Disease relevance of Helper Viruses

• Such transformants possessed typical SSV morphology, expressed simian sarcoma associated virus (SSAV) gag gene products in the absence of virus release, and released SSV after superinfection with a type C helper virus [1].
• A class of mouse neoplasms termed Abelson virus-induced plasmacytoid lymphosarcomas has previously been found to express abnormal myb transcripts due to a helper virus insertion into the 5' end of the c-myb locus [2].
• We investigated the role of the Moloney helper virus, Moloney murine leukemia virus (Mo-MuLV), in cell transformation and tumor induction by the defective Abelson murine leukemia virus (Ab-MuLV) [3].
• The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells [4].
• Defective herpes simplex virus vectors containing the B7-1-immunoglobulin (B7-1-Ig) fusion transgene (dvB7Ig) were generated using G207 as a helper virus and tested in the poorly immunogenic murine neuroblastoma, Neuro2a, in syngeneic A/J mice [5].

High impact information on Helper Viruses

• Adeno-associated viral (AAV) vectors are non-pathogenic, integrating DNA vectors in which all viral genes are removed and helper virus is completely eliminated [6].
• The induction of erythroid bursts was not caused by the murine type C helper viruses used to pseudotype either Ha-MuSV or Ki-MuSV, or by media from cells carrying the Ki-MuSV and Ha-MuSV genomes [7].
• During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein [8].
• We suggest the name Fhe for the new gene controlling susceptibility to Friend helper virus erythroblastosis [9].
• Leukemic spleen cells, 30-60 d after virus inoculation, expressed decreased amounts of ecotropic Friend murine leukemia helper virus gag- and env-encoded cell surface and intracellular proteins compared with leukemic cells tested 8-10 d after virus inoculation [10].

Chemical compound and disease context of Helper Viruses

• In contrast, in mice genetically resistant to the native helper virus of SFFV, the helper effect of LPS was optical when it was injected with SFFV and oil when given 5 days before or after the virus [11].
• Each was transfected into TK- cells along with MLV helper virus, and TK+ colonies were obtained by selection in the presence of hypoxanthine, aminopterin, and thymidine (HAT) [12].
• Synthetic peptide vaccines containing a single Th cell epitope identified in the gp70 envelope glycoprotein of Friend murine leukemia helper virus induced potent protective immunity against Friend virus infection [13].
• Adeno-associated virus replication. The effect of L-canavanine or a helper virus mutation on accumulation of viral capsids and progeny single-stranded DNA [14].
• Using a transfected defective interfering RNA which contains an IS and a reporter (chloramphenicol acetyltransferase) gene and JHM2c as a helper virus, we demonstrated that subgenomic mRNAs transcribed from the defective interfering RNAs were extremely heterogeneous [15].

Biological context of Helper Viruses

• Transfection of HPRT- cells followed by superinfection with various helper viruses has led to the rescue of chimeric virus capable of transmitting the HPRT+ phenotype to HPRT- rodent or human cells [16].
• Genes at this class II locus controlled the responsiveness of Th cells to envelope glycoprotein of Friend murine leukemia helper virus and affected the class switching of virus-neutralizing antibodies from IgM to IgG in FV-infected mice [17].
• Rfv-2 was physically and functionally distinct from the I-A-linked Ir gene that has been shown to control the responsiveness of Th cells to the envelope glycoprotein of Friend murine leukemia helper virus [18].
• The two packaging components, gag-pol and env, were placed on separate plasmids to reduce helper virus formation [19].
• By selection with Zeocin, a mixed population of pAM3-IRES-Zeo-transfected NIH3T3 cells (AMIZ cells) was maintained with little or no DNA methylation of the helper virus 5' LTR [20].

Anatomical context of Helper Viruses

• The high-titer virus-producing cell lines were assayed for absence of helper virus, synthesis of human IDUA, and for integrity of proviral structure [21].
• Distinct helper virus requirements for Abelson murine leukemia virus-induced pre-B- and T-cell lymphomas [22].
• To overcome host cell DNA methylation that suppresses viral gene expression, we constructed a chimeric retroviral helper virus, pAM3-IRES-Zeo, that contains Moloney murine leukemia virus as a helper virus and a picornavirus internal ribosome entry site (IRES) sequence followed by a Zeocin selection marker at the 3' end of the env sequence [20].
• Hybridomas producing anti-46K antibodies were established by fusion of mouse myeloma cells with spleen cells taken from mice bearing Sac tumour cells infected with Moloney helper virus [23].
• Artificially constructed dRNAs lacking sequences encoding the helicase and polymerase domains of the replicase proteins and portions of the MP were viable in protoplasts and plants in the presence of helper virus [24].

Gene context of Helper Viruses

• Vectors were constructed encoding beta-galactosidase (LacZ), CD80 (B7.1), or CD154 (CD40L) and were packaged using either a standard helper virus (HSVlac, HSVB7.1, and HSVCD40L) or a helper virus-free method (hf-HSVlac, hf-HSVB7.1, and hf-HSVCD40L) [25].
• Therefore, the amino acid sequence of the defective MAIDS virus p12gag region is not homologous to that of the helper virus and the Edv transcript because of the frameshift [26].
• Uninfected NR6 cells or NR6 cells infected by helper virus alone can be used as controls for the EGF specificity of growth stimulation [27].
• An increase in helper virus multiplicity gave an increase in beta-tubulin stimulation, but dl312 alone, even at a high multiplicity of infection, gave no induction, confirming the requirement for E1a. beta-Actin nuclear RNA was actively synthesized before infection, but it was not further stimulated by the virus [28].
• All of the transformed cells were relatively resistant to the growth-inhibitory effects of TGF-beta 1, compared to normal RLE cells and control cells infected with a helper virus [29].

Analytical, diagnostic and therapeutic context of Helper Viruses

• LPS did not affect helper virus expression in a standard cell culture (XC) assay, but it did increase helper virus replication in mice [11].
• Monkey cells infected with this virus and the appropriate helper virus produce dimeric hCG. hCG produced in this system was shown to chromatograph identically to standard hCG preparations on gel filtration and to be biologically active in the mouse uterine weight assay [30].
• The cloned DNA was analyzed by Southern blotting of restriction endonuclease digests and by electron microscopic visualization of R loops formed between the cloned DNA and MC29 or helper virus RNA [31].
• Finally, immunoprecipitation assays revealed the presence of a specific interaction between the capsid proteins of SPMV and its helper virus (PMV) [32].
• Only transplantation of helper virus-superinfected Sac cells led to the development of anti-46K antibodies in addition to antibodies against helper virus structural antigens [23].

References