Subgroup-E Avian-leukosis-virus-associated Disease in Chickens (original) (raw)

1. H. L. Robinson*,
2. M. N. Pearson*,
3. D. W. DeSimone*,
4. P. N. Tsichlis†, and
5. J. M. Coffin‡
6. *Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545; †Department of Medicine, and ‡Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111

Excerpt

One of the fascinating features of the biology of endogenous avian leukosis virus (ALV) is that these viruses, when introduced into chickens as exogenous infections, do not cause disease (Motta et al. 1975; Purchase et al. 1977; Crittenden et al. 1979a,b). This is in striking contrast to ALVs of exogenous origin, which are associated with a wide spectrum of acute and nonacute diseases (Purchase and Burmester 1977; Duesberg, this volume).

If one examines the genomes of endogenous and exogenous ALVs for a genetic basis for this phenomenon, one finds that the genomes of endogenous viruses are similar to those of exogenous viruses that cause nonacute disease. The genomes of both groups of viruses contain genes for virus replication, gag, pol, and env, and a C region. Genes such as src, erb, myb, and mac, which code for the oncogenic products expressed by ALVs that cause acute disease, do not appear...