Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/27/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: Lymphoid leukosis is an important tumor-like disease of older chickens caused by avian leukosis virus. Vaccine strains of Marek's disease virus (serotype 2) are not known to cause any disease and are widely used as vaccines to protect chickens against Marek's disease. Avian leukosis virus and vaccine strains of Marek's disease virus are distinctly different. Infection of certain susceptible chicken strains with avian leukosis virus results in a moderate rate of lymphoid leukosis. However, when such chickens are also infected vaccine strains of Marek's disease virus, they may develop a higher frequency of lymphoid leukosis than when infected by avian leukosis virus alone. Studies were conducted to investigate the basis for this enhancing effect of Marek's disease virus. Seven vaccine strains of Marek's disease virus were each found to cause an enhancing effect on lymphoid leukosis but 5 of the 7 strains lost this ability upon further cultivation in the laboratory. The loss of enhancing effect occurred sooner during the process of further cultivation than the loss of immunizing ability. One further passaged strain was found to retain good immunizing ability against Marek's disease but with reduced ability to enhance lymphoid leukosis. Such strains will be important to further studies on enhancement mechanisms and may provide safer vaccines for Marek's disease.
Technical Abstract: Two common vaccine strains of serotype 2 Marek's disease (MD) virus are known to enhance the frequency of lymphoid leukosis (LL) in certain retrovirus-infected chickens. Experiments were conducted to investigate whether this LL enhancement ability was influenced by viral strain or by serial passage in cell culture. Each of seven low-passage serotype 2 MD virus strains enhanced LL responses. The HN-1 strain was competent for LL enhancement at passage 19 but LL enhancement ability was absent at passages 26, 27 and 40. Enhancement of LL by strains 471B/1, 281MI/1, 287C/1 and 298B/1 was reduced by 40 to 64 serial passages in chicken embryo fibroblast cultures. Strains SB-1 and 301B/1 continued to demonstrate enhancement of LL through 66 and 40 passages, respectively. Thus LL enhancement appeared to be a general property of serotype 2 MD viruses but was susceptible in 5 of 7 strains to reduction (attenuation) by cell culture passage. Enhancement of LL was attenuated more rapidly by cell culture passage than the ability to protect against virulent MD virus challenge. One such LL enhancement-attenuated strain, 471B/1 (passages 33 and 40), when combined with turkey herpesvirus (HVT), induced protection against MD challenge (76 and 78%) that was comparable with that induced by SB-1 + HVT (82%) or 301B/1 + HVT (89%).