Two Different Molecular Defects in the Tva Receptor Gene Explain the Resistance of Two tvar Lines of Chickens to Infection by Subgroup A Avian Sarcoma and Leukosis Viruses

摘要: The subgroup A to E avian sarcoma and leukosis viruses (ASLVs) are highly related thought have evolved from a common ancestor. These use distinct cell surface proteins as receptors gain entry into cells. Chickens resistance infection by the ASLVs. We identified mutations responsible for block virus in chicken lines resistant ASLVs [ASLV(A)]. tva genetic locus determines susceptibility of cells ASLV(A) viruses. In quail, allele tvas encodes two forms Tva receptor; these translated alternatively spliced mRNAs. normal cellular function receptor is unknown; however, extracellular domain contains 40-amino-acid, cysteine-rich region that homologous ligand binding low-density lipoprotein (LDLR) proteins. cDNAs had not yet been fully characterized; we cloned A-susceptible chickens, line H6 0. Two types were obtained. encode longer shorter form quail. different defects ASLV(A)-resistant inbred C 72. Line tvar single base pair substitution, resulting cysteine-to-tryptophan change LDLR-like Tva. This mutation drastically reduces affinity TvaR envelope glycoproteins. 72 tvar2 4-bp insertion exon 1 causes reading frame, which blocks expression receptor.