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Biomedical subjects

R R Redfield

Publications and source records attributed to R R Redfield.

99 records · Page 6Linked to original sources
PubMed1985

A papular eruption associated with human T cell lymphotropic virus type III disease.

The clinical spectrum of human T cell lymphotropic virus type III (HTLV-III) disease is associated with myriad cutaneous findings, commonly of infectious origin. A clinically characteristic, yet histologically nonspecific, papular eruption was observed in seven of thirty-five patients followed up for HTLV-III disease (acquired immunodeficiency syndrome and the related complex). Noncoalescing 2- to 5-mm skin-colored papules of the head, neck, and upper trunk typify the lesions. Histologically, a chronic perivascular infiltrate of mononuclear cells was regularly present. The eruption was often, but not always, pruritic. The clinical course was chronic. Many patients had persistent lesions for more than 9 months; however, the number of papules tended to wax and wane with time. Although the cause of this eruption is unknown, it is sufficiently distinct and frequent to be recognized by clinicians as a cutaneous sign of human retrovirus infection.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Frequency of illness associated with epidemic hepatitis A virus infections in adults.

Hepatitis A virus infection is often described as mild or asymptomatic, particularly in children. The failure of most adults who are found to be immune to remember symptoms of an illness suggestive of hepatitis A virus supports this belief. In 1982, two large outbreaks occurred in well documented populations of military personnel. These outbreaks were each extensively studied epidemiologically and serologically. It was found that 28/29 (96.6%) hepatitis A infections recognized prior to immune serum globulin in Outbreak A and 35/46 (76.1%) infections in Outbreak A were symptomatic. Symptomatic cases failed to occur beyond eight days of immune serum globulin administration to these predominantly susceptible groups. Between 40 and 70% of patients were icteric. Apparent contrasts in symptoms associated with hepatitis A infection in adults and children suggest a basic age-dependent difference in immune response to such infection.

Adolescent↗
PubMed1984

HTLV-III in symptom-free seronegative persons.

Of 96 patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex and healthy individuals at risk for AIDS, 4 had no detectable antibodies to viral proteins, though human T-cell leukaemia (lymphotropic) virus type III was isolated from their lymphocytes. 3 of these subjects were symptom-free and 1 had lymphadenopathy. All 4 were sexual partners of patients with AIDS or AIDS-related complex. The occurrence of seronegative but virus-positive persons without clinical symptoms suggests that assays other than those detecting antibody to virus, perhaps based on detection of viral antigens or immune complexes, may be required to identify all infected individuals.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Primary isolation and serial passage of hepatitis A virus strains in primate cell cultures.

Although several primate cell types have been reported to support replication of hepatitis A virus, optimal conditions for the isolation and production of quantities of virus have not been defined. We therefore examined seven different primate cell types for their ability to support replication of primate-passaged and wild-type virus as reflected by intracytoplasmic accumulation of viral antigen (direct immunofluorescence and radioimmunoassay) and propagation of cell culture-adapted virus. Of the cells tested, low-passage African green monkey kidney (AGMK) cells were most sensitive for initial isolation. Viral replication was documented after inoculation of AGMK cells with seven of nine hepatitis A virus antigen-positive fecal specimens (from seven epidemiologically distinct sources). With six inocula, virus was successfully passed in serial cultures. AGMK-adapted virus was readily propagated in continuous AGMK (BS-C-1) cells. The optimal temperature for the growth of virus in BS-C-1 cells was 35 degrees C. Viral release into supernatant fluids was documented in the absence of any cytopathic effect, and infectivity titers in supernatant fluids 21 days after inoculation (50% tissue culture infective does [TCID50], 10(6.0)/ml) equalled or exceeded those in the cell fraction (TCID50, 10(5.5)/ml). Cells maintained in serum-free media readily supported viral growth, with yields of virus (TCID50, 10(6.5)/ml) equal to or greater than those obtained with cells maintained in 2% fetal bovine serum.

Animals↗
PubMed1974

The presence of unique DNA sequences after viral induction of leukemia in mice. (RNA tumor virus-nucleic acid hybridization-insertion of viral DNA).

From previous studies, lymphocyte DNA from human leukemias and DNA from involved tissues of patients with Hodgkin's disease or Burkitt's lymphoma contain sequences that are absent from their normal counterparts. These sequences are related to those found in particulate elements associated with these neoplasias and possessing biochemical properties characteristic of RNA tumor viruses. Similar observations have been made of unique sequences related to those of the feline virus RD-114 and found in spontaneous mastocytomas in cats. Here we extend these results to the classical murine model of virus-induced leukemias. Splenic DNA from BALB/c mice with leukemia induced by Rauscher leukemia virus (RLV) possess some RLV-related sequences that do not exist in normal BALB/c DNA. Furthermore, these leukemia-specific sequences were absent in all other mouse strains examined, including AKR, a strain with a high incidence of spontaneous leukemia. The DNA of all noninfected mouse strains possesses considerable homology with the RLV genome. Temperature denaturation studies indicate, however, that although the RLV-related sequences found in all normal mice are similar to each other, they are not exactly homologous with RLV sequences. We conclude that RLV-induced leukemia in BALB/c results in the insertion of RLV sequences into cellular DNA that itself possesses only partial homology with the RLV genome.

Animals↗
PubMedDate not supplied

Correlation of tumor suppressor P53 RNA expression with human immunodeficiency virus disease in rapid and slow progressors.

OBJECTIVE: To determine the relation between P53 tumor suppressor RNA expression and human immunodeficiency virus (HIV) disease progression. STUDY DESIGN/METHODS: A quantitative assay of P53 RNA expression was used to analyze a cohort of HIV-negative persons. The assay was then used in longitudinal and cross-sectional studies of HIV slow and rapid progressors. RESULTS: We demonstrate first that P53 expression in peripheral blood mononuclear cells from HIV-1-seronegative persons is minimal. Longitudinal studies in a small cohort of HIV-1-infected slow and rapid progressors reveal that rapid progressors seem to have greater P53 RNA expression over time. This was validated in a cohort of 26 HIV-1-infected persons in whom the expression of P53 RNA was significantly greater in persons with rapid progression of HIV-1 disease. CONCLUSION: These data suggest that P53 RNA expression may play a role in the pathogenesis of HIV-1 disease, though the mechanism of this interaction remains unknown.

Animals↗
PubMedDate not supplied

Differential human immunodeficiency virus-suppressive activity of reverse transcription inhibitors in resting and activated peripheral blood lymphocytes: implications for therapy.

OBJECTIVES: Because recent evidence indicates that human immunodeficiency virus type 1 (HIV-1) propagates in resting T lymphocytes in vivo, we wanted to evaluate the antiviral effects exerted by currently used nucleoside (NRTI) and non-nucleoside analog reverse transcription inhibitors in resting lymphocytes, and compare those effects to the ones obtained in activated lymphocytes. METHODS: Tissue culture antiviral assays in which target cells are lymphocytes present in a resting or activated state. Virus replication was measured by a reverse transcription (RT) assay. Cell viability was evaluated using a commercial 3-(4k5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS: In vitro results obtained with concentrations of zidovudine and stavudine equivalent to drug levels found in plasma, showed more than 99% HIV-1 inhibition in activated lymphocytes but less than 50% virus inhibition in resting lymphocytes. Conversely, plasma levels of didanosine-inhibited HIV-1 by approximately 50% and 98% in activated and resting lymphocytes, respectively. Plasma level concentration of zalcitabine, lamivudine, and abacavir inhibited viral replication by more than 90% in both resting and activated cells. CONCLUSIONS: These data demonstrate that specific NRTI antiretroviral agents have different activity against HIV RT, depending on the state of cell cycle of the infected cell. We suggest that the replication of HIV-1 in resting lymphocytes should be taken into account in the design of future clinical trials, as well as treatment antiretroviral regimens. Selection of combination RTIs so that they provide antiretroviral activity in both resting and activated lymphocytes may be a way to minimize treatment failure and the emergence of drug-resistant variants.

Anti-HIV Agents↗