Influence of long terminal repeat and env on the virulence phenotype of equine infectious anemia virus.
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abstract
The molecular clones pSPeiav19 and p19/wenv17 of equine infectious anemia virus (EIAV) differ in env and long terminal repeats (LTRs) and produce viruses (EIAV(19) and EIAV(17), respectively) of dramatically different virulence phenotypes. These constructs were used to generate a series of chimeric clones to test the individual contributions of LTR, surface (SU), and transmembrane (TM)/Rev regions to the disease potential of the highly virulent EIAV(17). The LTRs of EIAV(19) and EIAV(17) differ by 16 nucleotides in the transcriptional enhancer region. The two viruses differ by 30 amino acids in SU, by 17 amino acids in TM, and by 8 amino acids in Rev. Results from in vivo infections with chimeric clones indicate that both LTR and env of EIAV(17) are required for the development of severe acute disease. In the context of the EIAV(17) LTR, SU appears to have a greater impact on virulence than does TM. EIAV(17SU), containing only the TM/Rev region from the avirulent parent, induced acute disease in two animals, while a similar infectious dose of EIAV(17TM) (which derives SU from the avirulent parent) did not. Neither EIAV(17SU) nor EIAV(17TM) produced lethal disease when administered at infectious doses that were 6- to 30-fold higher than a lethal dose of the parental EIAV(17). All chimeric clones replicated in primary equine monocyte-derived macrophages, and there was no apparent correlation between macrophage tropism and virulence phenotype.
