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Biomedical subjects

M S Hirsch

Publications and source records attributed to M S Hirsch.

At least 163 records · Page 9Linked to original sources
PubMed1986

Detection of human T-cell lymphotropic virus type III-related antigens and anti-human T-cell lymphotropic virus type III antibodies by anticomplementary immunofluorescence.

Techniques presently available for detection of human T-cell lymphotropic virus type III (HTLV-III) antigens and antibodies are laborious or relatively nonsensitive. We adapted anticomplementary immunofluorescence (ACIF) for these purposes. In HTLV-III-infected cells, specific ACIF was demonstrated by a diffuse speckling pattern that often resulted in a peripheral cellular rim of fluorescence. A 97% concordance was demonstrated between the ACIF assay and other sensitive tests for HTLV-III antibody detection (Western blot and membrane immunofluorescence and fixed-cell immunofluorescence tests). The ACIF assay was both more sensitive and more specific when compared with the enzyme-linked immunosorbent assay. For detection of HTLV-III antigens, the ACIF assay appeared to be as sensitive as the reverse transcriptase assay and more sensitive, with less background reactivity, than the conventional immunofluorescence assay. The ACIF assay often detected low levels of HTLV-III antigens within 3 days of infection in vitro, compared with 5 to 7 days with the indirect immunofluorescence assay, and generally paralleled the reverse transcriptase assay. The ACIF assay is a simple, sensitive, and specific assay for detection of HTLV-III-related antigens and antibodies. It should prove useful in the diagnosis of HTLV-III infection, as well as in studies of pathogenesis.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Infection of monocyte/macrophages by human T lymphotropic virus type III.

Normal blood-derived monocyte/macrophages were found to be susceptible to infection in vitro by human T lymphotropic virus type III (HTLV-III), the etiologic agent of the acquired immunodeficiency syndrome. In addition, HTLV-III was recovered from monocyte/macrophages of patients infected with this virus. The above findings raise the possibility that HTLV-III-infected monocyte/macrophages may serve as a vehicle for the dissemination of virus to target organs and as a reservoir for viral persistence, as has been shown for other lentiviruses including visna virus and caprine arthritis encephalitis virus.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Isolation of HTLV-III from cerebrospinal fluid and neural tissues of patients with neurologic syndromes related to the acquired immunodeficiency syndrome.

We conducted virus-isolation studies on 56 specimens from the nervous system of 45 patients in order to determine whether human T-cell lymphotropic virus Type III (HTLV-III) is directly involved in the pathogenesis of the neurologic disorders frequently encountered in the acquired immunodeficiency syndrome (AIDS) and the AIDS-related complex. We recovered HTLV-III from at least one specimen from 24 of 33 patients with AIDS-related neurologic syndromes. In one patient, HTLV-III was isolated from the cerebrospinal fluid during acute aseptic meningitis associated with HTLV-III seroconversion. HTLV-III was also isolated from cerebrospinal fluid from six of seven patients with AIDS or its related complex and unexplained chronic meningitis. In addition, of 16 patients with AIDS-related dementia, 10 had positive cultures for HTLV-III in cerebrospinal fluid, brain tissue, or both. Furthermore, we cultured HTLV-III from the spinal cord of a patient with myelopathy and from the sural nerve of a patient with peripheral neuropathy. These findings suggest that HTLV-III is neurotropic, is capable of causing acute meningitis, is responsible for AIDS-related chronic meningitis and dementia, and may be the cause of the spinal-cord degeneration and peripheral neuropathy in AIDS and AIDS-related complex.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Inhibition of human T-cell lymphotropic virus type III in vitro by phosphonoformate.

Phosphonoformate, an inhibitor of reverse transcriptase in a number of retroviruses, was shown to have a dose-related inhibitory effect on human T-cell lymphotropic virus type III (HTLV-III) replication in the H9 cell line in vitro. HTLV-III replication was eliminated at a concentration of 680 mumol, a non-cytotoxic dose. A lower dose of 132 mumol inhibited HTLV-III replication by more than 98%, as measured by reverse transcriptase activity, compared with untreated infected cultures. Reverse transcriptase activity in HTLV-III particles was completely inhibited by 5.0 mumol phosphonoformate.

Cell Line↗
PubMed1985

Recombinant human interferon alfa-A suppresses HTLV-III replication in vitro.

Recombinant human interferon alfa-A (rIFN alpha A) had a dose-related suppressive effect on human T lymphotropic virus type III (HTLV-III) replication in vitro in normal peripheral-blood mononuclear cells (PBMC). Both single-dose and multiple-dose regimens were inhibitory. Such inhibitory concentrations (4-1024 units/ml) were not toxic to PBMC in culture, and were within the ranges achievable in blood after injection. These studies suggest that clinical trials of rIFN alpha A in early HTLV-III infection are warranted.

Deltaretrovirus↗
PubMed1985

Risk of nosocomial infection with human T-cell lymphotropic virus III (HTLV-III).

Infection with human T-cell lymphotropic virus III (HTLV-III) is closely linked to the acquired immunodeficiency syndrome (AIDS). We evaluated the risk of nosocomial infection with HTLV-III by testing for antibodies to HTLV-III among hospital employees, including victims of needle-stick exposure, endoscopists, pathologists, and laboratory workers. Assays for antibody against the virus were performed by enzyme-linked immunosorbent assay and electrophoretic (Western blot) techniques. Although all 22 of our patients with AIDS and 6 of 7 with AIDS-related complex were found to have antibodies to HTLV-III when both assays were employed, none of the 85 employees with nosocomial exposure to specimens from patients with AIDS were positive for HTLV-III antibody. These studies must be regarded as preliminary, but they suggest that when current hospital isolation procedures are employed, the risk of nosocomial transmission of HTLV-III is low.

Accidents, Occupational↗
PubMed1985

Acute viral encephalitis.

Clinical manifestations of acute viral encephalitis are described, differential diagnoses are outlined, and a diagnostic approach is recommended. Encephalitic syndromes caused by arboviruses, herpesviruses, enteroviruses, and parainfectious processes are discussed.

Acute Disease↗
PubMed1985

Phenotypic properties of atypical lymphocytes in cytomegalovirus-induced mononucleosis.

The phenotypic properties of the surface of the atypical lymphocytes seen in cytomegalovirus-induced (CMV) mononucleosis were evaluated. Mononuclear cells from peripheral blood were obtained from adult patients within seven to 35 days of the onset of acute CMV mononucleosis. Sheep red blood cell rosetting techniques were used to obtain populations depleted of, or enriched for, T cells. Cell populations were further purified for helper/inducer lymphocytes (T4), cytotoxic/suppressor lymphocytes (T8), or non-T-lymphocytes by monoclonal-antibody binding and by complement-lysis techniques. Cytocentrifuge preparations of the cell fractions were evaluated and atypical lymphocytes were identified by morphological characteristics. The appearance and disappearance of atypical lymphocytes paralleled and antedated the increase and subsequent decrease in T8 cells seen in these patients. A total of 69% +/- 22% of the atypical lymphocytes in the lymphocyte population were of the T8 phenotype, whereas 13% +/- 10% of the atypical lymphocytes were of the T4 phenotype and 18% +/- 13% were non-T lymphocytes. Thus, atypical lymphocytes in CMV mononucleosis reside predominantly, but not exclusively, in the T8 cell population.

Adult↗
PubMed1985

Treatment of cytomegalovirus retinitis with 9-[2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine.

Cytomegalovirus infections can cause significant morbidity and mortality in immunosuppressed patients, and present antiviral agents have had little efficacy against these infections. We describe the use of an acyclic nucleoside 9-[2-hydroxy-1-(hydroxymethyl) ethoxy methyl]guanine (BW B759U), in the treatment of two patients with cytomegalovirus retinitis. The efficacy of this agent was evident, with healing of retinal lesions and resolution of viremia and viral shedding. BW B759U appears to be similar pharmacokinetically to intravenous acyclovir in terms of half-life, peak serum levels, and renal excretion.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Prospects of therapy for infections with human T-lymphotropic virus type III.

Human T-lymphotropic virus type III is susceptible to attack at various sites during its replicative cycle. Inhibitors of reverse transcriptase activity, including suramin, antimoniotungstate (HPA-23), and trisodium phosphonoformate, have shown in-vitro activity against the virus in early clinical trials. Other significant antiviral agents are recombinant interferon alpha-A, ribavirin, and ansamycin. Double-blind, placebo-controlled clinical trials of interferon alpha, which inhibits viral replication at easily achievable serum levels, are underway. The development of optimal therapeutic regimens will require carefully controlled, multicenter collaborative trials with standardized criteria for evaluating responses. Prolonged treatment with combinations of antiviral and immunomodulating agents may be necessary for control of HTLV-III replication and for effective treatment of the acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Primary human T-lymphotropic virus type III infection.

Primary infection with the human T-lymphotropic virus type III (HTLV-III) was documented in three patients by virus isolation during acute illness and concurrent or subsequent HTLV-III seroconversion. All patients had fevers, rigors, arthralgias, and myalgias. Additional symptoms included truncal maculopapular rash, urticaria, abdominal cramps, and diarrhea. Lymphocytic meningitis accompanied the febrile illness in two patients. The estimated incubation period was 4 to 6 weeks, and the symptoms lasted 2 to 3 weeks. Seroconversion occurred 8 to 12 weeks after presumed exposure and was manifested by a characteristic antibody response pattern. Physicians should consider the possibility of primary HTLV-III infection when evaluating patients who belong to one of the risk groups for the acquired immunodeficiency syndrome and who have prolonged febrile illnesses.

Adult↗
PubMed1984

HTLV-III in the semen and blood of a healthy homosexual man.

Human T-lymphotropic virus type III (HTLV-III) is the probable etiologic agent for the acquired immune deficiency syndrome (AIDS). HTLV-III was isolated from semen and blood of a healthy homosexual man whose serum contains antibodies to HTLV-III. The finding of virus in semen supports epidemiologic data that suggest that AIDS can be transmitted sexually. In addition, the demonstration of HTLV-III in the blood and semen of a healthy individual establishes an asymptomatic, virus-positive carrier state which may be important in the dissemination of HTLV-III and, consequently, AIDS.

Adult↗
PubMed1984

Herpes virus infections in patients with neoplastic disease. Diagnosis and therapy.

Herpes viruses are among the most common and troublesome opportunistic pathogens infecting patients with neoplastic diseases. The recent development of partially effective and relatively nontoxic antiviral agents offers promise for the prophylaxis or therapy of these infections in high-risk groups. Vidarabine and acyclovir have shown efficacy in several herpes virus infections and are now licensed in the United States. Alpha interferon may also be useful in the prophylaxis or early therapy of certain herpes virus infections. Newer antiviral agents and combination therapies are under study. Early and rapid diagnosis of such infections is critical to the development of effective therapy.

Acyclovir↗
PubMed1984

Antineutrophil antibodies in infectious mononucleosis.

Antineutrophil antibodies were detected in the serum of 12 of 14 patients with acute Epstein-Barr virus-induced infectious mononucleosis. These antibodies were present in two patients with mononucleosis and severe neutropenia, and in 10 patients with mononucleosis uncomplicated by severe neutropenia. Antineutrophil antibodies were not detected in serum from five patients with cytomegalovirus-induced mononucleosis, or five renal allograft recipients with primary or reactivation Epstein-Barr virus infection. This study suggests that antineutrophil antibodies are among those produced by the polyclonal activation induced by Epstein-Barr virus during acute infectious mononucleosis.

Adult↗