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J S Epstein

Publications and source records attributed to J S Epstein.

At least 73 records · Page 4Linked to original sources
PubMed1989

Serological confirmation of human T-lymphotropic virus type I infection in healthy blood and plasma donors.

We wished to develop criteria for serological confirmation of human T-lymphotropic virus type I (HTLV-I) infection in healthy donors. Selected serum or plasma samples reactive by HTLV-I enzyme immunosorbent assay or gel-agglutination assays with at least one viral-specific band on Western immunoblot (WIB) were tested in six laboratories by four WIBs and four radioimmunoprecipitation assays (RIPAs) for antibodies to HTLV-I proteins encoded by gag (p19 and p24), env (gp46 and/or gp61), and tax (p40x) genes. One hundred forty-two donor sera were obtained from 38 Japanese, 69 American, and 35 Caribbean blood or plasma donors. Among these samples, WIB assays appeared more sensitive to p24 antibodies, whereas RIPAs were significantly more sensitive to gp61 antibodies. All sera (137) with gp61 antibodies had p24 antibodies. Of the 137 sera positive for p24 and gp61 antibodies, p19 antibodies were detected in 129 sera, and p40x antibodies were detected in 108. In sera with p19 antibodies and antibodies to env- or tax-encoded proteins, p24 antibodies were always present. Antibodies to p40x were not found in the absence of gp61 antibodies. Virological evidence of infection was found in seven American donors by lymphocyte coculture (one HTLV-I, one HTLV-II) or by polymerase chain reaction (three HTLV-I, two HTLV-II). Sera from all seven donors showed p24 and gp46 and/or gp61 antibodies. We suggest that seroreactivity to both p24 and gp46 and/or gp61 by WIB or RIPA or both are suitable criteria to confirm but not to distinguish HTLV-I and HTLV-II infections.

Blood Donors↗
PubMed1989

What do western blot indeterminate patterns for human immunodeficiency virus mean in EIA-negative blood donors?

To investigate the specificity of western blot indeterminate (WBi) patterns for antibodies to the human immunodeficiency virus type 1 (HIV-1), 100 enzyme immunoassay (EIA) negative donors from whom prospectively obtained recipient sera were available were tested by WB. 20 were WBi, with p24 being the predominant (70%) and generally the only band. Among recipients of WBi blood, 36% were WBi in their 6 month post-transfusion sample, but so were 42% of a control population that had received only WB-negative blood. When serial samples from recipients with a WBi pattern were tested on two occasions, only 35% of results were reproducible. No reciepient of WBi blood became EIA positive, true positive for WB, positive for HIV-1 antigen, or positive for EIA reactivity against recombinant p24 or gp41. The polymerase chain reaction was negative for gag and env HIV-1 sequences in all donors and recipients. Thus WBi patterns are exceedingly common in randomly selected donors and recipients and such patterns do not correlate with the presence of HIV-1 or the transmission of HIV-1 from donor to recipient.

Blood Donors↗
PubMed1989

Co-amplification of multiple regions of the HIV-1 genome by the polymerase chain reaction: potential use in multiple diagnosis.

We have used the polymerase chain reaction (PCR) to detect by co-amplification, multiple regions of the HIV-1 genome in infected cells. Genomic RNA and DNA from productively infected H9 cells were independently extracted and amplified in reactions with and without reverse transcriptase respectively using primer pairs to the gag, env, tat and nef regions of the viral genome in the same reaction mixture. PCR-products were analysed by liquid hybridization with end labelled oligonucleotide probes followed by gel-electrophoresis (oligomer hybridization). The primer pairs were capable of detecting as few as 10 copies of RNA and 10-20 copies of integrated proviral DNA. The ability to co-amplify multiple target regions in the same incubation mixture provides a method for detecting and confirming the presence of HIV-1 in samples for which limited nucleic acid is available. In addition, in reconstitution experiments, the same method was used to detect HIV-1 and HTLV-I simultaneously with comparable sensitivity (20-40 gene copies each). This offers the possibility of simultaneous diagnosis of multiple viral infections, such as those that occur in AIDS, on the same sample preparation.

DNA, Viral↗
PubMed1987

Detection of human immunodeficiency virus core protein in plasma by enzyme immunoassay. Association of antigenemia with symptomatic disease and T-helper cell depletion.

A sensitive enzyme immunoassay was developed for detecting human immunodeficiency virus (HIV) core antigen. Assay sensitivity was 3.67 pmol/L of purified HIV core protein, and 1 or 100 in-vitro infectious units/mL of HIV in purified virus preparations or cell culture supernatants, respectively. Enzyme immunoassay sensitivity exceeded that of reverse transcriptase assay by 1000-fold. Core antigen was detected in whole plasma from 41% of symptomatic subjects and 13% of asymptomatic subjects seropositive for HIV. After plasma fractionation, antigenemia was found in 60% of symptomatic subjects and in 33% of asymptomatic subjects seropositive for HIV. Fifty-seven percent of samples from which HIV could be isolated in lymphocyte culture had detectable quantities of core antigen in plasma. However, at least 87% of samples with measurable antigen in plasma had HIV isolated from lymphocyte cultures. Antigenemia was associated with reduced T-cell number and symptomatic disease, and may be a useful marker for disease progression.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Viral infections and cell-mediated immunity in immunodeficient homosexual men with Kaposi's sarcoma treated with human lymphoblastoid interferon.

Herpesviral infections and cellular immunity were studied in 19 patients with acquired immunodeficiency syndrome who were treated with human lymphoblastoid interferon for Kaposi's sarcoma. Before treatment, cytomegalovirus (CMV) and Epstein-Barr virus were isolated from 18 of 19 patients and 13 of 14 patients, respectively. Serum levels of interferon were measurable in all cases. Concanavalin A induced lymphocyte proliferation normally in 16 of 18 patients, but CMV induced proliferation in only nine of 18 patients. Natural killer cell activity was normal in 12 of 19 patients and was augmented in vitro by interferon in six of 19 subjects. CMV-specific HLA-restricted cytotoxic T cell activity was found in only two of 15 cases. With therapy, serum levels of interferon increased in 15 of 18 patients. There were two partial tumor remissions but no improvements in viral infections. Natural killer cell activity was decreased in 11 of 14 cases, and in vitro augmentation by interferon was absent in all five previous responders. CMV-specific T cell activity did not improve, but HLA-unrestricted cytotoxicity was increased in four of eight cases.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Selective defects in cytomegalovirus- and mitogen-induced lymphocyte proliferation and interferon release in patients with acquired immunodeficiency syndrome.

To examine the defect in cellular immunity in patients with acquired immunodeficiency syndrome (AIDS), we studied in vitro lymphocyte proliferation and interferon (IFN) release in response to cytomegalovirus (CMV) antigen and Concanavalin A mitogen in 40 homosexual men with AIDS, 10 homosexual men with chronic lymphadenopathy syndrome, 7 healthy homosexual men, and 18 healthy heterosexual subjects of either sex. CMV serology by an enzyme-linked immunosorbent assay and viral cultures for CMV were performed. Lymphocytes of patients with AIDS showed impaired CMV-specific release of IFN but normal mitogen-induced IFN release. The defect was not attributable to CMV infection per se. Cell proliferation in response to both CMV antigen and mitogen was impaired in patients with AIDS who had opportunistic infections. The defect could not be attributed to CMV viremia. We concluded that impaired release of IFN in response to a viral antigen is characteristic of lymphocytes in patients with AIDS and that this defect is distinct from a defect in mitogenic responsiveness, which coexists predominantly in patients with opportunistic infections.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Mechanisms of T-cell functional deficiency in the acquired immunodeficiency syndrome.

Cell-mediated immune responses to cytomegalovirus infections were studied to define mechanisms for deficient effector T-cell responses in patients with the acquired immunodeficiency syndrome (AIDS). Progressive cytomegalovirus infection is common in such patients and is accompanied by a failure to develop HLA-restricted cytotoxic T-cell responses. The mechanism for the cytotoxic T-cell deficiency is presumably the basis for susceptibility to opportunistic infections. Precursors to these effector cells circulate in the peripheral blood of patients, but maturation of these cells into cytotoxic T cells is arrested during an interleukin-2-dependent phase. Production of interleukin-2 by lymphocytes from patients with AIDS is deficient because sera from these patients contain an inhibitor of interleukin-2 production. Excess suppressor cell activity does not appear to account for this deficient production. Studies of the source of the serum inhibitor should provide insights into the pathogenesis of AIDS and possible leads for effective treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Comparative virulence and immunogenicity of the Towne strain and a nonattenuated strain of cytomegalovirus.

The Towne strain cytomegalovirus and a low-passage strain, Toledo-1, were compared for virulence and immunogenicity in healthy adult male subjects to determine the suitability of the Towne strain for vaccination. Five seropositive subjects who received the Toledo-1 strain developed infections ranging in severity from laboratory abnormalities to mild mononucleosis syndromes (mean incubation, 4.7 weeks). None of the four seronegative subjects receiving the Towne strain developed systemic infection, but all developed delayed local reactions at the injection sites. All subjects developed cytotoxic lymphocyte responses specific to cytomegalovirus, usually HLA-restricted, but these were of greater magnitude and duration in the Toledo-1 recipients. The latter also developed natural killer cell and interferon responses, atypical lymphocytosis, inversion of helper/suppressor cell ratios, and depressed responses to T-cell mitogens, none of which occurred in Towne strain recipients. The results further substantiate the avirulence and immunogenicity of the Towne strain cytomegalovirus.

Adult↗
PubMed1982

Efficacy of ceftriaxone in serious bacterial infections.

Ceftriaxone is a new semisynthetic cephalosporin with broad-spectrum in vitro activity and an unusually long serum half-life. The clinical efficacy of ceftriaxone was evaluated in 35 infections in 34 patients; 12 of these patients had skin and soft tissue infections, 10 had infections of the urinary tract, 8 had pneumonia, 2 had biliary tract infections, 1 had sinusitis, 1 had diverticulitis, and 1 had a retroperitoneal abscess. Of the 35 infections, 9 were bacteremic. The bacteria isolated included Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus faecalis, other streptococcal species, Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae, Serratia marcescens, Enterobacter cloacae, Haemophilus influenzae, Pseudomonas aeruginosa, Bacteroides fragilis, other Bacteroides species, and anaerobic cocci. Improvement or cure occurred in 32 episodes, for a response rate of 91%. There were three treatment failures in patients with soft tissue infections. No serious drug toxicities were observed. At a dosage regimen of 1 g every 12 h the peak and trough serum antibiotic concentrations were well above the minimal inhibitory concentrations of most pathogens. Our findings suggest that ceftriaxone is a safe and effective antibiotic for therapy of serious bacterial infections.

Adult↗