Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
MOLECULAR CHARACTERIZATION OF FV-2(RR)-ADAPTED VARIANTS OF FRIEND SPLEEN FOCUS-FORMING VIRUS
Diss Abstr Int [B]; 52(2):647 1991. Unique Identifier : AIDSLINE ICDB/92677947 Majumdar MK; Indiana State Univ.
Abstract:
Friend spleen focus-forming virus (F-SFFV) of the Friend erythroleukemia virus complex induces a rapid erythroleukemia in susceptible strains of mice. The env gene of F-SFFV encodes the oncoprotein gp52 that is responsible for inducing the erythroid precursor cells to proliferate. Susceptibility of mice to F-SFFV is controlled by the Fv-2 gene. Mice homozygous for the Fv-2r allele (eg, C57BL/6) are resistant to gp52-induced proliferative disease. To understand the mechanism of Fv-2-mediated resistance in mice, the env genes of two Fv-2rr-adapted variants of F-SFFV, BB6 and RBV, were characterized. The envelope protein of BB6 and RBV have apparent Mr of 42,000 (gp42) and 52,000 (gp52), respectively. The env genes of these variants were amplified by PCR, cloned, and sequenced. When the nucleotide sequences of these variants were compared with different strains of wild-type F-SFFV, BB6 and RBV were found to have 159-bp and 15-bp deletions, respectively. The deletions encompass part of the hydrophobic domain (membrane-spanning) of the ecotropic region of the envelope protein. In addition, BB6 and RBV have 12 and 9 amino acid substitutions, respectively, some of which are in the highly conserved region (amino acids 92 to 158) believed to be important to the induction of the erythroproliferative disease. Presumably, these changes in the envelope protein of BB6 and RBV are responsible for the ability of these variants to overcome the Fv-2rr resistance in mice. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD91-20984).
Keywords: Amino Acid Sequence Animal Base Sequence Friend Virus/*GENETICS *Genes, env Leukemia, Erythroblastic, Acute/*ETIOLOGY/GENETICS Mice Spleen Focus-Forming Viruses/*GENETICS Viral Envelope Proteins/ANALYSIS THESIS
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