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H L Robinson

Publications and source records attributed to H L Robinson.

At least 109 records · Page 6Linked to original sources
PubMed1985

Induction of angiosarcoma by a c-erbB transducing virus.

Recently, 12 new transductions of c-erbB have been identified in a series of Rous-associated virus type 1-induced erythroleukemias. During the passage of these new transducing viruses it has become apparent that the erythroleukemia in chicken 5005 contained two different c-erbB transducing viruses. One induces erythroblastosis, whereas the second induces angiosarcoma. The angiosarcoma- and erythroblastosis-inducing viruses appear to have had a common ancestor, since tumors induced by each contain a novel, 4.3-kilobase c-erbB-related EcoRI fragment. The angiosarcoma-inducing virus has been named avian angiosarcoma virus and is designated for the chicken in which it originated.

Animals↗
PubMed1985

Susceptibility to erbB-induced erythroblastosis is a dominant trait of 151 chickens.

Rous-associated virus-1 (RAV-1)-induced erythroblastosis results from proviral insertions into or viral transductions of the c-erbB region of the epidermal growth factor gene. Most chickens develop low incidences (less than 5%) of RAV-1-induced erythroblastosis. However, an inbred line of chickens (151) suffers high incidences (approximately 80%) of RAV-1-induced erythroblastosis. Analysis of 151, K28, and (K28 X 151) X K28 chickens for susceptibility to RAV-1-induced erythroblastosis revealed that susceptibility to RAV-1-induced erythroblastosis is a dominant trait of line 151 chickens. Analysis of 151 X K28 and K28 chicks for susceptibility to the induction of erythroblastosis by two new c-erbB-transducing viruses (avian erythroblastosis virus strains AEV-5005 and AEV-5009) revealed that susceptibility to transformation by new c-erbB-transducing viruses is also a dominant trait of 151 chickens. We think it is likely that both of these dominant traits are encoded by the same gene or genes. Our hypothesis is that this gene (or genes) potentiates the ability of the transmembrane and cytoplasmic domains of the epidermal growth factor receptor to transform cells.

Alpharetrovirus↗
PubMed1985

Sequences outside of the long terminal repeat determine the lymphomogenic potential of Rous-associated virus type 1.

Recombinant avian leukosis viruses have been constructed from the molecularly cloned DNAs of Rous-associated virus type 1 (RAV-1) and Rous-associated virus type 0(RAV-0). Virus encoded by the cloned RAV-1 DNA induced a high incidence of B-cell lymphoma and a moderate incidence of a variety of other neoplasms. Virus encoded by the cloned RAV-0 DNA did not cause disease. Virus recovered from DNA constructions that encoded the gag, pol, and 5' env sequences of RAV-0 and the 3' env and long terminal repeat sequences of RAV-1 did not cause a high incidence of lymphoma. Rather, these constructed viruses induced a low incidence of a variety of neoplasms. Virus recovered from reconstructed pRAV-1 DNA had the same disease potential as did virus recovered from the parental pRAV-1 DNA. These results indicate that the long terminal repeat sequences of RAV-1 do not confer the potential to induce a high incidence of B-cell lymphoma.

Animals↗
PubMed1984

New findings on the congenital transmission of avian leukosis viruses.

RAV-0, an endogenous avian leukosis virus, does not undergo congenital transmission in infected K28 chickens. In contrast, avian leukosis viruses of exogenous origin undergo highly efficient congenital transmission. The relative abilities of endogenous and exogenous viruses to undergo congenital transmission appear to be determined by the p27 capsid proteins of these viruses.

Animals↗
PubMed1983

Genomes of endogenous and exogenous avian retroviruses.

The endogenous viruses of chickens are closely related to the exogenous avian leukosis viruses (ALV) yet as a group differ from these viruses in their host range, growth rate, and oncogenicity. The present study was undertaken to determine the patterns of relationship among the genomes of endogenous and exogenous ALVs. Complete or partial T1 oligonucleotide maps were prepared from the genomes of endogenous viruses that reside at eight distinct loci in chickens. Selected endogenous viruses and recombinants of endogenous or endogenous and exogenous viruses were characterized for host range and growth rate. From these data we could infer the following: (1) Endogenous viruses form a distinct lineage of ALVs with the most distinctive differences occurring in the portion of env that encodes host range and the U3 portion of the long terminal repeat; (2) The U3 sequences of endogenous ALVs determine the low growth rates of these viruses; and (3) Endogenous ALVs have distinctive oligonucleotide markers that allow them to be subclassified into distinct lineages. Our results suggest that endogenous viruses are derived from one another and not from exogenous field strains of ALV. This phenomenon may be related to the unique env encoded host range of endogenous ALVs, their unique U3 encoded growth rates, or perhaps their unique access, as residents of germ line DNA, to germ line cells.

Animals↗
PubMed1982

At least two regions of the viral genome determine the oncogenic potential of avian leukosis viruses.

Recombinants of oncogenic and nononcogenic avian leukosis viruses were tested for their oncogenic potential in chickens. The results indicate that at least two regions of the viral genome determine the oncogenic potential of these viruses. The first region contains sequences that control viral mRNA synthesis. These sequences determine the potential of a virus to induce a low incidence of lymphomas, carcinomas, chondrosarcomas, fibrosarcomas, and osteopetrosis. The second region lies outside the sequences that control viral mRNAs synthesis. These sequences determine the ability of a virus to induce a high incidence of lymphomas or osteopetrosis.

Animals↗
PubMed1982

Role of methylation in the induced and spontaneous expression of the avian endogenous virus ev-1: DNA structure and gene products.

The endogenous avian provirus ev-1 is widespread in white leghorn chickens. Although it has no major structural defects, ev-1 has not been associated with any phenotype and is ordinarily expressed at a very low level. In this report, we describe a chicken embryo (Number 1836) cell culture containing both ev-1 and ev-6 which spontaneously expressed the ev-1 provirus. This culture released a high level of noninfectious virions containing a full complement of virion structural (gag) proteins but devoid of reverse transcriptase activity or antigen. These virions contained 70S RNA closely related to the genome of Rous-associated virus type 0, but identifiable as the ev-1 genome by oligonucleotide mapping. A fraction of the RNA molecules in the 70S complex were unusual in that they were polyadenylated 100 to 200 nucleotides downstream of the usual polyadenylation site. Eight sibling embryo cultures did not share this unusual phenotype with 1836, indicating that it was not inherited. However, an identical phenotype was inducible in the sibling cultures by treatment with 5-azacytidine, an inhibitor of DNA methylation, and the induced expression was stable for more than 10 generations. Analysis of chromatin structure and DNA methylation of the ev-1 provirus in 1836 cells revealed the presence (in a fraction of the proviruses) of both DNase I hypersensitive sites in the long terminal repeats and in gag and a pattern of cleavage sites for methyl-sensitive restriction endonuclease not found in a nonexpressing sibling. These results lend strong support to the role of DNA methylation in the control of gene expression. Additionally, they explain the lack of phenotype associated with ev-1 as due to a combination of its low expression and defectiveness in pol and env.

Animals↗
PubMed1981

Avian leukosis virus-induced tumors have common proviral integration sites and synthesize discrete new RNAs: oncogenesis by promoter insertion.

Unlike other RNA tumor viruses, avian leukosis viruses (which cause lymphomas and occasionally other neoplasms) lack discrete "transforming genes". We have analyzed the virus-related DNA and RNA of avian leukosis virus (ALV)-induced tumors in an attempt to gain insight into the mechanism of ALV oncogenesis. Our results show that viral gene products are not required for maintenance of neoplastic transformation. Primary and metastatic tumors are clonal and thus presumably derived from a single infected cell. Most importantly, tumors from different birds have integration sites in common. Tumor cells synthesize discrete new poly(A) RNAs consisting of viral sequences covalently linked to cellular sequences. These RNA species are expressed at high levels in tumor cells. Our results suggest that in lymphoid tumors, an ALV provirus is integrated adjacent to a specific cellular gene, and the insertion of the viral promoter adjacent to this gene results in its enhanced expression, leading to neoplasia. These results have potentially important implications for the mechanism of non-viral carcinogenesis.

Animals↗
PubMed1980

Ten genetic loci in the chicken that contain structural genes for endogenous avian leukosis viruses.

Our interpretation of the results presented here may be summarized as follows: (1) Endogenous viral genes can be located at any of a large number of sites in the chicken chromsome. (2) Different phenotypes of viral gene expression are observed, depending on the nature of the viral sequences at a given site and depending on whether the necessary sequence elements for expression are present. (3) Endogenous viral genes perform no essential function in the chicken.

Alpharetrovirus↗