HIV-1 Integrase INI1/hSNF5 Interaction Required for HIV-1
Jesse Creel
2222-2231, Vol. 78, No. 5 )
article, but if my understanding from the abstract is correct, the HIV-1
Integrase INI1/hSNF5 binding/interaction site must be highly conserved
and required for HIV-1 replication, and as such should make an excellent
candidate epitope/antigenic determinant for use in an HIV-1 Vaccine.
Further study of this and other host cell of replication budding
acquired molecules (BAMs) is surely important for HIV-1 Vaccine, notably
CypA (BAMs) come to mind.
Thanks
Jesse Creel
Vaccine Research Advocate
++++++++++++++++++++++++++++++++++++++++=
Journal of Virology, March 2004, p. 2222-2231, Vol. 78, No. 5
Specificity of Interaction of INI1/hSNF5 with Retroviral Integrases and
Its Functional Significance
Eric Yung,1, Masha Sorin,1, Emilie-Jeanne Wang,1 Seena Perumal,1 David
Ott,2 and Ganjam V. Kalpana1*
Department of Molecular Genetics, Albert Einstein College of Medicine,
New York, New York 10461,1 AIDS Vaccine Program, SAIC-Frederick Inc.,
National Cancer Institute at Frederick, Maryland 217022
Received 31 July 2003/ Accepted 8 November 2003
Integrase interactor 1 (INI1)/hSNF5 is a host factor that directly
interacts with human immunodeficiency virus type 1 (HIV-1) integrase and
is incorporated into HIV-1 virions. Here, we show that while INI1/hSNF5
is completely absent from purified microvesicular fractions, it is
specifically incorporated into HIV-1 virions with an
integrase-to-INI1/hSNF5 stoichiometry of approximately 2:1 (molar
ratio). In addition, we show that INI1/hSNF5 is not incorporated into
related primate lentiviral and murine retroviral particles despite the
abundance of the protein in producer cells. We have found that the
specificity in incorporation of INI1/hSNF5 into HIV-1 virions is
directly correlated with its ability to exclusively interact with HIV-1
integrase but not with other retroviral integrases. This specificity is
also reflected in our finding that the transdominant mutant S6,
harboring the minimal integrase interaction domain of INI1/hSNF5, blocks
HIV-1 particle production but not that of the other retroviruses in 293T
cells. Taken together, these results suggest that INI1/hNSF5 is a host
factor restricted for HIV-1 and that S6 acts as a highly specific and
potent inhibitor of HIV-1 replication.
* Corresponding author. Mailing address: Department of Molecular
Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave.,
Ullman 821, Bronx, NY 10461. Phone: (718) 430-2354. Fax: (718) 430-8778.
E-mail: kal...@aecom.yu.edu.
JVI -- Abstracts: Yung et al. 78 (5): 2222
Address:http://jvi.asm.org/cgi/content/abstract/78/5/2222?etoc
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