Effect of an in ovo infection with a Dutch avian leukosis virus subgroup J isolate on the growth and immunological performance of SPF broiler chickens

Abstract

The effect of an in ovo infection with a Dutch isolate of avian leukosis virus subgroup J (ALV-J) on the growth of specific pathogen free (SPF) broiler chickens was analysed. During this study, possible immune suppressive effects of ALV-J were assessed by measuring delayed-type hypersensitivity with keyhole limpet haemocyanin (KLH), natural killer (NK) cell activity, the production of radicals of nitric oxide (NO) by macrophages, humoral immune response against Newcastle and infectious bursal disease vaccine viruses, and automated total and differential leukocyte counts. In an attempt to elucidate the underlying causal mechanisms of the induced growth retardation, 3,39 ,5-triiodothyronine (T3) concentrations in serum were measured. Four experiments were conducted. In experiment 1, ALV-J-injected birds were compared with ALV subgroup A (ALV-A)-injected and negative control chickens. In experiment 2, ALV-J-injected birds were only compared with negative controls. Finally, in experiments 3a and 3b, ALV-J-injected chickens were compared with negative controls and a group of chickens in which only 10% of birds had been injected with ALV-J. Birds were injected in ovo at day 7 of incubation with 10 4 median tissue culture infectious dose (TCID 50 ) ALV-J or ALV-A, except in experiment 3a where 10 2 TCID 50 ALV-J was injected. Significant growth suppression was found in all 100% of ALV-J-infected groups. The average growth retardation of ALV-J-infected birds compared with negative controls at 6 weeks of age was approximately 8, 11, 2.5 and 6% for the four successive experiments performed. The delayed-type hypersensitivity test against KLH of ALV-J-infected birds showed a tendency towards lower wattle thickness; however, the difference with controls was not significant (P > 0.05). The same was true for NK cell activity and NO production by macrophages, although the difference was not significant. The total and differential leukocyte counts performed on blood samples from birds at 3, 4 and 6 weeks of age as well as the humoral immune response against Newcastle and infectious bursal disease vaccine viruses did not show significant differences between treatment groups either. Only the number of basophils were significantly higher (P = 0.02) in ALV-J-infected birds at 3 weeks of age. No significant lower T 3 levels were found in ALV-J-infected birds in weeks 2 and 3 (experiment 2) and weeks 3 and 5 (experiment 3b); however, at 4 weeks (experiment 2) and 6 weeks (experiment 3b) of age, T 3 levels were significantly lower suggesting mild hypothyroidism in these broilers. In conclusion, the present experiments show the occurrence of significant growth retardation in SPF broilers after an ALV-J in ovo infection. The various studies performed to assess the immune competence of ALV-J-infected chickens did not show significant differences in immune responsiveness. The assays on cellular immunity showed a tendency to a lower response in ALV-J-infected birds, but these differences were not statistically significant.

Differences in pathogenicity among strains of the same or different avian leukosis virus subgroups

“…The data on RAV-2 and RAV-49 document that within both subgroups, ALV-B and ALV-C, differences in pathogenicity exist between individual viral strains and indicate that both wasting and the lymphoid tissue alteration may be induced independently. This conclusion is also supported by recently published data on ALV-J pathogenicity for in ovo infected chickens, in which significant growth suppression was not accompanied by alteration of immune responsiveness (Landman et al, 2002). Endogenous avian retroviral sequences that participated in ALV-J formation (Bai et al, 1995) represent a potential source of genetic material for the occurrence of recombinants accommodating new pathogenic properties dif- Figure 1.…”

“…The main clinical sign of the wasting syndrome is progressive weight loss, which is accompanied by metabolic and hormonal disorders, depletion of lymphatic organs and immunosuppression, and in some cases also by osteopetrosis, anaemia and, occasionally, diarrhoea (Meyers et al, 1976;Smith & Van Eldik, 1978;Price & Smith, 1982;Rupp et al, 1982;Fadly et al, 1982;Landman et al, 2002;reviewed in Svoboda et al, 2003). Carter & Smith (1984) pointed out a specific pathogenic effect of subgroup C viruses, characterized by stunting, hypothyroidism, hyperinsulinaemia, alteration of lipid metabolism and lymphoblastoid infiltration of the liver, thyroid and pancreas.…”

A 205-Nucleotide Deletion in the 3′ Untranslated Region of Avian Leukosis Virus Subgroup J, Currently Emergent in China, Contributes to Its Pathogenicity

“…The proportion of infected chickens can reflect viral replication in vivo (12,32). As shown in Table 1, the SPF layers and commercial broilers infected with rHLJ09SH01 showed a higher infection proportion than the chickens infected with rHLJ09SH01A205 within the first 2 weeks after hatching.…”

“…Thus, the failure to detect neutralizing antibodies for either virus in these chickens 7 weeks after hatching was not unexpected. Cloacal swabs from the hatched chickens were tested for the p27 antigen to evaluate the success of the ALV-J infection process; generally, the proportion of infected chickens reflects the replication of virus in vivo (12,32). The cloacal swabs collected 1, 6, and 15 days after hatching showed that infection with rHLJ09SH01 resulted in a higher proportion of p27 ELISApositive SPF layers and commercial broilers than infection with rHLJ09SH01A205, indicating that the 205-nucleotide deletion confers a replication advantage on ALV-J in vivo (Table 1).…”

The MET Gene Is a Common Integration Target in Avian Leukosis Virus Subgroup J-Induced Chicken Hemangiomas

“…Since its discovery in the United Kingdom, a variety of ALV-J strains in diverse geographical areas, including North America, Europe, East Asia, Australia, and the Middle East, have been characterized (6)(7)(8)(9)(10)(11). It is believed that these isolates derive from a single common ancestor and are not the result of independent recombination events (6).…”