Restriction factors of retroviral replication: the example of Tripartite Motif (TRIM) protein 5α and 22

Amino Acids ◽  
2009 ◽  
Vol 39 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Anna Kajaste-Rudnitski ◽  
Cinzia Pultrone ◽  
Flavia Marzetta ◽  
Silvia Ghezzi ◽  
Tiziana Coradin ◽  
...  
Keyword(s):  
Restriction Factors ◽  
Trim Protein ◽  
Tripartite Motif ◽  
Retroviral Replication

Characterization of porcine tripartite motif genes as host restriction factors against PRRSV and PEDV infection

2019 ◽  
Vol 270 ◽  
pp. 197647 ◽  
Author(s):  
Ying Wei ◽  
Chuangchao Zou ◽  
Siying Zeng ◽  
Chunyi Xue ◽  
Yongchang Cao
Keyword(s):  
Restriction Factors ◽  
Host Restriction ◽  
Host Restriction Factors ◽  
Tripartite Motif

scholarly journals Restriction factors in human retrovirus infections and the unprecedented case of CIITA as link of intrinsic and adaptive immunity against HTLV-1

Retrovirology ◽  
2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Greta Forlani ◽  
Mariam Shallak ◽  
Elise Ramia ◽  
Alessandra Tedeschi ◽  
Roberto S. Accolla
Keyword(s):  
Adaptive Immunity ◽  
Mhc Class Ii ◽  
Molecular Mechanisms ◽  
Dual Function ◽  
Main Body ◽  
Virus Infections ◽  
Restriction Factors ◽  
Intrinsic Immunity ◽  
Retroviral Replication ◽  
Mhc Class Ii Transactivator

Abstract Background Immunity against pathogens evolved through complex mechanisms that only for sake of simplicity are defined as innate immunity and adaptive immunity. Indeed innate and adaptive immunity are strongly intertwined each other during evolution. The complexity is further increased by intrinsic mechanisms of immunity that rely on the action of intracellular molecules defined as restriction factors (RFs) that, particularly in virus infections, counteract the action of pathogen gene products acting at different steps of virus life cycle. Main body and conclusion Here we provide an overview on the nature and the mode of action of restriction factors involved in retrovirus infection, particularly Human T Leukemia/Lymphoma Virus 1 (HTLV-1) infection. As it has been extensively studied by our group, special emphasis is given to the involvement of the MHC class II transactivator CIITA discovered in our laboratory as regulator of adaptive immunity and subsequently as restriction factor against HIV-1 and HTLV-1, a unique example of dual function linking adaptive and intrinsic immunity during evolution. We describe the multiple molecular mechanisms through which CIITA exerts its restriction on retroviruses. Of relevance, we review the unprecedented findings pointing to a concerted action of several restriction factors such as CIITA, TRIM22 and TRIM19/PML in synergizing against retroviral replication. Finally, as CIITA profoundly affects HTLV-1 replication by interacting and inhibiting the function of HTLV-1 Tax-1 molecule, the major viral product associated to the virus oncogenicity, we also put forward the hypothesis of CIITA as counteractor of HTLV-1-mediated cancer initiation.

scholarly journals Structural basis for PRYSPRY-mediated tripartite motif (TRIM) protein function

2007 ◽  
Vol 104 (15) ◽  
pp. 6200-6205 ◽  
Author(s):  
L. C. James ◽  
A. H. Keeble ◽  
Z. Khan ◽  
D. A. Rhodes ◽  
J. Trowsdale
Keyword(s):  
Protein Function ◽  
Structural Basis ◽  
Trim Protein ◽  
Tripartite Motif

scholarly journals Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations

2020 ◽  
Vol 8 (12) ◽  
pp. 1965
Author(s):  
Guney Boso ◽  
Christine A. Kozak
Keyword(s):  
Adaptive Evolution ◽  
Restriction Factors ◽  
Complex Interactions ◽  
Evolutionary Conflict ◽  
Accelerated Evolution ◽  
Multiple Virus ◽  
Vertebrate Hosts ◽  
Cellular Pathways ◽  
Retroviral Replication ◽  
Viral Antagonists

The evolutionary conflict between retroviruses and their vertebrate hosts over millions of years has led to the emergence of cellular innate immune proteins termed restriction factors as well as their viral antagonists. Evidence accumulated in the last two decades has substantially increased our understanding of the elaborate mechanisms utilized by these restriction factors to inhibit retroviral replication, mechanisms that either directly block viral proteins or interfere with the cellular pathways hijacked by the viruses. Analyses of these complex interactions describe patterns of accelerated evolution for these restriction factors as well as the acquisition and evolution of their virus-encoded antagonists. Evidence is also mounting that many restriction factors identified for their inhibition of specific retroviruses have broader antiviral activity against additional retroviruses as well as against other viruses, and that exposure to these multiple virus challenges has shaped their adaptive evolution. In this review, we provide an overview of the restriction factors that interfere with different steps of the retroviral life cycle, describing their mechanisms of action, adaptive evolution, viral targets and the viral antagonists that evolved to counter these factors.

Lack of endogenous TRIM5α-mediated restriction in rhesus macaque dendritic cells

Blood ◽  
2008 ◽  
Vol 112 (9) ◽  
pp. 3772-3776 ◽  
Author(s):  
Nathalie J. Arhel ◽  
Sébastien Nisole ◽  
Laetitia Carthagena ◽  
Frédéric Coutant ◽  
Philippe Souque ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Rhesus Macaque ◽  
Rhesus Macaques ◽  
Cell Types ◽  
Primary Cells ◽  
Adaptive Immune ◽  
Trim Protein ◽  
Tripartite Motif ◽  
Hiv 1

Rhesus macaques are resistant to infection by HIV-1 as a result of an innate cellular restriction mechanism attributable to the expression of rhTRIM5α, a member of the large tripartite motif (TRIM) protein family. TRIM5α-mediated restriction, which occurs before reverse transcription through targeting of the HIV-1 capsid, has been identified in a number of macaque primary cells and cell lines and is thought to occur in all macaque cell types. We report, however, that rhesus macaque dendritic cells (DCs) lack TRIM5α-mediated restriction and are equally permissive to HIV-1 infection as human DCs. Evidence suggests that, although TRIM5α RNA levels are normal in these cells, the protein may be dysfunctional. We propose that abrogation of TRIM5α-mediated restriction in DCs, although still operative in cells that replicate HIV-1 (macrophages, T lymphocytes), illustrates the need for innate mechanisms to not inhibit adaptive immune responses to ensure an optimal fight against pathogens.

scholarly journals Correlated cryogenic fluorescence microscopy and electron cryo-tomography shows that exogenous TRIM5α can form hexagonal lattices or autophagy aggregates in vivo

2020 ◽  
Vol 117 (47) ◽  
pp. 29702-29711
Author(s):  
Stephen D. Carter ◽  
João I. Mamede ◽  
Thomas J. Hope ◽  
Grant J. Jensen
Keyword(s):  
Mammalian Cells ◽  
Light And Electron Microscopy ◽  
Protein Family ◽  
Native State ◽  
Cytoplasmic Bodies ◽  
Trim Protein ◽  
Tripartite Motif ◽  
Hiv 1

Members of the tripartite motif (TRIM) protein family have been shown to assemble into structures in both the nucleus and cytoplasm. One TRIM protein family member, TRIM5α, has been shown to form cytoplasmic bodies involved in restricting retroviruses such as HIV-1. Here we applied cryogenic correlated light and electron microscopy, combined with electron cryo-tomography, to intact mammalian cells expressing YFP-rhTRIM5α and found the presence of hexagonal nets whose arm lengths were similar to those of the hexagonal nets formed by purified TRIM5α in vitro. We also observed YFP-rhTRIM5α within a diversity of structures with characteristics expected for organelles involved in different stages of macroautophagy, including disorganized protein aggregations (sequestosomes), sequestosomes flanked by flat double-membraned vesicles (sequestosome:phagophore complexes), sequestosomes within double-membraned vesicles (autophagosomes), and sequestosomes within multivesicular autophagic vacuoles (amphisomes or autolysosomes). Vaults were also seen in these structures, consistent with their role in autophagy. Our data 1) support recent reports that TRIM5α can form both well-organized signaling complexes and nonsignaling aggregates, 2) offer images of the macroautophagy pathway in a near-native state, and 3) reveal that vaults arrive early in macroautophagy.

scholarly journals Isolation of an Active Lv1 Gene from Cattle Indicates that Tripartite Motif Protein-Mediated Innate Immunity to Retroviral Infection Is Widespread among Mammals

2006 ◽  
Vol 80 (15) ◽  
pp. 7332-7338 ◽  
Author(s):  
Laura M. J. Ylinen ◽  
Zuzana Keckesova ◽  
Benjamin L. J. Webb ◽  
Robert J. M. Gifford ◽  
Timothy P. L. Smith ◽  
...  
Keyword(s):  
World Monkey ◽  
Leukemia Virus ◽  
Retroviral Infection ◽  
Trim Protein ◽  
Immunodeficiency Virus ◽  
Tripartite Motif ◽  
Bovine Sequence ◽  
Species Specific ◽  
Hiv 1

ABSTRACT Lv1/TRIM5α (tripartite motif 5α) has recently emerged as an important factor influencing species-specific permissivity to retroviral infection in a range of primates, including humans. Old World monkey TRIM5α blocks human immunodeficiency virus type 1 (HIV-1) infectivity, and the human and New World monkey TRIM5α proteins are inactive against HIV-1 but active against divergent murine (N-tropic murine leukemia virus [MLV-N]) and simian (simian immunodeficiency virus from rhesus macaque [SIVmac]) retroviruses, respectively. Here we demonstrate antiviral activity of the first nonprimate TRIM protein, from cattle, active against divergent retroviruses, including HIV-1. The number of closely related human TRIM sequences makes assignment of the bovine sequence as a TRIM5α ortholog uncertain, and we therefore refer to it as bovine Lv1. Bovine Lv1 is closely related to primate TRIM5α proteins in the N-terminal RING and B-box 2 domains but significantly less homologous in the C-terminal B30.2 domain, particularly in the region shown to influence antiviral specificity. Intriguingly, some viruses restricted by bovine Lv1, including HIV-1 and MLV-N, are unable to synthesize viral DNA by reverse transcription, whereas restricted HIV-2 makes normal amounts of DNA. The data support the conclusion that TRIM protein-mediated restriction of retroviral infection is a more common attribute of mammals than previously appreciated.

Sign in / Sign up

Export Citation Format

Share Document