LEPTOMYCIN-B INHIBITS EQUINE INFECTIOUS-ANEMIA VIRUS REV AND FELINE IMMUNODEFICIENCY VIRUS REV FUNCTION BUT NOT THE FUNCTION OF THE HEPATITIS-B VIRUS POSTTRANSCRIPTIONAL REGULATORY ELEMENT

Citation
Gc. Otero et al., LEPTOMYCIN-B INHIBITS EQUINE INFECTIOUS-ANEMIA VIRUS REV AND FELINE IMMUNODEFICIENCY VIRUS REV FUNCTION BUT NOT THE FUNCTION OF THE HEPATITIS-B VIRUS POSTTRANSCRIPTIONAL REGULATORY ELEMENT, Journal of virology, 72(9), 1998, pp. 7593-7597
Citations number
42
Categorie Soggetti
Virology
Journal title
ISSN journal
0022538X
Volume
72
Issue
9
Year of publication
1998
Pages
7593 - 7597
Database
ISI
SICI code
0022-538X(1998)72:9<7593:LIEIVR>2.0.ZU;2-H
Abstract
Human immunodeficiency virus type 1 Rev export depends upon the presen ce of the nuclear export signal (NES), a leucine-rich stretch of hydro phobic amino acids. Recently, the nuclear NES-binding receptor has bee n identified as CRM1 or exportin 1. Rev export has been shown to be CR M1 dependent. The function of the atypical NES-containing Rev-like pro teins of equine infectious anemia virus (EIAV) and feline immunodefici ency virus (FN) is inhibited by leptomycin B, a drug that specifically blocks NES-CRM1 interactions. These data suggest that the function of atypical NES-containing proteins is CRM1 dependent. In contrast to th e inhibition of EIAV Rev and FIV Rev, the cytoplasmic accumulation of hepatitis B virus (HBV) posttranscriptional regulatory element (PRE)-c ontaining and Mason-Pfizer monkey virus (MPMV) constitutive transport element (CTE)-containing RNAs is not inhibited by leptomycin B treatme nt. We conclude that the HBV PRE, like the MPMV CTE, functions indepen dently of an NES receptor-exportin 1 interaction.