Nucleotide Sequence of the Envelope Gene of Gardner-Arnstein Feline Leukemia Virus B Reveals Unique Sequence Homologies with a Murine Mink Cell Focus-Forming Virus

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Abstract
The nucleotide sequence of the envelope gene and the adjacent 3'' long terminal repeat (LTR) of Gardner-Arnstein feline leukemia virus of subgroup B (GA-FeLV-B) was determined. Comparison of the derived amino acid sequence of the gp70-p15E polyprotein to those of several previously reported murine retroviruses revealed striking homologies between GA-FeLV-B gp70 and the gp70 of a Moloney virus-derived mink cell focus-forming virus. These homologies were located within the substituted (presumably xenotropic) portion of the mink cell focus-forming virus envelope gene and comprised amino acid sequences not present in 3 ecotropic virus gp70s. Areas of insertions and deletions, in general, were the same between GA-FeLV-B and Moloney mink cell focus-forming virus, although the sizes of the insertions and deletions differed. Homologies between GA-FeLV-B and mink cell focus-forming virus gp70 is functionally significant in that they both possess expanded host ranges, a property dictated by gp70. The amino acid sequence of FeLV-B contains 12 Asn-X-Ser/Thr sequences, indicating 12 possible sites of N-linked glycosylation as compared with 7 or 8 for its murine counterparts. Comparison of the 3 LTR or GA-FeLV-B to AKR and Moloney virus LTR revealed extensive conversation in several regions including the CCAAT and Goldberg-Hogness (TATA) boxes thought to be involved in promotion of transcription and in the repeat region of the LTR. The inverted repeats that flanked the LTR of GA-FeLV-B were identical to the murine inverted repeats, but were 1 base longer than the latter. The region of U3 corresponding to the .apprx. 75-nucleotide enhancer sequence is present in GA-FeLV-B, but contains deletions relative to AKR and Moloney virus and is not repeated. An interesting palindrome in the repeat region immediately 3'' to the U3 region was noted in all the LTR, but was particularly pronounced in GA-FeLV-B. Possible roles for this structure are discussed.