The myeloproliferative sarcoma virus not only transforms fibroblasts but also causes extensive expansion of the hematopoietic stem cell compartment on infection of adult mice. Similar to the Moloney sarcoma virus, it carries the mos oncogene. Moloney sarcoma virus, however, does not induce myeloproliferation and leukemia in adult mice. The difference between the two viruses was explored by using their molecularly cloned genomes and the cellular mos oncogene to construct recombinant genomes. It was shown that the U3 region of the viral long terminal repeat (LTR) has a decisive function in determining the target cell specificity of the myeloproliferative sarcoma virus. Any mos gene, whether of cellular or viral origin, is sufficient in conjunction with the proper LTR to induce myeloproliferation. Our results indicate that the pathogenicity of acutely transforming viruses is determined not only by the oncogene but also by sequences in the viral LTR.

A derivative of the myeloproliferative sarcoma virus (Neor-MPSV) carrying the mos oncogene and dominant selection marker for neomycin resistance (Neor) was introduced into embryonal carcinoma and embryo-derived cell lines by transfection and infection using pseudotypes with Friend helper virus (Friend murine leukemia virus [F-MuLV]). Cells resistant to G418 (a neomycin analog) were cloned and expanded. Transductants retained an undifferentiated phenotype as judged by morphology, tumorigenicity, and cell-surface antigen analyses. Nucleic acid analysis of infectants revealed both Neor-MPSV and F-MuLV proviruses, although no virus was released. G418-resistant transductants remained nonpermissive for the expression of other proviruses and for subsequent superinfection. Northern analysis showed expression of full-length Neor-MPSV, as well as mos-specific subgenomic RNA. mos sequences were deleted from Neor-MPSV (Neor mos-1), and pseudotypes were used to infect embryonal carcinoma cells. No morphological differences were observed in either mos+ or mos- transductants as compared with parental cell lines. However, mos+ transductants showed an enhanced anchorage-independent growth compared with that of mos- transductants in agar cloning. PCC4 transductants were induced to differentiate with retinoic acid and superinfected with F-MuLV. Infection with viral supernatant in fibroblasts and in mice confirmed the rescue of biologically active Neor-MPSV.

The mini plasmids deriving from pKN102, a copy mutant of the antibiotic resistance factor R1drd-19 of E. coli, share a common DNA sequence of 2.6 kb, which carries the minimal functions for autonomous replication. By cloning of two PstI fragments of this region it could be demonstrated that the "basic replicon" is a DNA segment not larger than 1.8 kb, which carries the orgin of replication and the genetic information for at least two proteins. Protein F (NW=11.000 dalton) seems to be synthesed in larger amounts in minicells of E. coli than protein C (20.000). Plasmids containing this isolated replicon of R1 are completely compatible with the parental plasmid R1drd-19.

A DNA copy of influenza B/Singapore/222/79 viral RNA segment 5, containing the gene coding for the nucleoprotein (NP), has been cloned in Escherichia coli plasmid pBR322, and its nucleotide sequence has been determined. The influenza B NP gene contains 1,839 nucleotides and codes for a protein of 560 amino acids with a molecular weight of 61,593. Comparison of the influenza B NP amino acid sequence with that of influenza A NP (A/PR/8/34) reveals 37% direct homology in the aligned regions, indicating a common ancestor. However, influenza B NP has an additional 50 amino acids at its N-terminal end. As is the case with influenza A NP, influenza B NP is a basic protein, with its charged residues relatively evenly distributed rather than clustered. The structural homology suggests functional similarity between the NP of influenza A and B viruses.

While an ethical obligation to report findings of clinical research to trial participants is increasingly recognised, the academic debate is often vague about what kinds of data should be fed back and how such a process should be organised. In this article, we present a classification of different actors, processes and data involved in the feedback of research results pertaining to an individual. In a second step, we reflect on circumstances requiring further ethical consideration. In regard to a concrete research setting--the one of clinico-genomic research--we discuss what kinds of difficulties have to be faced when returning individual research results to trial participants. In a last step, we elaborate on a stepwise model to trigger the individual feedback process. Hence, this paper gives guidance on how to feedback individual research results in a specific research setting and responds at the same time to new challenges in the debate on the duty to return individual research findings.