Rous sarcoma virus nucleotide sequences in cellular DNA: measurement by RNA-DNA hybridization

Kinetic analysis of the hybridization of 71S RNA from Prague strain of Rous sarcoma virus with an excess of DNA from virus induced sarcomas indicated the presence of the majority of the viral genome sequences in cellular DNA with a very low average frequency per cell. About one-third of the viral sequences were at least partially complementary to DNA sequences with a higher average frequency on the order of 50 to 100 per cell. Normal chick embryo DNA was distinctly different, but contained sequences at least partially homologous to some fraction of the viral RNA.     

A new class of endogenous human retroviral genomes

Human DNA contains multiple copies of a novel class of endogenous retroviral genomes. Analysis of a human recombinant DNA clone (HLM-2) containing one such proviral genome revealed that it is a mosaic of retroviral-related sequences with the organization and length of known endogenous retroviral genomes. The HLM-2 long terminal repeat hybridized with the long terminal repeat of the squirrel monkey virus, a type D retrovirus. The HLM-2 gag and pol genes share extensive nucleotide sequence homology with those of the M432 retrovirus (a type A-related retrovirus), mouse mammary tumor virus (a type B retrovirus), and the avian Rous sarcoma virus (a type C retrovirus). Nucleotide sequence analysis revealed regions in the HLM-2 pol gene that were as much as 70 percent identical to the mouse mammary tumor virus pol gene. A portion of the putative HLM-2 env gene hybridized with the corresponding region of the M432 viral genome.     

Virus-induced transformation without cell division

Interference with the cell cycle by vinblastine sulfate immediately after cells were infected with Rous sarcoma virus had little effect on the a development of two metabolic changes that occur in transformed cells. These results, along with an earlier demonstration of morphological changes developing in infected nondividing cells, demonstrate that the phenotypic development of the malignant state can occur without the intervention of cell divisions after infection by Rous sarcoma virus.     

Absence of polymerase protein in virions of alpha-type rous sarcoma virus

Noninfectious particles of a mutant of Rous sarcoma virus failed to exhibit DNA polymerase activity even with the use of the most sensitive synthetic template-primer complexes. A neutralization blocking test against antibody to DNA polymerase revealed that these mutants did not contain protein immunologically related to the DNA polymerase.     

1-Adamantanamine hydrochloride: inhibition of Rous and Esh Sarcoma viruses in cell culture

I-Adamantanamine hydrochloride, added to chick embryo cells, inhibited focus production upon subsequent inoculation of the cells with Rous and Esh sarcoma viruses. Addition of the chemical to suspensions of Rous and Esh viruses before they were added to chick cell cultures did not inactivate the viruses; and the addition to chick cells did not prevent plaque formation following their inoculation with Newcastle disease virus. This indicates that cells treated with 1-adamantanamine hydrochloride are capable of supporting viral replication, and these observations suggest that the drug inhibits growth of two oncogenic viruses by prevention of virus penetration, but not by a virucidal effect or cell intoxication.     

Wounding and its role in RSV-mediated tumor formation

Tumors induced in chickens by Rous sarcoma virus remain localized at the site of injection even though the animals become viremic. Tumors have now been shown to be inducible at other sites if a wound is inflicted or if the tissue is injured by administration of tumor promoters. These findings indicate that local wounding plays a role in the spread of tumorigenicity of Rous sarcoma virus.     

Molecular modeling of the HIV-1 protease and its substrate binding site

The human immunodeficiency virus (HIV-1) encodes a protease that is essential for viral replication and is a member of the aspartic protease family. The recently determined three-dimensional structure of the related protease from Rous sarcoma virus has been used to model the smaller HIV-1 dimer. The active site has been analyzed by comparison to the structure of the aspartic protease, rhizopuspepsin, complexed with a peptide inhibitor. The HIV-1 protease is predicted to interact with seven residues of the protein substrate. This information can be used to design protease inhibitors and possible antiviral drugs.     

Viral RNA subunits in cells transformed by RNA tumor viruses

Single-stranded 35S and 20S viral RNA species are synthesized in virus-producing mouse and rat cells transformed by the murine sarcoma virus. A transformed hamster cell line that does not produce virus synthesizes 35S, but not 20S viral RNA.     

Reversion of murine sarcoma virus transformed mouse cells: variants without a rescuable sarcoma virus

Murine sarcoma virus transformed mouse 3T3 cells, which are negative for murine leukemia virus and which yield sarcoma virus after superinfection with murine leukenmia virus, spotaneously give rise to flat variants front which murine sarcoma virus can no longer be rescued. The revertants support leukemia viruis growth and show an enhanced sensitivity to murine sarcoma superinfection and, like normal cells, do not release RNA-dependent DNA polymerase activity. Because revertants could be obtained with high frequency from progeny of single transformed cells, each cell that containts the sarconma virus genome seems to have the capacity to suppress or eliminate an RNA tumor virus native to its species of origin.     

Glycopeptides from the surface of control and virus-transformed cells

Glycopeptides were removed by trypsin digestion from the surface of control cells and cells transformed by Rous sarcoma virus, murine sarcoma virus, or polyoma virus. After digestion with pronase, the glycopeptides were analyzed by gel filtration. The elution profiles suggest that there are differences in the glycopeptides from the surface of control cells and those from transformed cells.     

Transformation of chick embryo neuroretinal cells by Rous sarcoma virus in vitro: induction of cell proliferation

Neuroretinal cells from 7-day-old chick embryos are transformed and induced to proliferate after infection with Rous sarcoma virus in vitro. Susceptibility of neuroretinal cells to the virus is also dependent on the stage of development since infection of cells from 10-day-old embryos is uneffective.     

Structure of the uncleaved human H1 hemagglutinin from the extinct 1918 influenza virus

The 1918 "Spanish" influenza pandemic represents the largest recorded outbreak of any infectious disease. The crystal structure of the uncleaved precursor of the major surface antigen of the extinct 1918 virus was determined at 3.0 angstrom resolution after reassembly of the hemagglutinin gene from viral RNA fragments preserved in 1918 formalin-fixed lung tissues. A narrow avian-like receptor-binding site, two previously unobserved histidine patches, and a less exposed surface loop at the cleavage site that activates viral membrane fusion reveal structural features primarily found in avian viruses, which may have contributed to the extraordinarily high infectivity and mortality rates observed during 1918.     

Low malignancy of Rous sarcoma cells as evidenced by poor transplantability in turkeys

Homologous and isologous transfers of Rous sarcoma cells in turkeys indicate that growth of the implanted cells contributes little, if at all, to the formation of these neoplasms. Infection of normal host cells by virus appears to be, at least in this species, the major factor in the induction and progressive growth of Rous sarcomas.     

污染疫苗的禽腺病毒分离和鉴定

在用非免疫鸡胚增殖鸭病毒性肝炎病毒(E52株)过程中，发现种毒受到污染。采用聚乙二醇沉淀．Sephadex G100柱层析法纯化污染病毒，在电镜下发现一大小为70～80nm，无囊膜，20面体对称的病毒颗粒。挑选4条随机引物对其进行反转录PCR扩增，共扩增出3条基因片段。序列分析结果表明，与禽腺病毒(鸡胚致死孤儿病毒)基因组部分序列同源性分别高达99．5％、99．6％和99．5％，从而证明禽腺病毒污染了鸭病毒性肝炎病毒鸡胚尿囊液种毒。     

Complement-fixing antigens in hamster tumors induced by the Bryan strain of Rous sarcoma virus

Hamster tumors transplanted subcutaneously from primary intracranial tumors which developed after inoculation of the Bryan strain of Rous sarcoma virus, contained virusspecific tumor antigens indistinguishable from those induced by the Schmidt-Ruppin strain.