Biomedical subjects

A M Fadly

Publications and source records attributed to A M Fadly.

At least 19 recordsLinked to original sources

PubMed2005

Novel criteria for the diagnosis of Marek's disease virus-induced lymphomas.

Several novel criteria have been tested to assist in the differential diagnosis of tumours induced by Marek's disease virus (MDV) from those induced by avian leukosis virus (ALV) and reticuloendotheliosis virus (REV). A collection of tumours induced by inoculation of specific strains of MDV, ALV and REV, alone or in combination, were tested for quantification of MDV DNA by real-time polymerase chain reaction, expression of the MDV oncogene Meq, expression of several cell markers associated with transformation (CD30, Marek's disease-associated surface antigen, and p53), and level of DNA methylation in the tumour cells. In addition, tissues latently infected with MDV and non-infected tissues were tested as controls. Tumours induced by MDV had about 10(2)-fold more copies of MDV DNA than either tissues latently infected by MDV or tumours induced by retrovirus in MDV-vaccinated chickens. Moreover, the MDV antigen Meq was consistently expressed in all MDV tumours but it could not be detected in tissues latently infected with MDV or in tumours induced by retrovirus in MDV-vaccinated chickens. Other markers studied were not specific for MDV and therefore had limited value for diagnosis. Nonetheless, some of these markers might have potential value in research as they will help to identify transformed cells.

Animals↗

PubMed2000

Hypervariability in the envelope genes of subgroup J avian leukosis viruses obtained from different farms in the United States.

Avian leukosis virus, subgroup J (ALV-J), has a wide host range, preferentially infecting meat-type birds, and produces a high incidence of myelocytomatosis and nephromas. Using the published sequences from HPRS-103 (ALV-J isolated in 1989 in Great Britain), we designed a set of PCR primers that amplified proviral DNA from nine U.S. field samples. The primers were specific for ALV-J, not amplifying DNA from uninfected cells or cells infected with ALV subgroups A-E. These primers expanded a 2.4-kb fragment that encompasses gp85, gp37, the E element, and most of the 3' LTR. We also developed a set of PCR primers that amplified a 2.1-kb fragment from ALV-J-infected cells and a 1.6-kb fragment from uninfected ev- chicken embryo fibroblasts (Line 0). Upon cloning and DNA sequencing, we determined that the 2.1- and 1.6-kb fragments contained ALV-J gp85- and gp37-like sequences. Comparison of the amino acid sequences demonstrated that the Line 0 sequences were 97.5% identical with the gp85 and gp37 of HPRS-103 and somewhat less identical with the other nine U.S. isolates. This suggests that the envelope genes of ALV-J may have arisen as a result of a recombination event between exogenous ALV and Line 0-like sequences in the chicken. Phylogenetic analysis also showed that the U.S. field isolates were closely related to one another and more distantly related to the European HPRS-103. The pattern of mutations in the U.S. field isolates suggests that the U.S. strains are slowly drifting away from their progenitor Line 0-like sequences. The development of effective vaccines and diagnostic tests is likely to become more problematic as the viruses continue to mutate.

Amino Acid Sequence↗

PubMed1999

A genetically engineered cell line resistant to subgroup J avian leukosis virus infection (C/J).

A cell line (DF-1¿J) expressing the envelope protein isolated from the ADOL-Hc1 strain of the avian leukosis virus subgroup J (ALV-J) was used to analyze receptor interference to six different isolates of ALV-J as well as ALV subgroups A-D. The traditional gag-specific enzyme-linked immunosorbent assay (ELISA) as well as flow cytometry was used to evaluate viral infection. The parental cell line (DF-1) was susceptible to all ALV subgroups tested while the DF-1¿J cell line was selectively resistant to the subgroup J isolates. The DF-1¿J cell line was resistant to infection by all six ALV-J isolates as determined using the gag-specific ELISA. There was no interference with the other ALV subgroups (A-D) induced by the expression of the ADOL-Hcl envelope. The ALV-J isolates used in this analysis are serologically distinct when analyzed by flow cytometry. Convalescent sera to ADOL-Hcl cross-reacts with all of the ALV-J isolates tested; however, sera to HPRS-103 did not bind to four of the six isolates. Based on the intensity and differential binding of these antisera using flow cytometry, the six ALV-J isolates used can be grouped into four categories. Thus the DF-1¿J cell line is resistant to infection by a serologically and genetically diverse group of ALV-J isolates and should be useful as a diagnostic tool.

Amino Acid Sequence↗

PubMed1998

Orbital lymphosarcoma associated with reticuloendotheliosis virus in a peafowl.

Lymphosarcoma associated with infection by avian reticuloendotheliosis virus was diagnosed in an Indian peafowl with exophthalmia and exposure keratitis. Exenteration of the orbit was complicated by a profound oculocardiac reflex and extensive hemorrhage during surgery. Orbital bleeding was controlled by direct pressure, electrocautery, topical administration of bovine thrombin, and application of sterile gelatin sponges and oxidized regenerated cellulose. A blood transfusion was also performed. In addition to describing methods of handling intraoperative complications of orbital exenteration in birds, to the authors' knowledge, this is the first report to describe an association of reticuloendotheliosis virus, which more commonly affects poultry, with lymphosarcoma in an Indian peafowl.

Animals↗

PubMed1998

The unique envelope gene of the subgroup J avian leukosis virus derives from ev/J proviruses, a novel family of avian endogenous viruses.

A new subgroup of avian leukosis virus (ALV), designated subgroup J, was identified recently. Viruses of this subgroup do not cross-interfere with viruses of the avian A, B, C, D, and E subgroups, are not neutralized by antisera raised against the other virus subgroups, and have a broader host range than the A to E subgroups. Sequence comparisons reveal that while the subgroup J envelope gene includes some regions that are related to those found in env genes of the A to E subgroups, the majority of the subgroup J gene is composed of sequences either that are more similar to those of a member (E51) of the ancient endogenous avian virus (EAV) family of proviruses or that appear unique to subgroup J viruses. These data led to the suggestion that the ALV-J env gene might have arisen by multiple recombination events between one or more endogenous and exogenous viruses. We initiated studies to investigate the origin of the subgroup J envelope gene and in particular to determine the identity of endogenous sequences that may have contributed to its generation. Here we report the identification of a novel family of avian endogenous viruses that include env coding sequences that are over 95% identical to both the gp85 and gp37 coding regions of subgroup J viruses. We call these viruses the ev/J family. We also report the isolation of ev/J-encoded cDNAs, indicating that at least some members of this family are expressed. These data support the hypothesis that the subgroup J envelope gene was acquired by recombination with expressed endogenous sequences and are consistent with acquisition of this gene by only one recombination event.

Amino Acid Sequence↗

PubMed1998

Independent isolates of the emerging subgroup J avian leukosis virus derive from a common ancestor.

A new subgroup of avian leukosis virus (ALV) that includes a unique env gene, designated J, was identified recently in England. Sequence analysis of prototype English isolate HPRS-103 revealed several other unique genetic characteristics of this strain and provided information that it arose by recombination between exogenous and endogenous virus sequences. In the past several years, ALV J type viruses (ALV-J) have been isolated from broiler breeder flocks in the United States. We were interested in determining the relationship between the U.S. and English isolates of ALV-J. Based on sequence data from two independently derived U.S. field isolates, we conclude that the U.S. and English isolates of ALV-J derive from a common ancestor and are not the result of independent recombination events.

Amino Acid Sequence↗

PubMed1998

Reticuloendotheliosis in captive greater and Attwater's prairie chickens.

Reticuloendotheliosis in captive greater (Tympanuchus cupido pinnatus) and Attwater's (T. cupido attwateri) prairie chickens is reported for the first time. Between September 1993 and August 1994, two adult female wild-caught greater prairie chickens housed at Texas A&M University (College Station, Texas, USA) were observed with multiple subcutaneous nodules. Both birds were euthanatized. Complete necropsy examinations revealed lesions limited to the skin of each bird. Histopathologic examination of lesions revealed pleomorphic lymphoreticular cells suggestive of reticuloendotheliosis and reticuloendotheliosis virus (REV) was demonstrated in tumor tissue by polymerase chain reaction and virus isolation. Between September 1994 and June 1995, five additional greater prairie chickens and two Attwater's prairie chickens were euthanatized or found dead with evidence of lymphoreticular neoplasia in multiple organ systems. Initial testing of the captive flock in December 1994 for evidence of viremia and antibody to reticuloendotheliosis virus revealed over 50% of the tested birds were viremic, but none developed antibodies. Subsequent testing between January 1995 and January 1996 indicated that once infected with reticuloendotheliosis virus, Attwater's prairie chickens tended to remain outwardly healthy despite persistent viremia compared to infected greater prairie chickens which had higher morbidity and mortality rates within 60 to 90 days after initial detection of viremia and did not usually develop persistent viremia. Antibodies to REV were detected in only three captive greater prairie chickens and only in 1995. Six of the nine birds that were euthanatized or found dead due to reticuloendotheliosis developed viremia prior to death; three birds were not tested prior to death. Testing of free-ranging greater and Attwater's prairie chickens for reticuloendotheliosis is recommended prior to translocation or release.

Animals↗

PubMed1997

Avian retroviruses.

Avian leukosis virus (ALV) and reticuloendotheliosis virus (REV) are the most common naturally occurring avian retroviruses associated with neoplastic disease conditions in domesticated poultry. Avian leukosis virus infects primarily chickens, whereas REV infects chickens, turkeys, and other avian species. In addition to causing tumors, both ALV and REV can reduce productivity and induce immunosuppression and other production problems in affected flocks.

Animals↗

PubMed1997

Role of contact and genetic transmission of endogenous virus-21 in the susceptibility of chickens to avian leukosis virus infection and tumors.

The role of contact and genetic transmission of endogenous virus-21 (EV21) on response of chickens to avian leukosis virus (ALV) infection and tumors was studied. F1 progeny of a cross between RPRL late-feathering (LF) line EV21+ males and RPRL early feathering (EF) line 15B1 females harboring or lacking EV21 were used. The EF chicks lacking EV21 were inoculated with a field strain of subgroup A ALV at hatch and contact exposed to LF, EV21+ hatchmates for various time intervals. In a second experiment, EV21 contact-exposed and unexposed EF chicks as well as LF, EV21+ hatchmates were inoculated with ALV at various ages. Chickens were tested for ALV-induced viremia and antibody and were observed for tumors until 24 wk of age. Antibody to EV21 in EF chickens contact-exposed to LF, EV21+ hatchmates varied from 10 to 65%, and was detected by 10 wk of age. By 24 wk of age, ALV-induced viremia and tumors in EF chickens varied from 5 to 30%, and from 15 to 32%, respectively, regardless of exposure to EV21. The incidence of ALV-induced tumors was significantly higher in LF chickens genetically infected with EV21 than in EV21 contact-exposed or unexposed EF chickens, but only in chickens inoculated with ALV at hatch. The data suggest that contact infection with EV21 has no influence on ALV infection and tumors. The data also suggest that genetic transmission of EV21 may increase susceptibility of chickens to ALV infection and tumors following infection with ALV at hatch, but not at 4 wk of age or older.

Animals↗

PubMed1994

Male-mediated venereal transmission of endogenous avian leukosis virus.

Congenital transmission of avian leukosis viruses (ALV) occurs readily through the egg, but transmission of ALV through male seminal fluid is considered to be nonexistent or rare. Progeny from mating endogenous late-feathering (LF), K/k+ males carrying an endogenous virus gene (ev21) with virgin early-feathering (EF) k+/w females were examined for the presence of infectious endogenous virus EV21 using an enzyme-labeled immunoassay for viral capsid antigen p27. All 177 LF chicks expressed EV21, p27, and 171 of 175 EF chicks did not express p27. Blood from the four p27-positive EF chicks revealed only infectious Subgroup E ALV as determined by subgroup-specific virus assays. Southern blot DNA hybridizations, however, ruled out germline integration of EV21 among the four infected EF progeny. Virus EV21 was not shed in albumens of the dams. Moreover, antibodies against ALV Subgroups A and E were not detected in dams 17 wk after the first insemination. Chicks infected with EV21 were found only in the first two of six hatches. Data suggested direct infection of the embryos from viremic semen rather than congenital infection through infected hens. Direct male transmission of EV21 to progeny may be the basis for persistence of refractory lines noted in some ALV eradication programs. Based on the absence of recombinants among 352 progeny, ev21 and K appear to be less than .3 cM apart.

Animals↗

PubMed1991

The influence of ev6 on the immune response to avian leukosis virus infection in rapid-feathering progeny of slow- and rapid-feathering dams.

Endogenous virus (EV) locus ev6 encodes only virus envelope glycoprotein. The influence of ev6 on the immune response to contact infection with hatchmates infected with avian leukosis virus (ALV) was compared in replicate hatches. The ALV Subgroup E-resistant, rapid-feathering (RF) female chickens produced by slow-feathering (SF) and RF dams with and without ev6 were exposed at hatch to hatchmates infected with ALV Subgroup A (Strain RPL-40). The RPL-40 viremia, shedding, and virus neutralizing antibodies were measured among pullets from two hatches at 22 wk of age. Although significant (P less than .05) differences between hatches in the immune response to contact infection were noted among ev6+ pullets, significantly fewer ev6+ pullets seroconverted than their ev6- hatchmates. At 22 wk of age, significantly more lymphomas were also found among ev6+ pullets than among ev6- hatchmates. In flocks wherein both parents and progeny were homozygous resistant to Subgroup E virus, there was no deterimental maternal effect on RF progeny from SF dams that carried ev21. These results also confirm that selection for genetic cellular resistance to Subgroup E ALV infection eliminates congenital transmission of EV21.

Animals↗

PubMed1990

Interactions between endogenous virus loci ev6 and ev21. 1. Immune response to exogenous avian leukosis virus infection.

The effects of ev6, ev21, sex, and hatch, were studied with respect to avian leukosis virus (ALV) viremia, cloacal shedding, and antibody response among RPL-40 virus-infected White Leghorns that carried ev6 and ev21 in all combinations. Among the four possible ev genotypes, chickens that carried only ev21 were the most immunologically tolerant to RPL-40 infection. Incidence of RPL-40 viremia was lowest among hatchmates that lacked both ev genes. Analysis of variance indicated significant interactions between ev6 and ev21 with respect to all responses. Among ev21+ slow-feathering (SF) chickens, the incidence of viremia and shedding of RPL-40 was reduced in the presence of ev6 when compared with ev6- hatchmates. Conversely, among ev21- rapid-feathering (RF) chickens, ev6 significantly enhanced the incidence of RPL-40 viremia when compared with ev6- hatchmates. The endogenous virus, ev6, markedly reduced recovery of the endogenous virus (EV21) from plasmas of slow-feathering chickens. When both flocks were terminated at 21 wk of age, significantly more ev21+ SF females had died from or developed RPL-40-induced tumors than ev21- hatchmates.

Animals↗

PubMed1990

Interactions between endogenous virus loci ev6 and ev21. 2. Congenital transmission of EV21 viral product to female progency from slow-feathering dams.

The influence of the endogenous virus ev6 on congenital transmission of EV21, the infectious viral product encoded by locus ev21, and the immune response to exogenous avian leukosis virus (ALV) infection was studied in rapid-feathering (RF) female progeny from four classes of slow-feathering (SF) (ev21+ and RF (ev21-) dams with and without ev6. Apart from transmitting infectious EV21 and ev6 to progency, dam ev genotype did not influence the immune response or shedding of RPL-40. The endogenous virus envelope glycoprotein encoded by ev6, however, completely restricted shedding and congenital transmission of infectious endogenous virus EV21, from SF dams. After 19 wk of exposure to ALV strain RPL-40 infected cage mates, only 11% of the congenitally infected female progeny mounted neutralizing antibodies against RPL-40, whereas 73% of their noncongenitally infected sisters seroconverted. More ev6+ female progeny, however, were shedders of RPL-40 and developed tumors than ev6- sisters. Among progeny from the four classes of dams, EV21 congenitally infected hens had the highest incidence (31%) of RPL-40-induced tumors.

Animals↗

PubMed1989

Augmentation of retrovirus-induced lymphoid leukosis by Marek's disease herpesviruses in White Leghorn chickens.

Our objective was to determine whether the cell-associated herpesvirus vaccines used in chickens to control Marek's disease tumors can augment development of lymphoid leukosis (LL) induced by exogenous avian leukosis virus (ALV). Various single or mixed Marek's disease vaccines were inoculated at day 1, and ALV was injected at 1 to 10 days, with chickens of several experimental or commercial strains. Development of LL was monitored at 16 to 48 weeks in various experiments. In several strains of chickens we repeatedly found that the widely used serotype 3 turkey herpesvirus vaccine did not augment LL in comparison with unvaccinated controls. However, LL development and incidence were prominently augmented in several chicken strains vaccinated with serotype 2 vaccines, used alone or as mixtures with other serotypes. In one chicken strain, augmentation was demonstrated after natural exposure to ALV or serotype 2 Marek's disease virus viremic shedder chickens. Augmentation of LL by virulent or attenuated Marek's disease viruses of serotype 1 was intermediate in effect. Serotype 2 Marek's disease virus augmentation of LL was prominent in three laboratory lines and one commercial strain of White Leghorns, but it was not observed in an LL-resistant laboratory line or four commercial strains susceptible to ALV infection. Chickens developed similar levels of viremia and neutralizing antibodies to ALV regardless of the presence of augmentation of LL, suggesting that the mechanism of enhanced LL did not result from differences in susceptibility or immune response to ALV. We postulate that the serotype 2 herpesviruses may augment LL through one of several possible influences on bursal cells that are subsequently transformed by exogenous ALV.

Animals↗

PubMed1988

Influence of congenital transmission of endogenous virus-21 on the immune response to avian leukosis virus infection and the incidence of tumors in chickens.

After contact exposure to Strain RPL-40 avian leukosis virus-infected hatchmates, a dilatory neutralizing antibody response and prolonged RPL-40 viremia was found among most pullets that were congenitally infected with endogenous virus 21 (EV21). Conversely, most of the hatchmates that were not congenitally infected seroconverted within 10 wk after exposure to Strain RPL-40 virus. Compared with noncongenitally infected hatchmates, EV-21 infection-induced tolerance to pathogenic avian leukosis viruses was reflected in a significantly higher incidence of lymphomas in congenitally infected hens. The rate of seroconversion and the incidence of RPL-40 virus-induced tumors among noncongenitally infected daughters from slow-feathering dams homozygous resistant to EV were similar to those found among daughters of rapid-feathering dams that lacked genetic locus ev21. Results suggest that selection for resistance to EV may eliminate tolerance toward oncogenic field strains of avian leukosis viruses and may improve the performance of progeny from a feather-sex cross.

Animals↗

PubMed1987

Embryonic infection with the endogenous avian leukosis virus Rous-associated virus-0 alters responses to exogenous avian leukosis virus infection.

We inoculated susceptible chicken embryos with the endogenous avian leukosis virus Rous-associated virus-0 (RAV-0) on day 6 of incubation. At 1 week after hatching, RAV-0-infected and control chickens were inoculated with either RAV-1 or RAV-2, exogenous viruses belonging to subgroups A and B, respectively. The chickens injected with RAV-0 as embryos remained viremic with exogenous virus longer and either failed to develop type-specific humoral immunity to exogenous virus or developed it later than the control chickens not inoculated with RAV-0. The RAV-0-injected chickens also developed neoplasms at a much higher frequency than did the control chickens. We suggest that the lower immune responses of the RAV-0-injected chickens were due to an immunological tolerance to envelope group-specific glycoproteins shared among endogenous and exogenous viruses.

Animals↗

PubMed1986

Resistance of line 6(3) chickens to reticuloendotheliosis-virus-induced bursa-associated lymphomas.

Chickens of lines 6(3) and 151(5) X 7(1) were inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) or with the Rous-associated virus-I of avian leukosis virus (ALV) at hatching. At 4, 10, 16, and 36 weeks post inoculation (PI), chickens were tested for REV- and ALV-induced viremia and antibody. The incidence of REV- or ALV-induced bursa-associated lymphomas in line 6(3) chickens was compared with that in line 151(5) X 7(1) chickens. Inoculation of REV at hatching resulted in immunological tolerance to the virus in line 6(3) but not in line 151(5) X 7(1) chickens. Between 70% and 100% of line 6(3) chickens remained viremic and lacked REV antibody throughout the experimental period of 36 weeks. In contrast, ALV-inoculated chickens of both lines had antibody by 16 weeks PI. The frequencies of REV- and ALV-induced bursa-associated lymphomas in line 6(3) chickens were significantly lower than in line 151(5) X 7(1) chickens. Further, the incidence of bursa-associated lymphomas induced by REV in line 151(5) X 7(1) chickens was significantly lower than that induced by ALV. These results suggest that: (1) the genetic constitution of the host may influence the immunological response to REV infection; (2) chickens resistant to ALV-induced bursa-associated lymphomas are equally resistant to such lymphomas induced by another unrelated avian retrovirus, REV; and (3) ALV is a more potent inducer of bursa-associated lymphomas than REV.

Animal Husbandry↗

PubMed1986

Tests of association of immunoglobulin allotype genes and viral oncogenesis in chickens.

Chickens from Regional Poultry Research Laboratory (RPRL) inbred line 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. In contrast, RPRL line 100 chickens are highly susceptible to MD and LL and are weaker regressors of Rous sarcomas than line 6(3). RPRL lines 100 and 6(3) differ for alleles at the IgG-1 (G-1) allotype locus, but have identical IgM-1 (M-1) allotype alleles. To test the possible association of the G-1 locus with variations in resistance to virally-induced tumors, homozygous and heterozygous genotypes among F3 crosses were infected. F3 chickens with different G-1 types were comparable in their resistance to MD tumors following inoculation with the JM strain of the MD virus, and for their ability to regress Rous sarcoma tumors induced by the Rous sarcoma virus (RSV) RAV-1. However, following RAV-1 virus infection a smaller proportion of G-1a/G-1aF3 or F4 birds developed LL tumors than G-1a/G-1e and G-1e/G-1e birds. Genes determining immunoglobulin heavy chains were therefore associated with a recessive resistance to B-cell lymphomagenesis in chickens.

Animals↗