Cloned human interferon complementary DNAs were used as hybridization probes to detect interferon alpha and beta gene families in restriction endonuclease digests of total genomic DNA isolated from a wide range of vertebrates and invertebrates. A complex interferon-alpha multigene family was detected in all mammals examined, whereas there was little or no cross-hybridization of human interferon-alpha complementary DNA to non-mammalian vertebrates or invertebrates. In contrast, human interferon-beta complementary DNA detected one or two interferon-beta genes in all mammals tested, with the exception of the cow and the blackbuck, both of which possessed a complex interferon-beta multigene family which has presumably arisen by a recent series of gene duplications. Interferon-beta sequences could also be detected in non-mammalian vertebrates ranging from birds to bony fish. Detailed restriction endonuclease mapping of DNA sequences neighbouring the interferon-beta gene in a variety of primates indicated a strong evolutionary conservation of flanking sequences, particularly on the 3' side of the gene.

A provisional sequence was determined by the plus and minus method (Sanger et al. 1977).1 It has now been completed using the termination method of Sanger et al. (1977).2 About 30 alterations have been made and therefore the numbering is somewhat different from that used in the provisional sequence. The DNA sequence given is that of the circular viral (plus) strand. Numbering is from the unique Pst site, but the sequence is written starting at the first nucleotide after the termination of the gene- H protein. The letters in the left-hand margin indicate the proteins whose sequence is given on the corresponding line. Restriction enzyme recognition sites are indicated by underlining. The single-letter code for the restriction enzymes is as follows: A, Alu I; F, Hin fI; H, Hha I; M, Mbo II; P, Pst I; Q, Hph I; R, Hin dII; T, Taq I; Y, Hap II; Z, Hae III. The position of the origin of viral-strand replication is based on the work of Langeveld et al. (1977).3 Other references are given in our earlier paper (Sanger et al. 1977)1 and elsewhere in this volume. The cs 70 mutation is cold sensitive and is believed to be a point mutation in the gene- F protein (C. A. Hutchison III, pers. comm.).