Purification, Characterization, and Comparison of the DNA Polymerases from Two Primate RNA Tumor Viruses

Abrell, John W.; Gallo, Robert C.

doi:10.1128/jvi.12.3.431-439.1973

Cited by 129 publications

(34 citation statements)

References 26 publications

(25 reference statements)

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“…The first approach would be based on assays for reverse transcriptase (RT), the special DNA polymerase discovered in 1970 by Mizutani & Temin (3) and independently by Baltimore (4). We made our assays as sensitive as possible and capable of discriminating between RT from a novel human retrovirus and RT of animal retroviruses, as well as all of the human cellular DNA polymerases (5–12).…”

Section: Discovery Of Htlv‐1mentioning

confidence: 99%

Human retroviruses after 20 years: a perspective from the past and prospects for their future control

Gallo

2002

Immunological Reviews

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Among viruses the human retroviruses may be of special interest to immunologists, because they target cells of the immune system, particularly mature CD4+ T cells, impair their function and cause them to grow abnormally (human T-cell leukemia virus, HTLV) or to die (human immunodeficiency virus, HIV). Human retroviruses cause disease ranging from neurological disorders and leukemias (HTLV-1) to AIDS (acquired immunodeficiency virus) (HIV) and promote development of several types of malignancies (HIV). They share many common features, but their contrasts are greater, especially the far greater replication and variation of HIV associated with its greater genomic complexity. Both have evolved striking redundancy for mechanisms which promote their survival. Thus, HTLV has redundant mechanisms for promoting growth of provirus containing T cells needed for virus continuity, because it is chiefly through its cellular DNA provirus that HTLV replicates and not through production of virions. Conversely, HIV has redundancy in its mechanisms for promoting virion replication and escape from the host immune system. It is via these redundant mechanisms that they produce disease: leukemias from mechanisms promoting T-cell proliferation (HTLV-1) and AIDS from mechanisms promoting virus replication and T-cell death (HIV). The practical challenges for the future are clear. For HTLV-1, education and control of breastfeeding. For HIV, the formidable tasks now ahead in part demand new kinds of talent, talents that will foster greater insights into the development of therapy for the developing countries, new forms of less toxic therapies for all infected persons, a continued and expanded commitment to education, and a persistent 'never say die' commitment to the development of a truly preventive vaccine with all the scientific and nonscientific challenges that these objectives face.

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Section: Discovery Of Htlv‐1mentioning

confidence: 99%

Human retroviruses after 20 years: a perspective from the past and prospects for their future control

Gallo

2002

Immunological Reviews

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“…The protein in the cell extracts was determined by the method of Lowry et al (1951). The activity of reverse transcriptase was determined by the method of Abrell and Gallo (1973).…”

Section: Assays For M U L Vmentioning

confidence: 99%

Changes in tumor‐specific antigen expression during passage in vitro and in vivo of newly derived methylcholanthrene‐induced sarcomas of BALB/c mice

Law¹

1980

Intl Journal of Cancer

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The characteristics of tumor antigens of the transplantation type, TATA, were studied in a series of methylcholanthrene-induced sarcomas in pedigreed BALB/cAN mice. Each of the six sarcomas exhibited unique TATA when assayed for tumor rejection in syngeneic hosts. In three instances, however, in sarcomas CI-I, CII-5 and CII-7, TATA activity was lost during early in vivo passages. This activity was reestablished invivo from the in vitro-passaged lines in CI-I and CII-7 and these sarcomas along with CI-3, CI-4 and CII-10 maintained a stable TATA phenotype throughout the 50 transplant passages; TATA was lost permanently, however, in CII-5. These results indicate a dimorphic nature of early-passage neoplasms. No cross-reacting antigens were detected among these sarcomas, including also Meth A, a sarcoma well characterized as to its membrane antigens; nor was any evidence obtained for the existence of alien (inappropriate) H-2 antigens employing tumor rejection assays in F1 hybrids of BALB/c with strains bearing several haplotypes and also with studies of H-2 serology. In three sarcomas, some evidence was obtained for the existence of alloantigens of the non-H-2 type since it was found that (BALB/c X DBA/2)F1 hybrids could not be immunized by respective sarcomas. These findings suggest the existence on these sarcomas of a tumor antigen that is expressed normally in DBA/2 mice, although no definitive evidence has been obtained. Assays for MuLV, for the viral structural proteins gp70 and p30 and for reverse transcriptase showed that three sarcomas were positive and three others, as well as Meth A, were negative. MuLV and its antigens had no influence on tumor rejection activity nor could the cross-reactivity observed in the radioisotopic footpad assay (IFP) be related to MuLV.

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“…The activity of RNA-dependent reverse transcriptase was performed with the technique described by Abrell and Gallo (1973).…”

Section: Reverse Transcriptuse Assuymentioning

confidence: 99%

Suppression of T cell‐mediated immunity by tumor cells: Immunogenicity versus immunosuppression and preliminary characterization of the suppressive factors

Ting

Rodrigues

Ting³

et al. 1979

Intl Journal of Cancer

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In studying the immunogenicity of spleen cells and tumor cells in the generation, of cytotoxic T lymphocyte (CTL) in the allogeneic mixed lymphocyte culture (MLC) or mixed lymphocyte tumor cell culture (MLTC) reactions, we have found that the tumor cells not only appear to be poorly immunogenic, but are also immunosuppressive. This was shown by the ability of the tumor cells or their cell-free extracts to suppress standard MLC reactions. This suppression was acting mainly at the induction phase of the cytotoxic response. It could not interfere with the killing activity of the fully generated CTLs. In a Friend virus-induced leukemia FBL-3 system, at least two major components could be attributed to the cause of immunosuppression; one was of viral origin and the other was of non-viral origin. The viral component was sensitive to UV-irradiation and could be pelleted after ultracentrifugation at 100,000 g. The non-viral component was UV-resistant and was retained in the supernatant fraction after ultracentrifugation. Friend virus and 12 commonly found murine viruses have been excluded as the possible candidates causing the immunosuppression. The immunosuppressive viruses are very likely of endogenous origin and are defective in replication as shown by electromicroscopy, and by the virus focus-inducing and reverse transcriptase assays. These findings indicate that probably all tumor cells possess the immunosuppressive factor(s) which may account for their apparent lack of immunogenicity and the lack of proper immune responses in the tumor-bearing hosts.

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Purification, Characterization, and Comparison of the DNA Polymerases from Two Primate RNA Tumor Viruses

Cited by 129 publications

References 26 publications

Human retroviruses after 20 years: a perspective from the past and prospects for their future control

Human retroviruses after 20 years: a perspective from the past and prospects for their future control

Changes in tumor‐specific antigen expression during passage in vitro and in vivo of newly derived methylcholanthrene‐induced sarcomas of BALB/c mice

Suppression of T cell‐mediated immunity by tumor cells: Immunogenicity versus immunosuppression and preliminary characterization of the suppressive factors

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