The catalytic properties of the reverse transcriptase of the lentivirus equine infectious anemia virus

1994 
The reverse transcriptase (RT) of equine infectious anemia virus (EIAV) shares sequence similarity with the RTs of other lentiviruses, particularly with the RTs of human immunodeficiency viruses types 1 and 2 (HIV-1 and HIV-2, respectively), the causative agents of acquired immunodeficiency syndrome (AIDS). There is a 41-42% sequence identity between EIAV RT and both HIV RTs (which have 61% sequence identity to each other). We have compared the enzymic properties of EIAV RT with those of HIV-1 RT. Several aspects of the activities of EIAV RT differ from the corresponding activities of HIV-1 RT. There are significant differences in the inhibition of the DNA polymerase activities by the deoxynucleoside triphosphate analogs, 3’-azido-2,3’-dideoxythymidine triphosphate, dideoxyTTP and dideoxyGTP and by the nonnucleoside inhibitor, tetrahydroimidazo[4,5,1-jk-l,4]benzodiazepin-2-(lH)-one and thione; in the dependence of DNA polymerase and RNase H activities on pH; in the inhibition of the DNA polymerase activities by the thiol-specific reagent N-ethylmaleimide; in the specific DNA polymerase activity; in the inhibition of the ribonuclease H activity by the zinc chelator orthophenanthroline. However, there are several cases in which EIAV RT and HIV-1 RT are more similar than was previously found for HIV-1 RT and HIV2 RT. These include the K,,, values for the DNA polymerase activities, the heat stability of the DNA polymerase functions and the specific activity of the RNase H function. Equine infectious anemia virus (EIAV) belongs to the lentivirus subfamily of retroviruses. This group of viruses also includes human immunodeficiency virus types-1 and 2 (HIV-1 and HIV-2, respectively), simian, bovine and feline immunodeficiency viruses, the maedi-visna virus of sheep and caprine arthritis encephalitis virus. All viruses in this subfamily share common structural, genetic and biological features, including high mutation rates, replication in cells of the immune system and, in many cases, a long incubation period that precedes the onset of the disease (Montagnier et al., 1984; Narayan et al., 1990; Montelaro et al., 1991; Stephens et al., 1986; Cullen, 1992).
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