the drug reduced death and severity of disease in experimental encephalitis in hamsters. High specificity, low toxicity, and reproducible efficacy in lower animals suggested that phosphonoacetate could be a useful new antiviral drug. Sensitivity to phosphonoacetate also is a useful research tool as a genetic marker for herpesviruses.

Animals↗
PubMed1977

Seroepidemiological investigation of patients and family contacts in an epidemic of hepatitis A.

Serial blood and faecal samples were collected from patients and family contacts during an outbreak of hepatitis A in a village and tested by a solid-phase competitive type radioimmunoassay for hepatitis A antigen and hepatitis A antibody. The amount and duration of excretion of hepatitis A antigen was correlated with the severity of the illness. In 2 severe clinical cases, hepatitis A antigen was demonstrated in faecal extracts 11 days before the onset of jaundice and continuing for 10 days thereafter, with maximum shedding during the late incubation period. Faecal antigen was demonstrated in low concentrations for only 2 days in a patient with mild disease and in a person with subclinical infection. There was an inverse correlation between the incidence of infection and prevalence of hepatitis A antibody and age. Of 24 infections, 19 (79%) occurred in persons in the age group 0 to 20 years, a group in which only 6% of individuals had pre-existing antibody. Hepatitis A antibody was present in the serum of 3 persons in low titres of 1:20 to 1:40 on the day jaundice developed. The antibody titres increased very rapidly during the following 2 weeks of illness and slowly during the following months, reaching titres of 1:900 to 1:3500. In a separate study, a mean antibody titre of 1:591 was found in 13 patients, 12 years after clinical hepatitis A with jaundice.

Adolescent↗
PubMed1976

Post-transfusion hepatitis: the role of hepatitis B antibody.

Aliquots from units of blood previously transfused as part of a prospective post-transfusion hepatitis (PTH) study were rescreened for the presence of hepatitis B antibody (anti-HBS) to determine the effect of transfusion of such material. Anti-HBS was more commin in commercial blood. Infusion of anti-HBS was not associated with an increased or decreased risk of PTH, hepatitis B, or hepatitis B (HB) exposure. Receipt of anti-HBS did not modify the hepatitis which occurred. Receipt of large amounts of anti-HBS may be associated with an increased incidence of HB events. Preexisting anti-HBS was not only not protective against PTH, but more PTH (67% versus 40%) and hepatitis B (47% versus 12%) were seen in those patients with it.

Antibodies↗
PubMed1975

Acute viral hepatitis in adults. Comparison of the radioimmunoassay and counterimmunoelectrophoresis methods of detecting HbsAg.

We compared the radioimmunoassay (RIA) and counterimmunoelectrophoretic (CIE) methods in detecting hepatitis B antigen (HBsAG) in 407 acute and 336 convalescent sera of adults with viral hepatitis. The CIE method demonstrated that 41% of acute and 28% of 14-to 17-day serum specimens were HBsAg-positive. The RIA method demonstrated seropositivity in 60% of acute and 56% of convalescent specimens (P less than .001). Eighty-four percent of coded specimens initially positive for HBsAg by RIA were found to have subtype antigenic determinants d or y; 92% of the HBsAg-negative controls were negative for subtype antigens, confirming the specificity of the RIA test. RIA subtyping data corroborated earlier work with immunodiffusion techniques.

Acute Disease↗
PubMed1975

Inhibition of DNA polymerase from herpes simplex virus-infected wi-38 cells by phosphonoacetic Acid.

Infection of Wi-38 cells with herpes simplex virus induced an elevated DNA polymerase activity which had many biochemical properties different from normal cell DNA polymerase. Phosphonoacetic acid specifically inhibited the virus-induced DNA polymerase as compared to the normal WI-38 cell DNA polymerase. The compound did not appear to inhibit enzyme activity by interacting with the DNA primer.

Journal Article↗