Equine Infectious Anemia Virus (EIAV) gag gene evolution in vivo

Abstract

ELR1 cDNA sequence, which resulted in a premature stop signal 813 codons downstream. This translational termination was predicted truncating the receptor at the C-terminus of the transmembrane domain. The other species (ELR1-DE) had a deletion of 109 nt and caused a shift of the open reading frame and an appearance of a stop codon 312 nt downstream. Because ELR1-DE presumably encoded a peptide of mere 23 residues, only ELR1-IN was further analyzed for potential functions on EIAV infection of target cells. Firstly, the expression of the soluble form ELR1 (sELR1) by ELR1-IN was confirmed by Western-blot and immunofluorescence analysis. Like ELR1, the transcription level of ELR1-IN varied in different individuals of horse and at different time points in same individuals. The radio of ELR1-IN mRNA species to that of ELR1 was approximate 1:2. However, the expressions of both forms of the receptor were significantly regulated by the infection of EIAV. Additionally, pre-incubation of the recombinant sELR1 with EIAV significantly inhibited the infection of EIAV on equine macrophages, which is the primary in vivo target cell of the virus. Fetal horse dermal (FHD) cells are susceptible to EIAV in vitro. The replication of EIAV in FHD cells transiently transfected with ELR1-IN was markedly reduced when compared with the replication in cells transfected with the empty vector. Taken together, our data implicate that sELR1 is an important cellular factor that inhibits the infection of EIAV on host cells.