Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
agricultural and biological sciences
Association of TRIM22 with the type 1 interferon response and viral control during primary HIV-1 infection
Journal of Virology, Volume 85, No. 1, Year 2011
Notification
URL copied to clipboard!
Description
Type 1 interferons (IFNs) induce the expression of the tripartite interaction motif (TRIM) family of E3 ligases, but the contribution of these antiviral factors to HIV pathogenesis is not completely understood. We hypothesized that the increased expression of select type 1 IFN and TRIM isoforms is associated with a significantly lower likelihood of HIV-1 acquisition and viral control during primary HIV-1 infection. We measured IFN-α, IFN-β, myxovirus resistance protein A (MxA), human TRIM5α (huTRIM5α), and TRIM22 mRNA levels in peripheral blood mononuclear cells (PBMCs) of high-risk, HIV-1-uninfected participants and HIV-1-positive study participants. Samples were available for 32 uninfected subjects and 28 infected persons, all within 1 year of infection. HIV-1-positive participants had higher levels of IFN-β (P = 0.0005), MxA (P = 0.007), and TRIM22 (P = 0.01) and lower levels of huTRIM5α (P < 0.001) than did HIV-1-negative participants. TRIM22 but not huTRIM5α correlated positively with type 1 IFN (IFN-α, IFN-β, and MxA) (all P < 0.0001). In a multivariate model, increased MxA expression showed a significant positive association with viral load (P = 0.0418). Furthermore, TRIM22 but not huTRIM5α, IFN-α, IFN-α, or MxA showed a negative correlation with plasma viral load (P = 0.0307) and a positive correlation with CD4 + T-cell counts (P = 0.0281). In vitro studies revealed that HIV infection induced TRIM22 expression in PBMCs obtained from HIV-negative donors. Stable TRIM22 knockdown resulted in increased HIV-1 particle release and replication in Jurkat reporter cells. Collectively, these data suggest concordance between type 1 IFN and TRIM22 but not huTRIM5α expression in PBMCs and that TRIM22 likely acts as an antiviral effector in vivo. Copyright © 2011, American Society for Microbiology. All Rights Reserved.
Authors & Co-Authors
Singh, Ravesh
South Africa, Durban
The Nelson R. Mandela Medical School
Gaiha, Gaurav Das
United States, Cambridge
Harvard University
Werner, Lise
South Africa, Congella
Centre for the Aids Programme of Research in South Africa
McKim, Kevin
United States, Cambridge
Harvard University
Mlisana, Koleka P.
South Africa, Congella
Centre for the Aids Programme of Research in South Africa
Luban, Jeremy
Switzerland, Geneva
Université de Genève
Walker, Bruce D.
South Africa, Durban
The Nelson R. Mandela Medical School
United States, Cambridge
Harvard University
United States, Chevy Chase
Howard Hughes Medical Institute
Abdool Karim, Salim S.
South Africa, Congella
Centre for the Aids Programme of Research in South Africa
Brass, Abraham L.
United States, Cambridge
Harvard University
Ndung'u, Thumbi P.
South Africa, Durban
The Nelson R. Mandela Medical School
United States, Cambridge
Harvard University
South Africa, Congella
Centre for the Aids Programme of Research in South Africa
Williamson, Carolyn
Unknown Affiliation
Morris, Lynn
Unknown Affiliation
Gray, Clive M.
Unknown Affiliation
Hide, Winston A.
Unknown Affiliation
van Loggerenberg, Francois
Unknown Affiliation
Statistics
Citations: 76
Authors: 15
Affiliations: 5
Identifiers
Doi:
10.1128/JVI.01810-10
ISSN:
0022538X
e-ISSN:
10985514
Research Areas
Infectious Diseases