TRIM5α degradation via autophagy is not required for retroviral restriction.
Maywood, United States. In J Virol, Feb 2016
Collectively, these results are consistent with observations that the turnover of TRIM5α proteins is sensitive to autophagy inhibition; however the data presented here do not support observations that the inhibition of autophagy abrogates retroviral restriction by TRIM5 proteins.
An overview of the lagomorph immune system and its genetic diversity.
Porto, Portugal. In Immunogenetics, Oct 2015
Regarding innate immunity, we review the most recent advances in identifying interleukins, chemokines and chemokine receptors, Toll-like receptors, antiviral proteins (RIG-I and Trim5), and the genes encoding fucosyltransferases that are utilized by rabbit hemorrhagic disease virus as a portal for invading host respiratory and gut epithelial cells.
Impact of TRIM5α in vivo.
Ōsaka, Japan. In Aids, Oct 2015
Genetic manipulation of the human TRIM5 gene could establish human cells totally resistant to HIV-1, which may lead to a cure for HIV-1 infection in the future.
HIV suppression by host restriction factors and viral immune evasion.
New Haven, United States. In Curr Opin Struct Biol, Apr 2015
Here we review the recent developments towards establishing the structural and biochemical bases of HIV inhibition by, and viral countermeasures of, the restriction factors TRIM5, MxB, APOBEC3, SAMHD1, and BST2/tetherin.
Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection.
London, United Kingdom. In Nature, 2013
For the pathogenic retrovirus human immunodeficiency virus type 1 (HIV-1), these include widely expressed restriction factors, such as APOBEC3 proteins, TRIM5-α, BST2 (refs 4, 5) and SAMHD1 (refs 6, 7), as well as additional factors that are stimulated by type 1 interferon (IFN).
TRIM5 structure, HIV-1 capsid recognition, and innate immune signaling.
Zürich, Switzerland. In Curr Opin Virol, 2012
TRIM5 is a restriction factor that blocks retrovirus infection soon after the virion core enters the cell cytoplasm. Restriction activity is targeted to the virion core via recognition of the capsid protein lattice that encases the viral genomic RNA.[Review]
TRIM5 acts as more than a retroviral restriction factor.
Columbus, United States. In Viruses, 2011
Findings have defined a novel function for TRIM5 as a pattern recognition receptor in innate immune recognition and provided valuable mechanistic insight into its role as a retroviral restriction factor.
TRIM5 is an innate immune sensor for the retrovirus capsid lattice.
Genève, Switzerland. In Nature, 2011
the retroviral restriction factor TRIM5 has two additional activities that are linked to restriction: it constitutively promotes innate immune signalling and it acts as a pattern recognition receptor specific for the retrovirus capsid lattice