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The genome structure of a newly isolated avian erythroblastosis virus, AEV-H, was analyzed. Using DNA probes specific for the LTR sequence of SR-RSV-A, and for the erbA gene and the erbB gene of the ES4 strain of AEV, we have shown that the genome of AEV-H is 35S in size and carries the erbB gene but not the erbA gene. Comparison of the restriction sites of molecularly cloned AEV-H DNA with that of cloned DNA of the associated virus revealed that the env gene of the associated virus was replaced with the erbB gene to generate AEV-H. The genome structure of AEV-H is, therefore, determined to be 5'-gag-pol-erbB-3'. Moreover, we have isolated a mutant of AEV-H, td-130, that can induce sarcomas but not erythroblastosis in chickens. The restriction analysis of proviral DNA of the td-130 showed that it carries a deletion of about 150 to 200 nucleotides in the erbB gene. These data indicate that the erbB protein is responsible for both erythroblastosis and sarcomas.
A new strain of avian erythroblastosis virus (AEV), designated "AEV-H," was established by serial passages of a field isolate of avian lymphatic leukemia virus subgroup A [LLV(A)] in chicks from a White Leghorn flock of line 151 chicks. One stock of AEV-H contained 10(4) focus-forming units/ml virus and 10(9) tissue culture infective dose/ml LLV(A). All of the chicks that received ip inoculations of 0.2 ml AEV-H developed erythroblastosis complicated by fibrosarcoma 16-24 days (approximately equal to 17.7 days) after inoculation. Pathologic changes of erythroblastosis were macroscopically observed, mainly in such visceral organs as the liver, spleen, and bone marrow. In addition, microscopic changes were observed in the lung, kidney, ovary, and heart. Pathologic changes of fibrosarcoma were so conspicuous that they were recognizable by the naked eye in the pancreas and in the serous membrane of the intestine.
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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.
We analyzed the viral mRNA's present in fibroblast nonproducer clones transformed by avian erythroblastosis virus. Two size classes of mRNA (28 to 30S and 22 to 24S) were identified by solution hybridization with both complementary DNA strong stop and complementary DNA made against the unique sequences of avian erythroblastosis virus. Based upon the kinetics of hybridization with complementary DNA made against the unique sequences of avian erythroblastosis virus, we estimated that there were 400 to 500 copies of the 28 to 30S RNA per cell and 200 to 250 copies of the 22 to 24S RNA per cell. Both RNA species were packaged in the virion. In vitro translation of the 28 to 30S virion RNA yielded a 75,000-dalton protein which was the 75,000-dalton gag-related polyprotein found in avian erythroblastosis virus-transformed cells. In vitro translation of the 22 to 24S virion RNA yielded two proteins (46,000 and 48,000 daltons). This indicates that there may be two genes in avian erythroblastosis virus, one coding for the 75,000-dalton gag-related polyprotein and the second coding for the 46,000- or 48,000-dalton protein or both.
Forty-two children who sustained a serum bilirubin (SBR) level above 339 mumol/L as newborn infants were assessed at our Growth and Development Clinic to determine presence of sequelae. Only one child (2.3%) had mild sensorineural deafness and one child (2.3%) performed below age-matched standards on psychological testing. As the SBR level rose the psychological scores were lower. Three infants had sepsis associated with the hyperbilirubinaemia. Two (maximum SBR levels of 371 and 366 mumol/L) children were normal (General Cognitive Index (GCI) 117 and 119, respectively) and one child (maximum SBR level 556 mumol/L) was borderline abnormal (GCI 74) on psychological testing; he also suffered from Rhesus erythroblastosis. Premature infants recorded a mean GCI of 109.9 (+/- 33.4) and for term infants mean GCI was 110.3 (+/- 17.3; NS); however, the youngest premature infant was 32 weeks' gestation. When maximum SBR level was correlated with GCI and Motor Index (MI) the only significant correlation (r = -0.7445; P = 0.03) occurred in infants with Rhesus erythroblastosis and GCI. Since exchange transfusion has a mortality of between 0.3 and 5.3% and an associated morbidity incidence of 5.2% we suggest that the standard indication for its use (SBR level of 342 mumol/L) should only apply to infants with Rhesus erythroblastosis. The actual SBR level which places a newborn infant at significant risk of bilirubin encephalopathy, where the cause of jaundice is other than Rhesus erythroblastosis, cannot be determined by this study.(ABSTRACT TRUNCATED AT 250 WORDS)
The H strain of avian erythroblastosis virus (AEV-H) was recently isolated from the liver emulsion of a chicken that suffered from erythroblastosis after being inoculated with subgroup A leukosis virus. AEV-H induced erythroblastosis or sarcoma when inoculated into chickens and transformed chick embryo fibroblasts (CEF) in vitro. Analysis of viral proteins synthesized in cells, which were named HNP, transformed by AEV-H but not producing transforming virus revealed tha the genome of AEV-H directed the synthesis of the gag gene products, Pr76gag and Pr180gag-pol, which was the precursor of active reverse transcriptase. Thus the HNP produced virions that were not infectious due to a defect of the env gene. Studies on the viral RNA showed that a 35 S RNA, estimated to be 8000 nucleotides long, was the genomic RNA of AEV-H and probably carried one transforming gene, which is most likely erbB gene. The gene organization of AEV-H was suggested to be 5'-gag-pol-onc-3'. These data imply that the single oncogene is responsible for both erythroblastosis and sarcoma.