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Biomedical subjects

I Karakoz

Publications and source records attributed to I Karakoz.

At least 19 recordsLinked to original sources
PubMed1996

Frequent detection of reviraemia in ducks persistently infected with avian leukosis retroviruses.

Ducks intraembryonally infected with avian leukosis viruses of subgroup C (ALV-C) were followed for a long period (up to 6.8 years), and the viraemia and production of virus-neutralizing antibodies were measured. In three independent experiments comprising ducks inoculated with uncloned and/or molecularly cloned ALV-C, we found that after the elimination of primary post-hatching viraemia, reviraemia could be detected in 60-70% of infected animals. Based on the course of viraemia, the individual ducks were assigned to four different groups: Group I (no reviraemia), Group II (one transient reviraemic period), Group III (one persistent reviraemic period), Group IV (fluctuating reviraemia). In comparison to sera from ducks included in Group I and/or II, a significant decrease in neutralizing activity of sera from animals comprised in Group III and/or IV was observed. Two out of four reviraemic viruses were not neutralized by antiserum against ALV-C, instead their infectivity was enhanced. Long-term follow-up of the cell-associated virus revealed that its rescuability by cocultivation with chicken embryo fibroblasts fluctuated in about 50% of animals. In the reviraemic phase of infection, integrated proviruses could be detected by Southern blotting in a majority of tissues examined. Our data document that many features recognized in lentiviruses are valid also for oncoviruses transmitted to heterologous hosts and substantiate further the suitability of ALV-C-infected ducks as a model for studying persistent retroviral infection.

Animals↗
PubMed1995

Vaccination with a low-oncogenic strain of Rous sarcoma virus prevents visceral tumors in chickens.

The oncogenic potential of different strains of Rous sarcoma virus (RSV) varies significantly in two Mhc(B) congenic chicken lines CB and CC and in their F1 hybrids with the unrelated inbred line IA. The Bryan high-titer pseudotype of RSV of antigenic subgroups D and B (BH-D, and BH-B) was highly oncogenic, eliciting mostly fatal, progressively growing tumors. Visceral tumor formation and erythroblastosis were seen after challenge with BH-B in CB and CC chickens, but not in their F1 hybrids with IA. Tumor regression induced by a low-oncogenic RSV strain PR-C elicited a protective immunity capable of preventing not only the progressive growth of challenge tumors at the site of inoculation, but also visceral tumor formation and erythroblastosis.

Animals↗
PubMed1994

Origin and evolution of the c-src-transducing avian sarcoma virus PR2257.

Avian sarcoma virus PR2257 transduced de novo the c-src gene and about 900 bp of 3' non-coding sequences belonging to the src locus. This virus contains only one mutation in the c-src coding sequence causing a reading frame shift after Pro-525. The molecular clone studied was derived from a cell line of transformed quail fibroblasts, C7. It contains endogenous virus (ev) derived sequences in the U5 and 3' non-coding regions, indicating that multiple recombination occurred with endogenous virus. Here we investigated the possible evolution of PR2257 when the original tumour was repeatedly passaged in vivo. After 16 passages a new virus, designated PR2257/16, appeared with a tenfold higher titre. The sequence of PR2257/16 was determined and showed that PR2257/16 resulted from recombination of PR2257 with the env gene of the helper virus (td daPR-C). This recombination expanded the env gene content in PR2257/16 and, in addition, five point mutations occurred in its genome. Because we thought that an endogenous virus might be involved in the mechanism of c-src transduction, we also reinvestigated the presence of ev sequences in PR2257 proviruses from several early passages of the original tumour. We found that in contrast with the first isolate from the C7 cell line, the provirus in these tumours did not contain such sequences. These results do not support the hypothesis that endogenous sequences were involved in the transduction process.

Animals↗
PubMed1994

New case of c-src gene transduction: the generation of virus PR2257.

PR2257 is a new replication-defective avian sarcoma virus which harbours in addition to the spliced version of the c-src gene also about 950 bp of no-coding cellular sequences located downstream from the c-src stop codon (Geryk et al., 1989). Comparison of the 950 bp region transduced by PR2257 with the chicken c-src cDNA (Dorai et al., 1991) and genomic sequences of the c-src 3' non-coding region from chicken and quail has shown that there are no additional introns. The c-src 3' non-coding region represents the largest c-src exon (No. 12) comprising about 2 kb. Absence of conserved open reading frames within this region in chicken and quail genomic DNAs excludes the possibility for coding a protein by these sequences. Also, the possibility was excluded that numerous endogenous virus-derived sequences identified in molecularly cloned PR2257 provirus played a role in the c-src transduction. After serial passaging of PR2257 virus in vivo a variant PR2257/16 was isolated. In PR2257/16, the size of the env gene was increased due to homologous recombination with a helper virus. In addition to mutations in the viral leader and the v-src coding region, a large deletion in transduced c-src 3' non-coding sequences was found in the PR2257/16 genome. The significance of genome modifications for selective advantage of this viral variant in vivo is discussed.

Animals↗
PubMed1992

Tumor induction by the LTR, v-src, LTR DNA in four B (MHC) congenic lines of chickens.

We report that the cloned DNA harboring the long terminal repeat (LTR), v-src, LTR proviral structure is tumorigenic in chickens of the Prague congenic lines. The growth rate of these tumors is by far the highest in the recombinant CC.R1 line, the B haplotype of which is composed of the B-F/L4 and B-G12 subregions originating from different naturally occurring haplotypes. Some of the tumors induced by the LTR, v-src, LTR DNA are repeatedly transplantable in syngeneic chickens, maintain unaltered provirus, and express v-src mRNA. Differences in the response to challenge with Rous sarcoma virus (RSV) and LTR, v-src, LTR DNA on a given experimental model are compared and possible involvement of an interaction between B-F/L and B-G region genes is considered. Regression of the LTR, v-src, LTR DNA-induced tumors did not prevent the formation and growth of tumors induced subsequently by RSV.

Animals↗
PubMed1991

Graft versus host reaction induced by thymectomized and bursectomized chicken blood.

Graft versus host reaction in chicken embryos was induced by blood taken from thymectomized or bursectomized or nonoperated donors. The intensity of graft versus host reaction induced by the blood of thymectomized chickens was increased comparing to the reaction induced by blood from control donors. No such result was recorded when the blood donors had the bursa of Fabricius removed.

Animals↗
PubMed1990

Ducks: a new experimental host system for studying persistent infection with avian leukaemia retroviruses.

Long-term persistence of the avian leukosis virus (ALV), the transformation-defective mutant of Prague strain Rous sarcoma virus subgroup C (td PR-C) was established in heterologous duck hosts after infection in mid-embryogenesis. Transient viraemia was observed for about 4 weeks after hatching and was lost in most of the infected ducks by about 6 months. Loss of viraemia was accompanied by the increasing synthesis of virus-neutralizing antibodies. In spite of strong virus-neutralizing antibodies, virus was detected by the cocultivation assay in duck tissues throughout the observation period up to 5 years. In the viraemic phase of infection, we found integrated proviruses in various tissues, preferentially in stomach muscle tissue and in the thymus. The long-term persistence of virus was frequently accompanied by liver necrosis and neoplastic diseases. Injection of td PR-C virus into early embryos resulted in more pronounced infection accompanied by an increased copy number of viral DNA per cell, high mortality and remarkable atrophy of thymus tissue in infected ducklings.

Animals↗
PubMed1989

Transduction of the cellular src gene and 3' adjacent sequences in avian sarcoma virus PR2257.

When injected into chickens, a transformation-defective mutant of the Prague C strain of Rous sarcoma virus induced tumors at low incidence and after a long latency. One such tumor released a replication-defective virus designated PR2257. We molecularly cloned and sequenced the proviral DNA from quail fibroblasts transformed by PR2257. Comparison of PR2257 sequence with that of Prague C, cellular src, and 3' adjacent cellular DNA showed that the spliced version of the c-src gene and about 950 base pairs (bp) of 3'-flanking cellular DNA were transduced into PR2257. This transduction eliminated nearly all replicative genes, since the gag gene splice donor site was linked to the splice acceptor site of the src gene and, on the 3' side, recombination occurred in the end of env gene. Insertion of two extra cytosines 23 bp before and 19 bp after the c-src stop codon resulted in an extension of the coding portion up to 587 amino acids, divergence of sequences after Pro-525 and replacement of Tyr-527 by a valine residue. In addition, it appears that the 5' and 3' untranslated regions of PR2257 result from multiple recombinations between exogenous and endogenous virus genomes. Limited digestion of p66src encoded by PR2257 with Staphylococcus aureus V8 protease yielded a V2 peptide (C-terminal moiety) with an apparent molecular mass of 31 kilodaltons, consistent with the 5.7-kilodalton increase expected from the DNA sequence. The structure of PR2257 suggests that the first step in the capture of c-src gene by avian lymphomatosis viruses is the trans splicing of the viral leader mRNA to exon 1 of c-src.

Amino Acid Sequence↗
PubMed1989

Prague inbred lines of chickens: a biological model for MHC research.

Evidence for further complexity of the genetic structure of chicken major histocompatibility complex (B) is reviewed, with a historical account showing mutual dependence of the development of an animal genetic model and the growth of scientific knowledge concerning the chicken MHC.

Animals↗
PubMed1989

B (MHC) antigen dependent modulation of GvH reactivity by neonatal thymectomy and alloimmunization.

Using Prague recombinant congenic lines of chickens, we found that neonatal thymectomy led either to a marked suppression (CC donors) or to a transient increase (CB donors) of GvH response against the B-F/L + B-G and B-F/L disparate congenic embryos. Similarly, preimmunization with the B (MHC) different blood led either to the suppression or increase of GvH reactivity of the CC and CB line donors depending on the antigenic difference (B-F/L + B-G, B-F/L, B-G) between the blood used for preimmunization, the immunized donor for GvH splenomegaly assay and the recipient embryos. In all cases, the suppression of GvH response of the CC line donors is accompanied with a marked increase in GvH reactivity against syngeneic and B-G 12 disparate embryos, suggesting an autoimmune state. Furthermore, the CC line chickens suffering from GvHD had lower GvH reactivity against the B (MHC) different embryos and a significantly raised reactivity against syngeneic embryos in comparison with controls. Chickens of the same group recovering from GvHD had an extremely high alloreactivity and only slightly or no increased GvH reactivity against syngeneic embryos.

Animals↗
PubMed1988

Genome structure of a new avian sarcoma virus PR2257 determined by restriction analysis.

The genome structure of a new avian src-containing acute transforming virus, designated PR2257, was studied by restriction analysis. PR2257 was isolated from a sarcoma grown in a 155-day-old chick inoculated intraembryonally with a transformation-defective mutant of daPR-C retaining no src sequences. The 4.4-kb genome of PR2257 consists of the following regions: 5' LTR--spliced version of chicken c-src--incomplete env gene--3' LTR. This structure clearly indicates that PR2257 was generated by recombination between a td daPR-C and chicken c-src.

Animals↗
PubMed1987

Humoral immune response in experimental allergic encephalomyelitis in inbred chicken lines.

Chickens of the inbred IA line develop clinical signs of experimental allergic encephalomyelitis (EAE) after immunization with myelin basic protein (MP) or spinal cord tissue (SCT). The disease is accompanied by convulsions and paralysis of wings and legs. EAE leads to a 100% mortality in IA line chickens. On the other hand, no clinical signs appear in WA line and (CB x IA) F1 chickens following immunization with either antigen. The IA line and (CB x IA)F1 chickens develop severe inflammatory changes in brain and spinal cord tissues after immunization with SCT, whereas no such alterations occur in WA line chickens. Immunization with MP does not lead to histopathological changes in any chicken line investigated. MP, however, induces high production of specific IgM antibodies in all lines. IgG antibody levels are elevated only in IA line chickens after immunization with either antigen.

Animals↗
PubMed1987

Haematological and pathomorphological studies on chickens inoculated with transformation-defective sarcoma virus.

A transformation-defective mutant of Rous sarcoma virus (td PR-RSV-C) inoculated into chicken embryos caused a number of pathological changes in chickens after hatching. Disturbances in haematopoiesis were manifested by anaemia of different degree and by the presence of immature blood elements in the peripheral blood. The haematological picture of erythroblastosis was confirmed histologically. In addition to erythroblastosis, lymphoid leukosis and a proliferative lymphosarcoma-like tumour were demonstrated histologically.

Animals↗
PubMed1986

Concomitant immunity leads to retardation or acceleration of the growth of Rous sarcomas in genetically resistant or susceptible inbred lines of chickens.

We report results on the age-dependent effect of the B (MHC) genotype on resistance to the growth of a second RSV tumour in chickens from highly inbred lines genetically resistant or susceptible to progressive growth of primary RSV-induced tumours. Furthermore, the second inoculation of RSV caused either accelerated or retarded growth of the primary tumours induced by the same virus. These two types of response to a second challenge with RSV were controlled by alleles of the chicken major histocompatibility (B) complex. The retarded growth of the primary tumours was found to be thymus-dependent. Furthermore, a clear-cut trans-complementation effect of two B alleles on the response to RSV challenge was demonstrated.

Age Factors↗
PubMed1986

Cyclophosphamide in allergic encephalomyelitis in chickens.

The studies concerned the effect of cyclophosphamide on immunological and biochemical indices of MBP-induced encephalomyelitis. Unlike isoprinosine, cyclophosphamide was observed to exert irregular effect. Contrary to the expected, the results obtained in some experimental systems show increased level of the parameters tested-IgG, antitrypsin and sialic acid. A suggestion has been put forward that the reason of the above phenomenon may be attributed not only to the type of drug applied but also to different course of treatment with regard to various affinity of the drug (different doses) to functionally different lymphocytes (suppressor, helper).

Animals↗
PubMed1985

Modulation of immunological reactivity in the course of allergic encephalomyelitis by isoprinosine.

It was observed that in the course of allergic encephalomyelitis (EAE) in chickens. Isoprinosine reduced the production of the specific IgA and IgM antibodies against encephalic antigen. Its influence on IgG production was slight. It was also found that isoprinosine reduced the antitrypsine activity in EAE. Its effect upon the level of antibodies and biochemical indices of inflammation was particularly pronounced on days 28-35 after immunization, i.e. at the time of the most intensive microscopic inflammatory changes in the brain. Histological analysis revealed an inhibition of plasmatic cells reproduction in the spleens of chickens receiving isoprinosine. No effect of the drug on the GvH reaction in chickens was found.

Animals↗
PubMed1985

Isolation of two transforming viruses from sarcomas obtained in chickens inoculated intraembryonally with a transformation defective mutant of Prague strain Rous sarcoma virus.

Sarcomas appeared after long latency with a frequency of about 2% in Brown Leghorn and (CB X IC)F1 chickens after intraembryonic and neonatal inoculation of transformation-defective mutants of ASVs subgroup C. Only the freshly isolated td mutants, td daPR-C and td daPR-C morphf, exhibited the tumorigenic activity, whereas the standard td mutants induced no sarcomas. Two (862 and 2257) out of four tumours could be transplanted in young chickens and produced low titres of transforming virus. The other two tumours were not transplantable and devoid of any transforming virus. Viruses 862 and 2257 are clearly defective in replication, virus 2257 cannot be complemented efficiently by any helper virus in vitro. The low titre of virus 2257 is not caused by interference with a helper virus of the same subgroup specificity. Both viruses are highly tumorigenic in vivo.

Animals↗