Biomedical subjects
Publications and source records attributed to M Linial.
We isolated 28 recombinants of Rous sarcoma virus at early (24 h) and late (7 days) times after infection. These recombinants were selected for wild type in the pol and src genes and analyzed for their env and gag phenotypes. We were unable to show strong linkage between any two markers, including two markers within a single gene (gag).
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We have isolated a nonconditional mutant of PR-RSV-E with unique properties. This virus (SE 21Q1b) is shed from a continuously growing culture of transformed quail cells. 21Q1b virions are unable to transform or replicate in other quail or chicken cells after exogenous infection, despite the fact that the viral particles contain normal envelope glycoproteins, internal structural proteins and RNA-dependent DNA polymerase. The lack of infectivity of 21Q1b virions is a consequence of the failure to package genomic 39S RNA. Instead, these virions contain a mixture of heterogenous-sized polyadenylated cellular RNAs and 4S RNA. Less than 1% of the encapsulated RNA is viral-specific, although in the 21Q1b-producing cells, amounts of 39S, 28S and 21S viral RNAs comparable to those in wild-type virus-infected cells are synthesized and function as mRNAs for the viral proteins. Thus 21Q1b can be considered an RNA packaging mutant. Superinfection of 21Q1b cells with either RAV-1 or PR-A leads to production of about 10% or more of the normal titer of superinfecting virus, but none of the 21Q1b genetic markers are rescued. After superinfection, the 21Q1b cells continue to synthesize 21Q1b particles containing cellular RNAs in the same amounts as before infection. Thus superinfection does not appear to "switch off" the aberrant packaging of cellular RNA, but allows packaging of the superinfecting RNA. One explanation for the phenotype of 21Q1b is that the genome is lacking a signal necessary for efficient genomic RNA packaging (but not for translation) and that the 21Q1b genome encodes a "packaging factor" with an altered specificity so that cellular RNAs are efficiently packaged. 21Q1b virions do contain RNA-dependent DNA polymerase which has normal endogenous synthetic activity. The cDNA product made in vitro from detergent-lysed 21Q1b virions hybridizes equally well to uninfected quail and 21Q1b-producing quail cell RNAs, with kinetics suggesting that the endogenous product consists of transcripts of cellular RNAs present in low amounts in the cells.
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Chicken fibroblasts derived from the H & N flock, which have been characterized as resistant to subgroup B avian oncornaviruses in focus assays, can be infected in suspension shortly after trypsinization by subgroup B sarcoma and leukosis viruses. Once cells are plated, resistance to infection reappears rapidly. C/BE cell suspensions obtained by treatment with EDTA instead of trypsin are not as sensitive to infection. Late interference established by preinfection with subgroup B leukosis viruses is not overcome by trypsinization. In addition to C/BE H & N chicken cells, C/ABE RPRL line 7 cells can also be infected by subgroup B viruses shortly after trypsinization; however, none of the cell types can be made sensitive to subgroup E infection. These results are discussed in relation to current information on the genetic control of resistance to avian oncornaviruses.
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We studied the course of infection of the female-specific bacteriophage phiII in male and female cells isogenic except for the presence of the substituted sex factor, F'lac. Both male and female cells are killed by phiII; however, only limited phage replication occurs in male cells. Host macromolecular synthesis stops abruptly at 4 to 6 min after infection of male cells, and synthesis of phage components cannot be detected. Experiments with chloramphenicol indicate that phage deoxyribonucleic acid (DNA) penetrates into male cells, since protein synthesis after infection is required to stop synthesis of DNA in males. Phage DNA becomes membrane-associated in both female and male cells. In male cells, parental phage DNA does not dissociate from the membrane during the latent period as is the case with females, indicating a block in phage DNA replication. Isolation of nonrestricting F'lac mutations indicates involvement of a specific episome product in phiII restriction.