Public Health Relevance

HIV-1 is the causative agent of acquired immune deficiency syndrome [AIDS];however emerging evidence implicates HIV-1 in a broader illness that includes systemic immune system activation. This study will determine the mechanism of HIV-1-induced macrophage activation while also developing novel approaches to suppress harmful inflammation. The findings of this study will directly impact human health by bringing about changes to current HIV-1 therapy regimens to include drugs that treat inflammation while still striving to suppress HIV-1 replication. The scientific goals of the proposed study support my career goals by providing a basis for long-term funding and a pathway to independence.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Career Transition Award (K22)
Project #
1K22AI095015-01A1
Application #
8210482
Study Section
Acquired Immunodeficiency Syndrome Research Review Committee (AIDS)
Program Officer
Petrakova, Eva
Project Start
2012-05-01
Project End
2014-04-30
Budget Start
2012-05-01
Budget End
2013-04-30
Support Year
1
Fiscal Year
2012
Total Cost
$162,000
Indirect Cost
$12,000
Name
University of Florida
Department
Pathology
Type
Schools of Medicine
DUNS #
969663814
City
Gainesville
State
FL
Country
United States
Zip Code
32611
Appelberg, K Sofia; Wallet, Mark A; Taylor, Jared P et al. (2017) HIV-1 Infection Primes Macrophages Through STAT Signaling to Promote Enhanced Inflammation and Viral Replication. AIDS Res Hum Retroviruses 33:690-702
Wallet, Mark A; Buford, Thomas W; Joseph, Anna-Maria et al. (2015) Increased inflammation but similar physical composition and function in older-aged, HIV-1 infected subjects. BMC Immunol 16:43
Wallet, Mark A; Reist, Caroline M; Williams, Julie C et al. (2012) The HIV-1 protease inhibitor nelfinavir activates PP2 and inhibits MAPK signaling in macrophages: a pathway to reduce inflammation. J Leukoc Biol 92:795-805