Previous Article | Next Article ![]()
Journal of Virology, August 2001, p. 7193-7197, Vol. 75, No. 15
Departments of Microbiology and Medicine,
College of Physicians and Surgeons, Columbia Univeirsity, New York,
New York, 10032
Received 31 October 2000/Accepted 3 May 2001
The human immunodeficiency virus type 1 (HIV-1) nucleocapsid
mutation R10A/K11A abolishes viral replication when present in proviral
clone HIV-1HXB-2, but it was found to have minimal effect on replication of the closely related HIV-1NL4-3.
Functional mapping demonstrated that a nonconservative amino acid
change at nucleocapsid residue 24 (threonine in HIV-1HXB-2,
isoleucine in HIV-1NL4-3) is the major determinant of the
different R10A/K11A phenotypes in these two proviruses.
Threonine-isoleucine exchanges appear to modify the R10A/K11A phenotype
via effects on virion RNA-packaging efficiency. The improved packaging
seen with hydrophobic isoleucine is consistent with solution structures
localizing this residue to a hydrophobic pocket that contacts guanosine
bases in viral genomic RNA stem-loops critical for packaging.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.15.7193-7197.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Context-Dependent Phenotype of a Human
Immunodeficiency Virus Type 1 Nucleocapsid Mutation
and
*
Corresponding author. Mailing address: Departments of
Microbiology and Medicine, Columbia University, College of Physicians and Surgeons, 701 W. 168th St., New York, NY 10032. Phone: (212) 305-8706. Fax: (212) 305-0333. E-mail: JL45{at}columbia.edu.
Present address: Ecole Normale Supérieure de Lyon, 69364 Lyon, France.
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
|---|
| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
|---|