The RNA of avian acute leukemia virus MC29.
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The RNA of myelocytoma virus MC29, a replication-defective avian acute leukemia virus, was investigated. Sedimentation and electrophoretic analyses indicated that the virus contains a distinct 28S RNA with about 5700 nucleotides. It is the smallest avian tumor virus RNA detected to date. The small size of the RNA suggests that the defectiveness of the virus is due to deletions in replicative genes. The RNA shared 3 to 5 of 30 large RNase T 1 -resistant oligonucleotides with the RNA of other avian leukosis and sarcoma viruses. Hybridization indicated that 61% of the viral RNA contains sequences in common with other avian sarcoma and leukosis viruses. At least 32% of the RNA (about 1800 nucleotides) appear to be MC29-specific and may represent the transforming information of the virus. Sequences of the conserved transforming gene of avian sarcoma viruses were not detected in MC29 RNA. It was concluded that the transforming sequences of MC29 RNA define a new class of avian tumor viral transforming genes.Keywords:
Tumor Virus
The RNA of myelocytoma virus MC29, a replication-defective avian acute leukemia virus, was investigated. Sedimentation and electrophoretic analyses indicated that the virus contains a distinct 28S RNA with about 5700 nucleotides. It is the smallest avian tumor virus RNA detected to date. The small size of the RNA suggests that the defectiveness of the virus is due to deletions in replicative genes. The RNA shared 3 to 5 of 30 large RNase T 1 -resistant oligonucleotides with the RNA of other avian leukosis and sarcoma viruses. Hybridization indicated that 61% of the viral RNA contains sequences in common with other avian sarcoma and leukosis viruses. At least 32% of the RNA (about 1800 nucleotides) appear to be MC29-specific and may represent the transforming information of the virus. Sequences of the conserved transforming gene of avian sarcoma viruses were not detected in MC29 RNA. It was concluded that the transforming sequences of MC29 RNA define a new class of avian tumor viral transforming genes.
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The RNAs of several avian tumor virus recombinants that had inherited their focus-forming ability from a sarcoma virus and their host range marker from a leukosis virus were investigated. Electrophoretic analyses showed that the cloned sarcoma virus recombinants contained only size class a RNA, although they had acquired a marker that resided on class b RNA in the leukosis virus parent. Class a RNA of different recombinant clones, derived from the same pair of parental viruses and selected for the same biological markers, differed slightly in electrophoretic mobility from each other and from the parental sarcoma virus. They were also found to have different fingerprints of RNase T1-resistant oligonucleotides. The average complexity of the 60-70S RNA prepared from Prague Rous sarcoma virus of subgroup B was estimated to be 3.5 × 10 6 daltons from the size of 20 RNase T1-resistant oligonucleotides, which represented 3.9% of the RNA and that of a recombinant to be 3.3 × 10 6 daltons from 23 oligonucleotides, which represented 4.7% of the RNA. This result suggests that the genome of wild-type and of recombinant RNA tumor viruses is polyploid. The sum of these observations led us to propose that recombination among avian tumor viruses occurred by crossing-over between homologous pieces of nucleic acid.
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Cells derived from the majority of chick embryos, although free of presently known avian tumor virus particles, appear to contain genetic materials similar to those found in this virus group. After infection of these cells with avian leukosis or Rous sarcoma virus, the genetic factor was recovered by incorporation into mature infectious virus. The newly isolated virus (RAV-60) did not require the assistance of another virus for its replication. The virus had most of the attributes of an RNA-containing avian leukosis virus, and its outer structure resembled the Rous sarcoma virus known as RSV(0).
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Abstract Persistence of RNA viruses is often, but not always, associated with the production of defective interfering (DI) particles. To investigate possible roles of DI particles and helper viruses in RNA virus persistence, persistent infection with Japanese encephalitis virus (JEV) was established in baby hamster kidney (BHK‐21) cells. At the 6th and 7th serial undiluted passages of JEV on BHK‐21 cells, viral persistence was established spontaneously with DI RNA generation. Seven cell clones exhibiting persistent infection were obtained from the initial BHK‐21 cell batches exhibiting JEV persistence, and maintained for over 400 days. Most cell clones produced infectious particles (10 1 –10 5 PFU/ml) continuously, expressed viral proteins, and resisted homologous superinfection. Two helper viruses, chvBS6‐3 and chvBS7‐1, were isolated from two of the seven cell clones, and characterized to investigate their roles in JEV persistence. While chvBS6‐3 was restored to its full cytopathicity in the absence of DI RNA, chvBS7‐1 exhibited almost no cytopathicity, regardless of DI RNA co‐replication. Attenuation of chvBS7‐1 did not appear to be due to inadequate adsorption or genome replication, but due to inefficient egress of the assembled progeny virions, suggesting altered helper virus emergence during JEV persistence in BHK‐21 cells. These observations suggest that at least two mechanisms are involved in JEV persistence; a DI RNA‐dependent mechanism, where DI RNA co‐replication nullifies the helper virus's cytopathicity, or a DI RNA‐independent mechanism, where the helper virus is self‐attenuated. This study provides a useful in vitro tool for understanding the mechanisms underlying RNA virus persistent infections. J Med. Virol. 85:1990–2000, 2013 . © 2013 Wiley Periodicals, Inc.
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Torque teno virus
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Immunodiffusion analysis of the PMF virus which was detected in malignant permanent human cell lines revealed positive reactions with antisera against the Mason-Pfizer monkey virus (MPMV). No cross-reactivity was demonstrated with murine leukemia virus (MuLV), rat leukemia virus (RaLV), hamster leukemia virus (HaLV), feline leukemia virus (FeLV), simian (woolly monkey) sarcoma virus (SSV-1) and mouse mammary tumor virus (MTV). The cross-reactive antigens of the PMF virus and the MPMV are considered as evidence for the human origin of the PMF virus.
Feline leukemia virus
Viral transformation
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Immunodiffusion
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Antibodies against the RNase H domain of human hepatitis B virus P protein(s) are frequent markers of acute and chronic virus infection (T. Weimer, K. Weimer, Z.-X. Tu, M.-C. Jung, G. R. Pape, and H. Will, J. Immunol. 143:3750-3756, 1989). In the present study, these antibodies were determined in serial serum samples of experimentally infected chimpanzees and naturally infected human patients with acute and chronic hepatitis B virus infection. Anti-P antibodies were found in the sera of both chimpanzees and humans early in infection shortly after the immunoglobulin M anti-HBc response; they persisted in chronic carriers with ongoing viral replication but declined and disappeared at the time of virus clearance from the sera. These data demonstrate that antibodies to the RNase H domain of the hepatitis B virus P protein are early markers of infection and a signal of ongoing virus replication. Falling titers indicate the decline or end of active virus production and may therefore be a prognostic sign of virus elimination in natural infection and after antiviral therapy.
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SUMMARY The synthesis of 3H-uridine-labelled complete virus, virus RNA and presumed replicative form (RF) were studied during the replication of southern bean mosaic virus (SBMV) in soybean callus cells. The inoculated cells were pre-incubated at 6 °C for 4 days and then moved to 25 °C to improve the synchronization of virus multiplication. The synthesis of complete virus, measured by the incorporation of 3H-uridine into virions and by infectivity assays, rose rapidly during 0 to 34 h after transfer to 25 °C. An RNA with a mol. wt. approximating to that of the postulated RF of SBMV-RNA and exhibiting partial resistance to RNase digestion was synthesized in significant amounts. This occurred after a 16 to 24 h incubation, preceding the major period of virus RNA synthesis which reached maximum during 40 to 48 h. Pulse-chase experiments, within limits, suggested the possible precursor role of the postulated RF in the synthesis of virus RNA. Accumulation of an RNA with electrophoretic properties similar to the presumptive RF of SBMV-RNA, was found in inoculated cells incubated at 6 °C from 84 to 96 h, suggesting a possible blockage of virus replication at the double-stranded RNA stage in these cells.
Nuclease protection assay
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