Disease relevance of Avian Leukosis

• Using the insertional activation model of c-myc by avian leukosis virus in the induction of bursal lymphoma in chickens, we have now characterized the c-myc locus in feline tissues and investigated the possibility that FeLV may also insert within feline c-myc [1].
• In the course of attempting to define these signals by testing virus incorporation of CD4-Env chimeric proteins, normal human CD4 was found to be efficiently and selectively assembled into avian leukosis virus particles in quail cells [2].
• Mutational analysis of the candidate internal fusion peptide of the avian leukosis and sarcoma virus subgroup A envelope glycoprotein [3].
• We tested the ability of the thymidine analog 3'-azido-3'-deoxythymidine (BWA509U) to inhibit the replication of the retrovirus avian leukosis virus [4].
• The DNA product from the endogenous RNA-directed DNA polymerase reaction of the RNP complex hybridized to REV RNA but not to avian leukosis virus RNA [5].

High impact information on Avian Leukosis

• This protein was not found in cells infected by trnasformation-defective mutants with either a partial or complete deletion of the src gene, nor in cells infected by a nontransforming avian leukosis virus [6].
• The vector, pDAH5, was obtained by removing the CAAT and TATA boxes of the 3'LTR of the avian leukosis virus RAV-2 and inserting the H5 sequence [7].
• Activation of c-erbB in avian leukosis virus-induced erythroblastosis leads to the expression of a truncated EGF receptor kinase [8].
• We now report a significant improvement made to this viral targeting method by using a related bridge protein, designated TVB-EGF, comprised of the extracellular domain of the TVB receptor for subgroup B avian leukosis virus fused to epidermal growth factor (EGF) [9].
• The mature avian leukosis virus subgroup A envelope glycoprotein is metastable, and refolding induced by the synergistic effects of receptor binding and low pH is coupled to infection [10].

Chemical compound and disease context of Avian Leukosis

• Messenger activity of virion RNA for avian leukosis viral envelope glycoprotein [11].
• 3'-Azido-3'-deoxythymidine inhibits the replication of avian leukosis virus [4].
• From the envelope gene of an avian leukosis virus of subgroup A, we have constructed a set of SU mutants in which these regions were replaced by the coding sequence of FLA16, a 16-amino-acid RGD-containing peptide known to be the target for several cellular integrin receptors [12].
• Identification and characterization of a shared TNFR-related receptor for subgroup B, D, and E avian leukosis viruses reveal cysteine residues required specifically for subgroup E viral entry [13].
• Analysis of these immune reactions by polyacrylamide gel electrophoresis revealed that avian leukosis virus-challenged and Rous sarcoma virus-challenged chickens recognized only two major cell surface antigens of 100000 and 29000 mol. wt. which were present on transformed and non-transformed virus-producing cells [14].

Biological context of Avian Leukosis

• In several bursal lymphoma cell lines in which c-myc transcription is regulated by avian leukosis virus (ALV) long terminal repeat (LTR) sequences, protein synthesis inhibition decreases the transcriptional activity of c-myc as well as other LTR driven viral genes [15].
• We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding epidermal growth factor receptor [16].
• Nucleotide sequence 5' of the chicken c-myc coding region: localization of a noncoding exon that is absent from myc transcripts in most avian leukosis virus-induced lymphomas [17].
• We tested several c-myc alleles cloned from normal and tumor tissues of chicken and human origin and found that only LL4myc (derived from a bursal lymphoma in which an avian leukosis virus long terminal repeat resides within the first c-myc intron in the same transcriptional orientation) had cotransforming activity [18].
• A 3' region of a previously unknown retroviruslike element named ART-CH (avian retrotransposon from chicken genome) was obtained in the course of polymerase chain reaction-mediated cloning of avian leukosis virus long terminal repeats (LTRs) from DNAs of infected chicken cells [19].

Anatomical context of Avian Leukosis

• B-cell lymphomas induced in chickens infected with avian leukosis viruses are characterized by integration of the virus within the cellular myc locus and alteration of c-myc expression [20].
• The isolates were classified as ALV-J by 1) their ability to propagate in chicken embryo fibroblasts (CEF) that are resistant to avian leukosis virus (ALV) subgroups A and E (C/AE) and 2) positive reaction in a polymerase chain reaction with primers specific for ALV-J [21].
• Six-week-old broiler chickens negative for exogenous avian leukosis viruses or congenitally infected with avian leukosis virus subgroup J were inoculated intravenously with 10(6) colony-forming units of Staphylococcus aureus, and pre- and postinoculation heterophil function was assessed [22].

Gene context of Avian Leukosis

• TVB receptors are death receptors of the tumor necrosis factor receptor (TNFR) family and serve as cellular receptors for cytopathic subgroups B and D and noncytopathic subgroup E of the avian leukosis viruses (ALVs) [23].
• In most avian leukosis virus-induced lymphomas proviral integration has occurred within, or downstream of, the first exon, thus presumably displacing the regulatory sequences that normally control c-myc expression [17].
• The genome of NK24 was 5.3 kilobases long and had a 1,126-base-pair sequence of cellular origin in place of a viral sequence of avian leukosis virus containing the 3' half of the gag gene and the 5' half of the pol gene [24].
• Sequence of host-range determinants in the env gene of a full-length, infectious proviral clone of exogenous avian leukosis virus HPRS-103 confirms that it represents a new subgroup (designated J) [25].
• The DNA product of the endogenous DNA polymerase reaction is hybridizable to REV RNA, but not to avian leukosis virus RNA [26].

Analytical, diagnostic and therapeutic context of Avian Leukosis

• A microplate enzyme-linked immunosorbent assay (ELISA) for detecting antibodies to avian leukosis virus (ALV) of subgroups A and B in infected chickens was developed with the use of Rous-associated virus (RAV)-1 (subgroup A) and RAV-2 (subgroup B) antigens purified by sucrose-gradient centrifugation [27].
• Development and application of reverse transcriptase nested polymerase chain reaction test for the detection of exogenous avian leukosis virus [28].
• Use of reverse transcriptase polymerase chain reaction for detection of vaccine contamination by avian leukosis virus [29].

References