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Biomedical subjects

R Gallo

Publications and source records attributed to R Gallo.

At least 127 records · Page 7Linked to original sources
PubMed1985

Detection of a surface antigen on NIH3T3 cells transfected with a human leukemia oncogene.

This study was conducted to examine the cell surface changes associated with oncogene induced transformation. Using the transfection technique the DNA of a human acute lymphocytic leukemia (ALL) was used to transform murine NIH3T3 cells. Balb/c mice were immunized with these transfectants and their immune splenocytes were used to produce a monoclonal antibody (17-9H3). Antibody 17-9H3 was demonstrated to bind to the cell membranes of transfectants and leukemia cells but not normal 3T3 cells in an enzyme linked immunosorbent assay. Fresh human leukemias, cultured leukemia lines and normal hemopoietic cells were examined with immunoperoxidase staining techniques to determine the specificity of 17-9H3. Our data suggest that the antigen associated with a human acute lymphocytic leukemia oncogene is ubiquitous, distributed among both neoplastic and normal hemopoietic cells. Among fresh human leukemias the antigen appears to be present primarily on fresh null ALLs and chronic myelogenous leukemia (CML) in blast crisis. This antigen was also found to be expressed by the majority of cultured T-cell lines tested.

Animals↗
PubMed1985

Antibodies to human T lymphotropic virus type III demonstrated by a dot immunobinding assay.

A dot immunobinding (DIB) technique was applied to the demonstration of antibodies to human T-lymphotropic virus type III (HTLV-III). By this technique IgG antibodies to HTLV-III were demonstrated in six of six Swedish patients with acquired immune deficiency syndrome and in 37 of 39 (95%) Swedish homosexual men with persistent generalized lymphadenopathy but in none of 50 Swedish healthy blood donors. Findings obtained by this method showed complete concordance with those obtained by an enzyme-linked immunosorbent assay. All sera positive by DIB were also positive by Western blotting. The DIB assay is simple and well suited for screening of sera for HTLV-III antibodies.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Molecular biology of human T-lymphotropic retroviruses.

The generic name for a family of human T-lymphotropic retroviruses is HTLV. Two of the three members in this family have been linked etiologically to human diseases: HTLV-I with adult T-cell leukemia and HTLV-III with the acquired immunodeficiency syndrome. In addition to their T-cell tropism and a number of other common biological and biochemical properties, the most unique common features of these viruses from a molecular biological point of view are the presence of the x-lor gene towards the 3' end of the genome and the phenomenon of a virus-induced trans-acting factor in activation of transcription initiated in the viral long terminal repeat. These features may not only be key in understanding the mechanism of transformation or cell killing by these viruses, but they also provide a basis for new classification of retroviruses. In spite of these similarities among HTLV-I, -II, -III, and bovine leukemia virus, the genome of HTLV-III is only distantly related to these other viruses. Instead, it shows greater homology to members of the Lentivirus family. Therefore, all these viruses may have a common progenitor. Two other salient features arose from the analyses of HTLV-III and acquired immunodeficiency syndrome. (a) HTLV-III frequently infects the brain of acquired immunodeficiency syndrome patients who suffer from central nervous system disorders. This not only identifies HTLV-III as the direct candidate in these central nervous system disorders but also poses the problem of crossing the blood-brain barrier in therapy strategies to eradicate the virus. (b) Different HTLV-III isolates comprise a spectrum of related viruses, with the degree of divergence varying from virtual identity to 10-15% difference. The most divergent region resides in the envelope gene. Whether this finding has implications in the development of an effective vaccine for acquired immunodeficiency syndrome remains to be determined.

Acquired Immunodeficiency Syndrome↗
PubMed1985

HTLV-III infection in homosexuals and hemophiliacs in Sweden.

Two hundred and three homosexual (HS) men and 114 hemophiliacs in Sweden were examined for serum antibodies to human T-lymphotropic virus type III (HTLV-III) and for alterations of T-lymphocyte subsets. Sera were screened for HTLV-III antibodies by an enzyme-linked immunosorbent assay and/or a dot immunobinding assay, and positive reactions were confirmed by Western blotting. HTLV-III antibodies were demonstrated in 13 of 13 (100%) HS men with acquired immune deficiency syndrome, in 63 of 67 (94%) HS men with persistent generalized lymphadenopathy, in 17 of 45 (38%) symptomatic HS men, and in 6 of 78 (8%) asymptomatic HS men but in none of 108 male blood donors. Seropositive HS men had significantly lower T4/T8 (helper/suppressor) cell ratios and T4 cell numbers than had seronegative HS men. Seronegative HS men had decreased T-cell ratios compared to controls but not decreased T4 cell numbers. Among hemophilia A patients, HTLV III antibodies were demonstrated in 40 of 48 (83%) cases treated with American factor VIII concentrate and in 17 of 29 (59%) cases treated with both American and Swedish concentrates but in none of 13 cases treated exclusively with Swedish factor VIII. Twenty-one hemophilia B patients treated with Swedish factor IX concentrates were all seronegative, whereas one of 3 hemophilia B cases treated with imported factor IX was seropositive. T4/T8 cell ratios were significantly lower in seropositive as compared to seronegative hemophilia A patients.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Unique pattern of HTLV-III (AIDS-related) antigen recognition by sera from African children in Uganda (1972).

Of 75 sera collected in the West Nile district of Uganda over a 1-year period between 1972 and 1973, 50 (66%) had antibody reactivity to human T-cell lymphotropic virus subgroup III (HTLV-III) at low titer levels. Sera were initially screened by HTLV-III enzyme linked immunosorbent assay and sera with values less than normal mean + 2 SD were removed from testing. The remaining sera were tested for positivity by an amplified Western blotting procedure which incorporated a three-layer immunoperoxidase procedure. Immunoglobulin reactive with HTLV-III Mr 24,000, 41,000, and 76,000 proteins were present in nearly all positive sera. The antibody status of this group was unlike any normal or acquired immunodeficiency syndrome-risk group previously tested. The high prevalence and relatively low titers suggest the detection as early as 1972 of a relative or predecessor of HTLV-III or of HTLV-III itself but existing in a population acclimated to its presence. It further suggests a likely African origin of HTLV-III.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Antibody seronegative human T-lymphotropic virus type III (HTLV-III)-infected patients with acquired immunodeficiency syndrome or related disorders.

The human T-lymphotropic virus type III (HTLV-III) is the primary cause of the acquired immunodeficiency syndrome (AIDS) and related disorders (ARC). Prior studies have reported that nearly all symptomatic patients with AIDS or ARC manifest antibody to HTLV-III. This observation has engendered efforts to screen for HTLV-III, especially prior to blood donation, with assays for antibody to HTLV-III. We report the first two cases, one with AIDS and one with ARC, that are HTLV-III virus positive but antibody negative. Accurate diagnosis of HTLV-III infection in some cases may require direct virus culture or tests for antigen. In addition, lack of HTLV-III antibody may indicate an atypical clinical course of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Preferential stimulation of rabbit alpha globin mRNA translation by a cap-binding protein complex.

A cap-binding protein complex (Edery et al. (1983) J. Biol. Chem. 258, 11398-11403) is shown here to stimulate preferentially the translation of endogenous alpha versus beta globin mRNA in a rabbit reticulocyte lysate. Several initiation factors (eIF-2, eIF-3, eIF-4A, eIF-4B, eIF-4C, eIF-4E and eIF-5) and elongation factor 1 were found to have no such discriminatory effect. These results are in contrast to several previous reports and demonstrate that the only factor capable of relieving translational competition between alpha and beta globin mRNAs is the cap-binding protein complex.

Animals↗
PubMed1984

Transmission of HTLV-III infection from human plasma to chimpanzees: an animal model for AIDS.

Two of three chimpanzees given plasma from patients with acquired immune deficiency syndrome (AIDS) or pre-AIDS showed serum antibodies to type III human T-cell leukemia virus (HTLV-III) 10 to 12 weeks after transfusion. One animal also developed lymphadenopathy, transient depression of the ratio of T4 to T8 lymphocytes, and impaired blastogenic responses. No opportunistic infections occurred. Adenopathy persisted for 32 weeks, and antibody to HTLV-III persisted for at least 48 weeks. This transmission of HTLV-III by lymphocyte-poor plasma confirms the potential risk of such plasma or plasma derivatives to recipients. The susceptibility of the chimpanzee to HTLV-III infection and the ability to simulate the human lymphadenopathy syndrome in this animal makes it a valuable model for further study of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Repetitive structure in the long-terminal-repeat element of a type II human T-cell leukemia virus.

The majority of human T-cell leukemia virus isolates (HTLV-I) are associated with clinically aggressive adult T-cell leukemia/lymphomas. By contrast, HTLV-II has been isolated from a patient with a relatively benign hairy T-cell leukemia. To characterize differences in the viral genomes that might contribute to these different pathologies, we determined the nucleotide sequence of the long terminal repeat (LTR) of a HTLV-II provirus. Comparison with the type I HTLV LTR reveals that, whereas the overall structural features are similar, the two sequences differ markedly throughout most of the length of the LTR. Despite the overall differences, the sequences of several functional regions of the two LTRs are conserved. These include the 5' boundary of U3, the RNA cap site, and the tRNAPro-binding site immediately 3' to the LTR. Another point of similarity is a 21-base sequence that is repeated four times in the U3 region of HTLV-II and three times in the U3 region of HTLV-I. This sequence has a formal analogy to, but no common sequence with, viral transcriptional enhancers. The U3 region of HTLV-II possesses a series of imperfect tandem direct repeats, 42 bases long, 21 bases long, 19 bases long, and 7 bases long. These structures differ from those of HTLV-I except for the 21-base repeat sequence. Thus, the structure of HTLV-II differs substantially from that of HTLV-I in the region that governs transcriptional initiation and tissue specificity. Such differences may account for some of the differences in clinical presentation of HTLV-associated adult T-cell leukemia/lymphomas and hairy T-cell leukemia.

Base Sequence↗
PubMed1984

Adult T-cell leukemia/lymphoma in Jamaica and its relationship to human T-cell leukemia/lymphoma virus type I-associated lymphoproliferative disease.

We had shown previously that the prevalence of human T-cell leukemia/lymphoma virus type I (HTLV-I)-antibody positivity is high in Jamaican non-Hodgkin's lymphoma (NHL) patients and that virus-positive patients have the clinical features and poor prognosis of adult T-cell leukemia/lymphoma (ATL). Sixty-two % of 45 NHL patients diagnosed consecutively between 2/1/82 and 1/31/84 and studied prospectively were HTLV-I-antibody positive. Skin involvement (38%), hypercalcemia (44%), and leukemia (40%) were unusually prevalent and there was a strong association (p less than 0.05) with HTLV-I-antibody positivity. Fifty-two % of the patients had bone marrow infiltration, and 74% of these patients were HTLV-I-antibody positive (p = 0.06). Lymphadenopathy (96%), hepatomegaly (60%), and splenomegaly (25%) were detected with about the same frequency as in other series of NHL patients with advanced disease, and 61-88% of these patients were HTLV-I-antibody positive. Patients were classified into those with "typical ATL" (NHL associated with 2 of the 4 features i) hypercalcemia; ii) histologically proven skin infiltration; iii) leukemia; and iv) bone marrow infiltration, providing that the morphology of infiltrating or leukemic cells was characteristic of ATL; those "consistent with ATL" (NHL associated with 1 of these 4 features); and "non-ATL" (NHL without any of these 4 additional features). Thirty-two (71%) of the NHL patients were ATL patients, i.e., had features typical of or consistent with ATL, and 78% of these were HTLV-I-antibody positive. HTLV-I provirus was detected in tumour cells of all HTLV-I-antibody positive patients tested. Three (23%) of the non-ATL patients were HTLV-I-antibody positive. There was no correlation between histopathological features and the clinical classification or HTLV-I-antibody positivity. Median survival of ATL and non-ATL patients was 16 and 53 weeks. Although the disease was usually fulminant, 34% of the ATL patients had a subacute or chronic course. Skin involvement and leukemia were prominent in these patients. Hypercalcemia was the chief prognostic determinant. Median survival of hypercalcemic and normocalcemic ATL patients was 13 and 86 weeks (p less than 0.05). Hypercalcemia caused 10 deaths, infections 12, and death was due to tumour progression in 4 patients. Infections were usually due to pyogenic organisms and only 2 patients had systemic opportunistic infections. Six (27%) of 22 chronic lymphocytic leukemic (CLL) patients were HTLV-I-antibody positive.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Oncogene expression in human leukemia.

The transforming genes of retroviruses (v-onc) are derived from normal cellular genes referred to as proto-oncogenes. These cellular genes have the capacity for conversion to oncogenes (c-onc) that are capable of inducing or maintaining the transformed state when they are overly expressed or altered by mutation or rearrangement. To study the possible involvement of these genes in human leukemia, we have analyzed their expression in a variety of fresh samples. We found that a number of oncogenes are expressed in different leukemic types and that although the transcript size did not vary for each gene, the copy number did. The myc gene (2.4 kb transcript) and the rasHa gene (1.5 kb transcript) were universally expressed. But in contrast to rasHa, the myc signal intensity varied. Myb (4.5 kb transcript) was expressed in all samples except B cell diseases. We detected low levels of abl expression (multiple mRNA species) in all leukemic types analyzed. Sis gene (4.2 kb transcript) expression was restricted to one patient sample with chronic myelogenous leukemia in blast transformation.

Acute Disease↗
PubMed1983

[Etiological aspects of leukemias in primates including man].

Attempts have been made to induce viral leukemia in monkeys (Papio hamadryas and Macaca arctoides) by inoculating them with blood from humans with different types of leukemias. In hamadryas baboons, the disease spread horizontally. By today 218 P. hamadryas and 5 M. arctoides monkeys had died of malignant lymphoma. The following viruses have been isolated from sick monkeys: lymphotropic baboon herpes virus (HVP), endogenous baboon C type viruses--xenotropic (BILN), and ecotropic (EVPG). C type oncovirus called "plasmic", which differs immunologically from the endogenous one, was also detected in the blood of sick animals. Altogether 165 sera from baboons, different species of macacas and chimpanzee were examined by the immunofluorescent technique for antibodies to HTLV virus isolated recently from sick humans with T cell leukemia/lymphoma. Antibodies to HTLV virus were detected only in monkeys (P. hamadryas and M. arctoides) with malignant lymphomas or in those which had been in close contact with them. Possible origin of simian HTLV-like virus is discussed. It originates either from leukemic patients or there is a family of primate HTLV like viruses related to the occurrence of leukemia.

Animals↗
PubMed1981

Muzolimine: a new high-ceiling diuretic suitable for patients with advanced renal disease.

Muzolimine was administered by mouth to 24 patients with creatinine clearances ranging from 4 to 28 ml/min to treat oedema or hypertension, or both. In four of these 24 patients muzolimine was given after intravenous high-dose frusemide had been unsuccessful. Muzolimine significantly increased urine volume and excretions of sodium, chloride, and potassium ions. Its diuretic efficacy was further shown by a mean reduction in body-weight of 8% and by the disappearance of oedema in all affected patients, even those refractory to intravenous frusemide. No rebound phenomenon was observed after the drug was stopped. Mean blood pressure was reduced in all hypertensive patients. Blood pressure was restored to normal in five out of seven patients treated with muzolimine alone and 10 out of 11 in whom muzolimine had been added to previously unsatisfactory antihypertensive treatment. Muzolimine was well tolerated by all patients. Muzolimine appears to be the diuretic of choice when treating patients with advanced renal disease.

Adolescent↗
PubMed1981

Echocardiographic detection of cardiac effects of arterio-venous dialysis fistula.

The effects of the dialysis fistula were evaluated by echocardiography in 10 patients with terminal renal failure. Echocardiography was performed the day before creation of the fistula (E0) and was then repeated 24 hours after surgery (E1), the day before the first dialysis (E2), the day following the fourth dialysis (E3) and, finally, after 6 months of RDT (E4). Left ventricular internal diameter was measured both in diastole (LVIDd) and in systole (LVIDs), allowing calculation of ventricular diameter percent shortening (LVID%), of ventricular diastolic (EDV) and systolic volume (ESV). In E1 the fistula caused a significant increase in LVIDd, accounting for a rise also in EDV. This ventricular dilation persisted in E2, but was abolished in E3 and in E4. LVIDs, ESV, and LVID% were unmodified throughout the study. these results show that the dialysis fistula causes an immediate rise in cardiac pre-load, which is rapidly reversed by RDT.

Adolescent↗
PubMed1980

[Treatment of arterial hypertension with minoxidil in renal insufficiency].

Minoxidil was administered to 13 patients with arterial hypertension resistant to ordinary antihypertensive drugs and with various degrees of renal failure. Four patients were followed in this way for 50 weeks. Blood pressure values fell from 208 +/- 9.8/124 +/- 4.8 to 153.1 +/- 7.8/86.9 +/- 2.6 at the end of the treatment period. Propanolol and furosemide were used to offset sodium retention and reflex tachycardia. There was no decrease in renal function. In patients examined for the longest period, the minoxidyl dose, after an intermediate reduction stage, reached the 8th week value. Hypertrichosis was the most disturbing side-effect, especially for the female patients. The question of pericarditis is discussed.

Adult↗
PubMed1979

Detection of integrated type-C viral DNA fragments in two primates (human and gibbon) by the restriction enzyme blotting technique.

We have shown that 1. partial provirus integration can be a possible result of a natural infection, and may serve as a model in animal systems where a viral etiology is implicated but detection of a major fraction of the virus genome is rare; 2. All human DNA contains some sequences that hybridize specifically with genomes of SiSV-SiSAV, suggesting that viruses of this group have infected humans in the past and recombined with human cellular DNA. 3. Finally, DNA from uncultured leukocytes of two leukemic patients, one being HL23, which yielded the virus HL23V in culture, was shown to have virus specific fragments related to BaEV. Another human DNA sample revealed virus specific fragments related to SiSV(SiSAV). These fragments are probably acquired by infection.

Animals↗