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Biomedical subjects

A M Fadly

Publications and source records attributed to A M Fadly.

At least 37 records · Page 2Linked to original sources
PubMed1986

Gene insertion into the chicken germ line by retroviruses.

We injected chick syncytial strain of reticuloendotheliosis virus (CS-REV) and wild type and recombinant avian leukosis virus (ALV) near the blastoderm of unincubated fertilized embryos and CS-REV intra-abdominally at day of hatch, and we progeny tested the surviving ALV viremic males and REV viremic males and females for transmitted viral genetic material. A number of positive progeny were identified and their deoxyribonucleic acid (DNA) analyzed for restriction enzyme fragments that hybridized with viral genetic material. Most of the progeny had simple restriction enzyme patterns unlike the viremic parents or congenitally infected progeny. This is suggestive evidence that retroviral genetic information has been inserted into the germ line of chickens.

Animals↗
PubMed1986

Design of retroviral vectors for the insertion of foreign deoxyribonucleic acid sequences into the avian germ line.

Because the available avian leukosis viral (ALV) vectors are moderately oncogenic in vivo, they are not suitable for insertion into the germ line. A significant reduction in the oncogenicity of the ALV vectors can be achieved by substituting the noncoding long terminal repeats (LTR) regions of the ALV virus with the LTR of the nononcogenic endogenous RAV-O virus. There is good evidence that the resulting RAV-O LTR vectors can be inserted into the germ line of domestic chickens and have the potential for inserting cloned sequences that can be used for poultry improvement.

Animals↗
PubMed1985

Tests of association of lymphocyte alloantigen genotypes with resistance to viral oncogenesis in chickens. 2. Rous sarcoma and lymphoid leukosis in progeny derived from 6(3) X 15(1) and 100 X 6(3) crosses.

Chickens from inbred line RPRL 6(3) are resistant to virally-induced Marek's disease (MD) and lymphoid leukosis (LL) and are relatively strong regressors of virally induced Rous sarcomas. Line 6(3) chickens are homozygous for three independent loci determining surface alloantigens of lymphocytes, Th-1 and Ly-4 on thymus-derived (T) cells and Bu-1 on bursa-derived (B) cells. In contrast, RPRL Lines 100 and 15(1) are highly susceptible to MD and LL and are weaker regressors of Rous sarcomas than 6(3). RPRL Lines 100 and 15(1) are homozygous for different alleles at the Th-1 and Ly-4 loci than 6(3), whereas only Line 100 differs from 6(3) at Bu-1. To test the possible association of these three antigen loci with variations in resistance to virally-induced tumors, homozygous genotypes among later generations derived from 6(3) X 15(1) and 100 X 6(3) crosses were identified by means of immunofluorescence testing of peripheral blood lymphocytes. Test progeny were then bred from matings of homozygous parents. No association was found between Rous sarcoma regression and the Th-1 and Ly-4 T cell alloantigen loci in F6 (6(3) X 15(1)) chickens, but the Bu-1 locus influenced rate of regression in F3 (100 X 6(3)) chickens. The Ly-4 in F6 (6(3) X 15(1)) and Bu-1 in the F3 (100 X 6(3)) chickens did not influence the incidence of LL. However, Th-1 influenced LL in F3 (100 X 6(3)) chickens (P less than .05) and possibly influenced LL in F6 (6(3) X 15(1)) chickens (P less than .09).

Animals↗
PubMed1985

Responses of chickens lacking or expressing endogenous avian leukosis virus genes to infection with exogenous virus.

Line 0 chickens that lack endogenous viral (ev) genes and 15I5 X 7 chickens that carry and express ev genes were inoculated with the avian leukosis virus, RAV-1, at 1 day of age or as embryos, and maintained to 70 days of age. Comparable uninoculated controls were also kept. Most of the day-old inoculated chickens developed antibody by 70 days, but as expected, most of the embryo inoculated chickens remained viremic. Major differences in response between the lines were only noted after day-old inoculation. About 40% of Line 0 died of a specific nonneoplastic syndrome (NNS) while none of the 15I5 X 7 chickens did. Line 0 also developed neutralizing antibodies at a much earlier age than 15I5 X 7 and, consequently, virus was cleared from the serum much earlier. Day-old RAV-1 infection of Line 0 also lowered hematocrit more at 14 and 21 days of age than in 15I5 X 7 chickens. Body weight was clearly reduced at all ages in both lines of chickens by both day-old and embryo inoculation. After embryo inoculation, hematocrit was lowered in both lines of chickens between 28 and 42 days of age. Immune response to sheep red blood cells and Brucella abortus was only slightly and inconsistently reduced by inoculation of RAV-1 by both routes in both lines of chickens. It was concluded that the major influences of ev gene expression was to reduce the incidence of NNS and the neutralizing antibody response after RAV-1 inoculation of day-old chicks.

Animals↗
PubMed1984

Influence of sex-linked feathering phenotypes of parents and progeny upon lymphoid leukosis virus infection status and egg production.

Data were collected on egg production, livability, lymphoid leukosis virus and antibody incidence, and hemagglutinin response to sheep red blood cells for slow- and fast-feathering female progeny from slow- and fast-feathering dams with known lymphoid leukosis virus infection status. Analyses of these results indicate that when the offspring or the dams are of the slow-feathering type, the offspring experience an increased rate of horizontal infection. This infection seemingly leads to an immunologically tolerant condition with an inability to produce specific lymphoid leukosis virus antibodies, thereby allowing the viremia to persist. This immunologically tolerant condition, which also occurs in the progeny of virus positive dams due to congenital transmission, is associated with depressed egg production performance. However, a hypothesized lack of immunological competence was not found in the hemagglutinin response to sheep red blood cells late in life. Our results suggest that fast-feathering progeny of slow-feathering dams may also be adversely influenced by increased congenital infection from their dams.

Animals↗
PubMed1983

Tumor induction by direct injection of cloned v-src DNA into chickens.

The in vitro transforming potential of Rous sarcoma viruses has been shown to reside in a gene segment, v-src. To provide direct proof that the isolated v-src sequence contains all the information necessary for sarcoma induction in vivo, we have injected subgenomic and genomic cloned DNA carrying v-src directly into chickens. We report that v-src, without the complements of other viral genes, can effectively induce sarcomas in the host within weeks after injection. The sarcoma tumors generated by subgenomic v-src DNA are of mono- or oligoclonal origin. They have acquired v-src sequences in the genome and expressed high levels of src messages. Intact long terminal repeats do not seem to be essential in the tumorigenic process.

Animals↗
PubMed1982

Immunocompetence of chickens during early and tumorigenic stages of Rous-associated virus-1 infection.

A study was designed to determine the effects of congenital infection with the Rous-associated virus-1 (RAV-1) on the immune function chickens during the early and late tumorigenic stages of infection. In another experiment, the effects of niridazole on the immune competence and the tumor incidence in chickens congenitally infected with RAV-1 were studied. Lymphocyte stimulation by phytohemagglutinin, the phytohemagglutinin skin test, the response to immunization with sheep erythrocytes and Brucella abortus, and histological evaluation of lymphoid organs were used to determine the immune competence in normal and infected chickens. Results indicated that both B- and T-cell immune functions during the early and late stages of RAV-1 infection were comparable to those of normal uninfected chickens. Administration of niridazole to congenitally infected chickens at 5 weeks of age for 7 or 21 days had no effect on the T-cell-mediated immunity; however, administration of the drug for 21 days eliminated lymphoma development. Unlike infection with other oncogenic viruses such as those causing Marek's disease and reticuloendotheliosis, infection with RAV-1 caused no detectable immunodepression during the early and late stages of infection.

Animals↗
PubMed1982

Studies of avian leukosis virus infection in chickens from a commercial breeder flock.

Progeny chicks from a commercial breeder flock with a high rate of avian leukosis virus (ALV) infection were classified as congenitally or contact infected with ALV on the basis of virus tests on their meconia at hatching and the presence or absence of antibodies at 20 weeks of age. The ALV infection profile, shedding, tumor mortality, and egg production in the congenitally-infected chickens were compared with those in the contact-infected hatchmates. Results show that viremic-tolerant hens classed as congenitally infected consistently shed virus into albumen of their eggs and progeny and 18% died from tumors. In contrast, hens classified as contact infected had a transient viremia; most of them developed antibody to ALV, and only 10% shed virus into albumen and progeny. No mortality from tumors occurred in this group of chickens during the 48-week experimental period, and egg production was significantly higher than in the group classified as congenitally infected. In addition, progeny chickens hatched from the contact-infected group maintained a low rate (2.9 to 3.8%) of ALV infection for the next two generations without further selection. These data further document principles and procedures for reduction of ALV infection in commercial flocks and the considerable economic benefits to be derived therefrom.

Animals↗
PubMed1981

Analysis of avian leukosis virus DNA and RNA in bursal tumours: viral gene expression is not required for maintenance of the tumor state.

Each of twelve tumors induced by either Rous-associated virus-1 or -2 (RAV-1 or RAV-2) contained a predominant population of cells with ALV proviruses integrated at common sites, consistent with a clonal origin. Seven of nine RAV-2-induced bursal tumors contained single proviruses, and all seven solitary proviruses had suffered deletions. The detailed structures of four of these proviruses show that major deletions had occurred near or at the 5' ends, spanning sequences potentially important in the production of viral RNA. One provirus also lacked most of the information coding for the replicative functions of the virus. Restriction maps suggest that these four proviruses were inserted in similar regions of the host genome. We have studied virus-specific RNA in four bursal tumors and four cell lines derived from bursal tumors. No normal viral RNA species were detectable in three tumors containing single aberrant proviruses. However, transcripts of 2.2. kb which reacted only with a hybridization probe specific for the 5' end of viral RNA were observed in one of these three tumors. Analogous species, varying in length from 1.5 to 6.0 kb, were observed in a fourth bursal tumor with multiple proviruses and in all four cell lines. (This tumor and the cell lines also contained normal species of ALV mRNA and apparently normal proviral DNA). The structures of the aberrant proviruses and the absence of normal viral RNA in some tumors indicate that expression of viral genes is not required for maintenance of the tumor phenotype. In at least some cases, the mechanism of oncogenesis may involve stimulation of transcription of flanking cellular sequences by a viral promoter.

Animals↗
PubMed1981

On the mechanism of retrovirus-induced avian lymphoid leukosis: deletion and integration of the proviruses.

There is considerable evidence that infection by avian lymphoid leukosis viruses can led to tumor development in the target organ of the host. The mechanism by which virus-induced oncogenic transformation occurs, however, is not clearly understood. As a first step toward deciphering this process, we have characterized the proviruses of the lymphoid leukosis viruses in DNAs extracted from the leukotic and metastatic tumors by using restriction enzyme digestion and filter hybridization analysis with radioactive probes specific for the infecting genome. Our results indicate (i) that lymphoid leukosis tumors are clonal in origin; (ii) that there are multiple sites in the cellular genome of the target tissue where the virus DNA can integrate and that, in the majority of the tumors, at least one such site of each tumor is adjacent to a cellular sequence related to the oncogene of MC-29 virus; and (iii) that deletions and other structural alterations in the proviral DNA may facilitate tumorigenesis.

Animals↗
PubMed1981

Relative efficiency of test procedures to detect lymphoid leukosis virus infection.

A total of 2544 comparisons were used to study the relative efficiency of various test procedures currently used to detect lymphoid leukosis virus infection in chickens. Meconium, blood, cloacal swabs, and egg albumen were collected from day-old chicks and adult hens from four breeder flocks. The phenotypic mixing was used as the biological assay for infectious virus. The complement fixation test and enzyme-linked immunosorbent assays were used as direct assays for the group-specific antigen of the avian leukosis-sarcoma viruses. Analysis of test results of biological assays has shown that blood from virus-infected chicks was more frequently positive than meconium. Also, direct assay for group-specific antigen was as efficient as the biological assays for detection of positive albumen samples from freshly laid eggs. The rate of false-positive reactors recognized by direct assays was lower in albumen samples than in cloacal swabs collected from hens that produce endogenous virus or group-specific antigen. Data also showed a relatively high concordance, ranging from 71 to 100%, between various assays with test materials from adult hens. Progress in reducing rates of exogenous lymphoid leukosis virus infection can be significant if dams are selected on the basis of any one of the test procedures examined. For complete eradication however, day-old chicks should be selected on the basis of the biological assay of blood of individual chicks reared in small groups.

Animals↗
PubMed1981

Tumor latency in avian lymphoid leukosis.

Transfer of bursa cells from older chicken infected with lymphoid leukosis (LL) virus into young recipient chicks depleted of bursal lymphocytes by cyclophosphamide shortened the latency period for lymphoma development in recipient chickens by an amount equivalent to the age of the donor. Chickens were crosses between males of the Regional Poultry Research Laboratory, East Lansing, Michigan, inbred line 151, subline 5, and females of inbred line 7, subline 2. In a further experiment with intact infected chicks, artificial metastasis at various ages by surgical bursectomy and inoculation of bursa cells into the bloodstream of the host did not shorten the latency period. These results suggest that latency in avian LL is a property of target B-cells and is unrelated to maturational events of the host physiology.

Age Factors↗
PubMed1980

Induction of neoplasms by subgroup E recombinants of exogenous and endogenous avian retroviruses (Rous-associated virus type 60).

Chickens susceptible to infection with subgroup E viruses were inoculated with four independent isolates of Rous-associated virus type 60 (RAV-60) that are subgroup e recombinants of endogenous and exogenous virus. Neoplasms developed in each inoculated group. Therefore, nontransforming viruses of subgroup E can induce lymphoid leukosis at a moderate rate compared with RAV-0, a subgroup E endogenous virus, suggesting that oncogenicity is not a viral envelope (env)-related characteristic. Since the common (c) regions of the RAV-60s examined were of exogenous origin, we suggest that the c region rather than env is important for a high rate of induction of lymphoid leukosis and related neoplasms.

Animals↗
PubMed1978

Vaccination against infectious bronchitis and the immunosuppressive effects of infectious bursal disease.

An immunosuppressive effect was demonstrated in chickens which were infected with infectious bursal disease virus (IBDV) early in life and prior to or shortly after vaccination with infectious bronchitis virus (IBV). This effect was evident by an increased susceptibility to respiratory tract infection with IBV and reduced virus-serum neutralizing antibody levels. Chickens which were hatched from dams susceptible to infectious bursal disease (IBD) were less responsive to IBV immunization attempts, if exposed to IBDV, than were those individuals hatched from IBD immune dams. However, in some cases, chickens from IBD immune dams were also more susceptible to IBV challenge when they had been exposed to IBDV and when compared to birds unexposed to IBDV but vaccinated against IB. An effect of cyclophosphamide on the bursa of Fabricius also had an immunosuppressive action on IBV immunity which was similar to the results from IBDV exposure. The data engendered from these trials may explain the unsatisfactory immunity sometimes observed under field conditions when broilers and replacement pullets are vaccinated at an early age.

Animals↗
PubMed1977

Immunization of chickens against adenovirus infection.

Chickens were vaccinated with monovalent and polyvalent adenovirus vaccines using three different serotypes, types 1, 2, and 3. No cross-protection was elicited by the heterologous serotypes but satisfactory protection from lesions and the shedding of challenge virus was induced by the homologous serotypes in the monovalent and polyvalent vaccines. The virus neutralizing (VN) titers were occasionally lower where the polyvalent vaccines were used when compared to those from chickens given the monovalent vaccines. This suggested possible interference though protection did exist against the appearance of lesions. Where chickens were vaccinated at an early age and in the presence of congenital homologous VN antibodies, protection against the effects of infection was satisfactory whereas the VN antibody titers were low or insignificant by the assay methods employed. The vaccine virus was not shed beyond 28 days after vaccination. No physical effects of vaccination were noted in any of the chickens during the post-vaccination period.

Adenoviridae Infections↗
PubMed1976

Variant infectious bronchitis virus isolated from Indiana chickens.

Infectious bronchitis virus (IBV) associated with a catarrhal tracheitis, sudden decline in egg production, and reduced shell quality was isolated from an Indiana White Leghorn breeder flock. It was found to be serologically different from Massachusetts, Connecticut, Iowa 97, Iowa 609, Florida, Arkansas 99, JMK, Holte, Gray and SE 17 IBV serotypes. Two different Massachusetts vaccine strains protected chickens from respiratory signs but not against virus infection using the isolant for challenge in laboratory trials. The isolant was passed through a 0.22 mu. filter. It was heat (56 C), acid pH (3.0), ether and chloroform labile. In embryos it produced deaths or lesions of infectious bronchitis in one to five days after inoculation. It is suggested that this IBV isolant be designated Indiana-type.

Animals↗
PubMed1975

Potential for polyvalent infectious bronchitis vaccines.

Numerous antigenic types and subtypes of infectious bronchitis virus (IBV) have been isolated and characterized from field epornitics of infectious bronchitis (IB). Thus obvious failures in obtaining the necessary protection from vaccination have been documented and they underscore the urgent need for vaccines which stimulate a broader spectrum of protection from heterologous IBV challenge than is presently obtained. If polyvalent IB vaccines are to be employed, assurance must be provided that variant IBV serotypes are not indiscriminately spread throughout the country or globe. Furthermore, possible interference, alteration, and reduction in immune response with the component antigens should be critically evaluated. Differences and comparative levels of postvaccinal respiratory signs with the different antigens, used singly and in combination, should be determined. As an alternative to polyvalent IB vaccines, certain Massachusetts-type strains, e.g., a Holland isolate IBV, at different passage levels in the authors' laboratory, have induced heterologous and homologous protection to some serotypes causing vexing field problems. Advantages are present in using a single antigenic type IB vaccine, if it is safe and effective, when compared to polyvalent vaccines. The absence of a serologic relationship to the results of immunity challenge is frequent with IBV isolates, which emphasizes that challenge results are considerably more important. In some IB problems, on a local or regional basis, autogenous vaccines may be indicated. Because of the multiplicity of IBV serotypes, however, it is doubtful that completely effective and safe IB vaccines will be forthcoming in the near future to satisfy the diverse needs of a dynamic poultry industry.

Animals↗