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Grant: Operating Grant

University of Saskatchewan

$580,750.00

The virus infectivity factor (Vif) of HIV-1: mechanisms of inhibiting APOBEC3 immune factors

FY 2013-14

Summary
The Human Immunodeficiency Virus-1 (HIV-1) causes the disease of Acquired Immunodeficiency Syndrome (AIDS). There are currently estimated to be 35 million people world-wide living with HIV/AIDS. When HIV-1 infects a person there are many barriers that that virus must overcome to establish a long term infection that results in AIDS. However, HIV-1 can overcome these barriers in most people because it produces many different proteins that specifically inhibit the function of proteins in the human immune system. We study a specific interaction between the HIV-1 protein called Vif and the APOBEC3 family of human immune system proteins. The HIV-1 Vif protein causes APOBEC3 proteins to become unstable in cells so that they cannot do their job. In the absence of Vif the APOBEC3 proteins are able to restrict the replication of HIV-1 by mutating its genetic information so that the virus can no longer produce the proteins that it needs to function. If we understand how Vif interacts with APOBEC3 proteins we can identify new avenues of blocking the virus and releasing the natural anti-HIV activity of our immune system. This research proposes experiments to help us better understand the relationship of Vif and APOBEC3 proteins with an ultimate goal of uncovering new strategies for HIV-1 therapies.
Program
Operating Grant
Location
Saskatchewan, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
305325
Name
Chelico Linda
Region
Saskatchewan
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Virology & Viral Pathogenesis
Projecttitle
The virus infectivity factor (Vif) of HIV-1: mechanisms of inhibiting APOBEC3 immune factors
Programtype2
Operating Grants
Orgnameinp2
University of Saskatchewan
Cihramount2
$580,750
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Apobec3; Deoxycytidine Deaminases; Hiv-1; Host-Pathogen Interface; Mutagenesis; Nucleic Acid-Protein Interactions; Protein-Protein Interactions; Restriction Factor; Reverse Transcription; Ubiquitination
Abstract
The Human Immunodeficiency Virus-1 (HIV-1) causes the disease of Acquired Immunodeficiency Syndrome (AIDS). There are currently estimated to be 35 million people world-wide living with HIV/AIDS. When HIV-1 infects a person there are many barriers that that virus must overcome to establish a long term infection that results in AIDS. However, HIV-1 can overcome these barriers in most people because it produces many different proteins that specifically inhibit the function of proteins in the human immune system. We study a specific interaction between the HIV-1 protein called Vif and the APOBEC3 family of human immune system proteins. The HIV-1 Vif protein causes APOBEC3 proteins to become unstable in cells so that they cannot do their job. In the absence of Vif the APOBEC3 proteins are able to restrict the replication of HIV-1 by mutating its genetic information so that the virus can no longer produce the proteins that it needs to function. If we understand how Vif interacts with APOBEC3 proteins we can identify new avenues of blocking the virus and releasing the natural anti-HIV activity of our immune system. This research proposes experiments to help us better understand the relationship of Vif and APOBEC3 proteins with an ultimate goal of uncovering new strategies for HIV-1 therapies.
Competitiondate
201403
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Chelico, Linda
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $580,750~ $0~