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Viruses, Volume 3, Issue 7 (July 2011), Pages 941-1311

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Research

Jump to: Review, Other

Open AccessCommunication Herpesviruses and Intermediate Filaments: Close Encounters with the Third Type
Viruses 2011, 3(7), 1015-1040; doi:10.3390/v3071015
Received: 2 February 2011 / Revised: 7 June 2011 / Accepted: 24 June 2011 / Published: 4 July 2011
Cited by 6 | PDF Full-text (464 KB)
Abstract
Intermediate filaments (IF) are essential to maintain cellular and nuclear integrity and shape, to manage organelle distribution and motility, to control the trafficking and pH of intracellular vesicles, to prevent stress-induced cell death, and to support the correct distribution of specific proteins. [...] Read more.
Intermediate filaments (IF) are essential to maintain cellular and nuclear integrity and shape, to manage organelle distribution and motility, to control the trafficking and pH of intracellular vesicles, to prevent stress-induced cell death, and to support the correct distribution of specific proteins. Because of this, IF are likely to be targeted by a variety of pathogens, and may act in favor or against infection progress. As many IF functions remain to be identified, however, little is currently known about these interactions. Herpesviruses can infect a wide variety of cell types, and are thus bound to encounter the different types of IF expressed in each tissue. The analysis of these interrelationships can yield precious insights into how IF proteins work, and into how viruses have evolved to exploit these functions. These interactions, either known or potential, will be the focus of this review. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessArticle C7a, a Biphosphinic Cyclopalladated Compound, Efficiently Controls the Development of a Patient-Derived Xenograft Model of Adult T Cell Leukemia/Lymphoma
Viruses 2011, 3(7), 1041-1058; doi:10.3390/v3071041
Received: 17 May 2011 / Revised: 17 June 2011 / Accepted: 17 June 2011 / Published: 5 July 2011
Cited by 7 | PDF Full-text (762 KB)
Abstract
Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive disease that occurs in individuals infected with the human T lymphotropic virus type 1 (HTLV-1). Patients with aggressive ATLL have a poor prognosis because the leukemic cells are resistant to conventional chemotherapy. We have [...] Read more.
Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive disease that occurs in individuals infected with the human T lymphotropic virus type 1 (HTLV-1). Patients with aggressive ATLL have a poor prognosis because the leukemic cells are resistant to conventional chemotherapy. We have investigated the therapeutic efficacy of a biphosphinic cyclopalladated complex {Pd2 [S(−)C2, N-dmpa]2 (μ-dppe)Cl2}, termed C7a, in a patient-derived xenograft model of ATLL, and investigated the mechanism of C7a action in HTLV-1-positive and negative transformed T cell lines in vitro. In vivo survival studies in immunocompromised mice inoculated with human RV-ATL cells and intraperitoneally treated with C7a led to significantly increased survival of the treated mice. We investigated the mechanism of C7a activity in vitro and found that it induced mitochondrial release of cytochrome c, caspase activation, nuclear condensation and DNA degradation. These results suggest that C7a triggers apoptotic cell death in both HTLV-1 infected and uninfected human transformed T-cell lines. Significantly, C7a was not cytotoxic to peripheral blood mononuclear cells (PBMC) from healthy donors and HTLV-1-infected individuals. C7a inhibited more than 60% of the ex vivo spontaneous proliferation of PBMC from HTLV-1-infected individuals. These results support a potential therapeutic role for C7a in both ATLL and HTLV-1-negative T-cell lymphomas. Full article
(This article belongs to the Special Issue Recent Developments in HTLV Research)
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Open AccessArticle Proposed Ancestors of Phage Nucleic Acid Packaging Motors (and Cells)
Viruses 2011, 3(7), 1249-1280; doi:10.3390/v3071249
Received: 4 June 2011 / Revised: 7 July 2011 / Accepted: 12 July 2011 / Published: 20 July 2011
Cited by 6 | PDF Full-text (878 KB)
Abstract
I present a hypothesis that begins with the proposal that abiotic ancestors of phage RNA and DNA packaging systems (and cells) include mobile shells with an internal, molecule-transporting cavity. The foundations of this hypothesis include the conjecture that current nucleic acid packaging [...] Read more.
I present a hypothesis that begins with the proposal that abiotic ancestors of phage RNA and DNA packaging systems (and cells) include mobile shells with an internal, molecule-transporting cavity. The foundations of this hypothesis include the conjecture that current nucleic acid packaging systems have imprints from abiotic ancestors. The abiotic shells (1) initially imbibe and later also bind and transport organic molecules, thereby providing a means for producing molecular interactions that are links in the chain of events that produces ancestors to the first molecules that are both information carrying and enzymatically active, and (2) are subsequently scaffolds on which proteins assemble to form ancestors common to both shells of viral capsids and cell membranes. Emergence of cells occurs via aggregation and merger of shells and internal contents. The hypothesis continues by using proposed imprints of abiotic and biotic ancestors to deduce an ancestral thermal ratchet-based DNA packaging motor that subsequently evolves to integrate a DNA packaging ATPase that provides a power stroke. Full article
(This article belongs to the Special Issue Bacteriophage Assembly)
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Review

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Open AccessReview Alphaherpesviruses and the Cytoskeleton in Neuronal Infections
Viruses 2011, 3(7), 941-981; doi:10.3390/v3070941
Received: 11 May 2011 / Revised: 3 June 2011 / Accepted: 17 June 2011 / Published: 27 June 2011
Cited by 16 | PDF Full-text (644 KB)
Abstract
Following infection of exposed peripheral tissues, neurotropic alphaherpesviruses invade nerve endings and deposit their DNA genomes into the nuclei of neurons resident in ganglia of the peripheral nervous system. The end result of these events is the establishment of a life-long latent [...] Read more.
Following infection of exposed peripheral tissues, neurotropic alphaherpesviruses invade nerve endings and deposit their DNA genomes into the nuclei of neurons resident in ganglia of the peripheral nervous system. The end result of these events is the establishment of a life-long latent infection. Neuroinvasion typically requires efficient viral transmission through a polarized epithelium followed by long-distance transport through the viscous axoplasm. These events are mediated by the recruitment of the cellular microtubule motor proteins to the intracellular viral particle and by alterations to the cytoskeletal architecture. The focus of this review is the interplay between neurotropic herpesviruses and the cytoskeleton. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview Correlates of Immunity to Filovirus Infection
Viruses 2011, 3(7), 982-1000; doi:10.3390/v3070982
Received: 14 April 2011 / Revised: 14 June 2011 / Accepted: 16 June 2011 / Published: 27 June 2011
Cited by 13 | PDF Full-text (173 KB)
Abstract
Filoviruses can cause severe, often fatal hemorrhagic fever in humans. Recent advances in vaccine and therapeutic drug development have provided encouraging data concerning treatment of these infections. However, relatively little is known about immune responses in fatal versus non-fatal filovirus infection. This [...] Read more.
Filoviruses can cause severe, often fatal hemorrhagic fever in humans. Recent advances in vaccine and therapeutic drug development have provided encouraging data concerning treatment of these infections. However, relatively little is known about immune responses in fatal versus non-fatal filovirus infection. This review summarizes the published literature on correlates of immunity to filovirus infection, and highlights deficiencies in our knowledge on this topic. It is likely that there are several types of successful immune responses, depending on the type of filovirus, and the presence and timing of vaccination or drug treatment. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview Anti-Apoptotic Effect of Tax: An NF-κB Path or a CREB Way?
Viruses 2011, 3(7), 1001-1014; doi:10.3390/v3071001
Received: 9 May 2011 / Revised: 9 June 2011 / Accepted: 11 June 2011 / Published: 27 June 2011
Cited by 9 | PDF Full-text (207 KB)
Abstract
The NF-κB pathway is intimately linked to the survival of mammalian cells, and its activation by Tax has consequently been considered important for human T-cell leukemia/lymphoma virus type 1 (HTLV-1)-infected cell resistance to death. Very little emphasis has been given to other [...] Read more.
The NF-κB pathway is intimately linked to the survival of mammalian cells, and its activation by Tax has consequently been considered important for human T-cell leukemia/lymphoma virus type 1 (HTLV-1)-infected cell resistance to death. Very little emphasis has been given to other mechanisms, although Tax regulates the expression and activity of several cellular genes. The finding that CREB protein is activated in HTLV-1 infected cells underlines the possibility that other mechanisms of survival may be implicated in HTLV-1 infection. Indeed, CREB activation or overexpression plays a role in normal hematopoiesis, as well as in leukemia development, and CREB is considered as a survival factor in various cell systems. A better understanding of the different molecular mechanisms used by Tax to counteract cell death will also help in the development of new therapeutic strategies for HTLV-1 associated diseases. Full article
(This article belongs to the Special Issue Recent Developments in HTLV Research)
Open AccessReview T Cells and Pathogenesis of Hantavirus Cardiopulmonary Syndrome and Hemorrhagic Fever with Renal Syndrome
Viruses 2011, 3(7), 1059-1073; doi:10.3390/v3071059
Received: 31 March 2011 / Revised: 30 June 2011 / Accepted: 1 July 2011 / Published: 6 July 2011
Cited by 31 | PDF Full-text (214 KB)
Abstract
We previously hypothesized that increased capillary permeability observed in both hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS) may be caused by hantavirus-specific cytotoxic T cells attacking endothelial cells presenting viral antigens on their surface based on clinical observations [...] Read more.
We previously hypothesized that increased capillary permeability observed in both hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS) may be caused by hantavirus-specific cytotoxic T cells attacking endothelial cells presenting viral antigens on their surface based on clinical observations and in vitro experiments. In HCPS, hantavirus-specific T cell responses positively correlated with disease severity. In HFRS, in one report, contrary to HCPS, T cell responses negatively correlated with disease severity, but in another report the number of regulatory T cells, which are thought to suppress T cell responses, negatively correlated with disease severity. In rat experiments, in which hantavirus causes persistent infection, depletion of regulatory T cells helped infected rats clear virus without inducing immunopathology. These seemingly contradictory findings may suggest delicate balance in T cell responses between protection and immunopathogenesis. Both too strong and too weak T cell responses may lead to severe disease. It is important to clarify the role of T cells in these diseases for better treatment (whether to suppress T cell functions) and protection (vaccine design) which may need to take into account viral factors and the influence of HLA on T cell responses. Full article
(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)
Open AccessReview HTLV-3/STLV-3 and HTLV-4 Viruses: Discovery, Epidemiology, Serology and Molecular Aspects
Viruses 2011, 3(7), 1074-1090; doi:10.3390/v3071074
Received: 11 May 2011 / Revised: 21 June 2011 / Accepted: 6 July 2011 / Published: 8 July 2011
Cited by 24 | PDF Full-text (395 KB)
Abstract
Human T cell leukemia/lymphoma virus Type 1 and 2 (HTLV-1 and HTLV-2), together with their simian counterparts (STLV-1, STLV-2), belong to the Primate T lymphotropic viruses group (PTLV). The high percentage of homologies between HTLV-1 and STLV-1 strains, led to the demonstration [...] Read more.
Human T cell leukemia/lymphoma virus Type 1 and 2 (HTLV-1 and HTLV-2), together with their simian counterparts (STLV-1, STLV-2), belong to the Primate T lymphotropic viruses group (PTLV). The high percentage of homologies between HTLV-1 and STLV-1 strains, led to the demonstration that most HTLV-1 subtypes arose from interspecies transmission between monkeys and humans. STLV-3 viruses belong to the third PTLV type and are equally divergent from both HTLV-1 and HTLV-2. They are endemic in several monkey species that live in West, Central and East Africa. In 2005, we, and others reported the discovery of the human homolog (HTLV-3) of STLV-3 in two asymptomatic inhabitants from South Cameroon whose sera exhibited HTLV indeterminate serologies. More recently, two other cases of HTLV-3 infection in persons living in Cameroon were reported suggesting that this virus is not extremely rare in the human population living in Central Africa. Together with STLV-3, these human viral strains belong to the PTLV-3 group. A fourth HTLV type (HTLV-4) was also discovered in the same geographical area. The overall PTLV-3 and PTLV-4 genomic organization is similar to that of HTLV-1 and HTLV-2 with the exception of their long terminal repeats (LTRs) that contain only two 21 bp repeats. As in HTLV-1, HTLV-3 Tax contains a PDZ binding motif while HTLV-4 does not. An antisense transcript was also described in HTLV-3 transfected cells. PTLV-3 molecular clones are now available and will allow scientists to study the viral cycle, the tropism and the possible pathogenicity in vivo. Current studies are also aimed at determining the prevalence, distribution, and modes of transmission of these viruses, as well as their possible association with human diseases. Here we will review the characteristics of these new simian and human retroviruses, whose discovery has opened new avenues of research in the retrovirology field. Full article
(This article belongs to the Special Issue Recent Developments in HTLV Research)
Open AccessReview The Natural Killer Cell Cytotoxic Function Is Modulated by HIV-1 Accessory Proteins
Viruses 2011, 3(7), 1091-1111; doi:10.3390/v3071091
Received: 14 June 2011 / Revised: 23 June 2011 / Accepted: 24 June 2011 / Published: 8 July 2011
Cited by 12 | PDF Full-text (528 KB)
Abstract
Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK [...] Read more.
Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK cell surface. Because of the importance of ligand-receptor interactions in modulating the NK cell cytotoxic response, HIV has developed strategies to regulate various NK cell ligands making the infected cell surprisingly refractory to NK cell lysis. This is perplexing because the HIV-1 accessory protein Vpr induces expression of ligands for the NK cell activating receptor, NKG2D. In addition, the accessory protein Nef removes the inhibitory ligands HLA-A and -B. The reason for the ineffective killing by NK cells despite the strong potential to eliminate infected cells is due to HIV-1 Vpu’s ability to down modulate the co-activation ligand, NTB-A, from the cell surface. Down modulation of NTB-A prevents efficient NK cell degranulation. This review will focus on the mechanisms through which the HIV-1 accessory proteins modulate their respective ligands, and its implication for NK cell killing of HIV-infected cells. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Systems-Biology Approaches to Discover Anti-Viral Effectors of the Human Innate Immune Response
Viruses 2011, 3(7), 1112-1130; doi:10.3390/v3071112
Received: 9 May 2011 / Revised: 26 June 2011 / Accepted: 29 June 2011 / Published: 11 July 2011
Cited by 3 | PDF Full-text (290 KB)
Abstract
Virus infections elicit an immediate innate response involving antiviral factors. The activities of some of these factors are, in turn, blocked by viral countermeasures. The ensuing battle between the host and the viruses is crucial for determining whether the virus establishes a [...] Read more.
Virus infections elicit an immediate innate response involving antiviral factors. The activities of some of these factors are, in turn, blocked by viral countermeasures. The ensuing battle between the host and the viruses is crucial for determining whether the virus establishes a foothold and/or induces adaptive immune responses. A comprehensive systems-level understanding of the repertoire of anti-viral effectors in the context of these immediate virus-host responses would provide significant advantages in devising novel strategies to interfere with the initial establishment of infections. Recent efforts to identify cellular factors in a comprehensive and unbiased manner, using genome-wide siRNA screens and other systems biology “omics” methodologies, have revealed several potential anti-viral effectors for viruses like Human immunodeficiency virus type 1 (HIV-1), Hepatitis C virus (HCV), West Nile virus (WNV), and influenza virus. This review describes the discovery of novel viral restriction factors and discusses how the integration of different methods in systems biology can be used to more comprehensively identify the intimate interactions of viruses and the cellular innate resistance. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Molecular Determinants of Human T-lymphotropic Virus Type 1 Transmission and Spread
Viruses 2011, 3(7), 1131-1165; doi:10.3390/v3071131
Received: 9 May 2011 / Revised: 1 July 2011 / Accepted: 2 July 2011 / Published: 12 July 2011
Cited by 18 | PDF Full-text (471 KB)
Abstract
Human T-lymphotrophic virus type-1 (HTLV-1) infects approximately 15 to 20 million people worldwide, with endemic areas in Japan, the Caribbean, and Africa. The virus is spread through contact with bodily fluids containing infected cells, most often from mother to child through breast [...] Read more.
Human T-lymphotrophic virus type-1 (HTLV-1) infects approximately 15 to 20 million people worldwide, with endemic areas in Japan, the Caribbean, and Africa. The virus is spread through contact with bodily fluids containing infected cells, most often from mother to child through breast milk or via blood transfusion. After prolonged latency periods, approximately 3 to 5% of HTLV-1 infected individuals will develop either adult T-cell leukemia/lymphoma (ATL), or other lymphocyte-mediated disorders such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The genome of this complex retrovirus contains typical gag, pol, and env genes, but also unique nonstructural proteins encoded from the pX region. These nonstructural genes encode the Tax and Rex regulatory proteins, as well as novel proteins essential for viral spread in vivo such as, p30, p12, p13 and the antisense encoded HBZ. While progress has been made in the understanding of viral determinants of cell transformation and host immune responses, host and viral determinants of HTLV-1 transmission and spread during the early phases of infection are unclear. Improvements in the molecular tools to test these viral determinants in cellular and animal models have provided new insights into the early events of HTLV-1 infection. This review will focus on studies that test HTLV-1 determinants in context to full length infectious clones of the virus providing insights into the mechanisms of transmission and spread of HTLV-1. Full article
(This article belongs to the Special Issue Recent Developments in HTLV Research)
Open AccessReview Beclin-1 Targeting for Viral Immune Escape
Viruses 2011, 3(7), 1166-1178; doi:10.3390/v3071166
Received: 23 June 2011 / Revised: 4 July 2011 / Accepted: 5 July 2011 / Published: 12 July 2011
Cited by 19 | PDF Full-text (302 KB)
Abstract
Macroautophagy is a catabolic pathway in eukaryotic cells that has recently been shown to facilitate pathogen detection, pathogen restriction and pathogen-derived antigen presentation to CD4+ T cells. Due to these protective functions during immune responses, several pathogens, including RNA and DNA [...] Read more.
Macroautophagy is a catabolic pathway in eukaryotic cells that has recently been shown to facilitate pathogen detection, pathogen restriction and pathogen-derived antigen presentation to CD4+ T cells. Due to these protective functions during immune responses, several pathogens, including RNA and DNA viruses, have developed strategies to inhibit autophagosome generation or maturation. Interestingly, most of the respective viral proteins exert these functions via binding to Beclin-1, an essential macroautophagy protein that constitutes part of the phosphatidylinositol-3 kinase complexes that mark membranes for autophagosome generation and facilitate autophagosome fusion with lyososomes. The viruses that inhibit macroautophagy by this pathway include herpesviruses, HIV and influenza A virus. Inhibition either before or after autophagosome formation seems to benefit their viral replication by different mechanisms, which are discussed here. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Open AccessReview Innate Antiviral Response: Role in HIV-1 Infection
Viruses 2011, 3(7), 1179-1203; doi:10.3390/v3071179
Received: 24 May 2011 / Revised: 28 June 2011 / Accepted: 29 June 2011 / Published: 14 July 2011
Cited by 15 | PDF Full-text (335 KB)
Abstract
As an early response to infection, cells induce a profile of the early inflammatory proteins including antiviral cytokines and chemokines. Two families of transcriptional factors play a major role in the transcriptional activation of the early inflammatory genes: The well-characterized family of [...] Read more.
As an early response to infection, cells induce a profile of the early inflammatory proteins including antiviral cytokines and chemokines. Two families of transcriptional factors play a major role in the transcriptional activation of the early inflammatory genes: The well-characterized family of NFkB factors and the family of interferon regulatory factors (IRF). The IRFs play a critical role in the induction of type I interferon (IFN) and chemokine genes, as well as genes mediating antiviral, antibacterial, and inflammatory responses. Type I IFNs represent critical components of innate antiviral immunity. These proteins not only exert direct antiviral effects, but also induce maturation of dendritic cells (DC), and enhance functions of NK, T and B cells, and macrophages. This review will summarize the current knowledge of the mechanisms leading to the innate antiviral response with a focus on its role in the regulation of HIV-1 infection and pathogenicity. We would like this review to be both historical and a future perspective. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Preventive and Therapeutic Strategies for Bovine Leukemia Virus: Lessons for HTLV
Viruses 2011, 3(7), 1210-1248; doi:10.3390/v3071210
Received: 21 May 2011 / Revised: 28 June 2011 / Accepted: 29 June 2011 / Published: 19 July 2011
Cited by 38 | PDF Full-text (306 KB)
Abstract
Bovine leukemia virus (BLV) is a retrovirus closely related to the human T-lymphotropic virus type 1 (HTLV-1). BLV is a major animal health problem worldwide causing important economic losses. A series of attempts were developed to reduce prevalence, chiefly by eradication of [...] Read more.
Bovine leukemia virus (BLV) is a retrovirus closely related to the human T-lymphotropic virus type 1 (HTLV-1). BLV is a major animal health problem worldwide causing important economic losses. A series of attempts were developed to reduce prevalence, chiefly by eradication of infected cattle, segregation of BLV-free animals and vaccination. Although having been instrumental in regions such as the EU, these strategies were unsuccessful elsewhere mainly due to economic costs, management restrictions and lack of an efficient vaccine. This review, which summarizes the different attempts previously developed to decrease seroprevalence of BLV, may be informative for management of HTLV-1 infection. We also propose a new approach based on competitive infection with virus deletants aiming at reducing proviral loads. Full article
(This article belongs to the Special Issue Recent Developments in HTLV Research)
Open AccessReview Viruses, Autophagy Genes, and Crohn’s Disease
Viruses 2011, 3(7), 1281-1311; doi:10.3390/v3071281
Received: 8 June 2011 / Revised: 12 July 2011 / Accepted: 13 July 2011 / Published: 21 July 2011
Cited by 12 | PDF Full-text (955 KB)
Abstract
The etiology of the intestinal disease Crohn’s disease involves genetic factors as well as ill-defined environmental agents. Several genetic variants linked to this disease are associated with autophagy, a process that is critical for proper responses to viral infections. While a role [...] Read more.
The etiology of the intestinal disease Crohn’s disease involves genetic factors as well as ill-defined environmental agents. Several genetic variants linked to this disease are associated with autophagy, a process that is critical for proper responses to viral infections. While a role for viruses in this disease remains speculative, accumulating evidence indicate that this possibility requires serious consideration. In this review, we will examine the three-way relationship between viruses, autophagy genes, and Crohn’s disease and discuss how host-pathogen interactions can mediate complex inflammatory disorders. Full article
(This article belongs to the Special Issue Autophagy and Viruses)

Other

Jump to: Research, Review

Open AccessCommentary TRIM5 Acts as More Than a Retroviral Restriction Factor
Viruses 2011, 3(7), 1204-1209; doi:10.3390/v3071204
Received: 20 June 2011 / Revised: 7 July 2011 / Accepted: 10 July 2011 / Published: 15 July 2011
Cited by 3 | PDF Full-text (664 KB)
Abstract
The retrovirus restriction factor TRIM5α blocks post-entry infection of retroviruses in a species-specific manner. As a cellular E3 ubiquitin ligase, TRIM5α binds to the retroviral capsid lattice in the cytoplasm of an infected cell and accelerates the uncoating process of retroviral capsid, [...] Read more.
The retrovirus restriction factor TRIM5α blocks post-entry infection of retroviruses in a species-specific manner. As a cellular E3 ubiquitin ligase, TRIM5α binds to the retroviral capsid lattice in the cytoplasm of an infected cell and accelerates the uncoating process of retroviral capsid, thus providing a potent restriction to HIV-1 and other retrovirus infections. The precise mechanism by which this restriction is imposed remains under scrutiny, and evidence is lacking to link the E3 ubiquitin ligase activity of TRIM5α to its ability to restrict retrovirus infection. In a recent study, Pertel and colleagues have uncovered the link between the two, providing compelling evidence to suggest that following the interaction with the retroviral capsid, TRIM5 triggers an antiviral innate immune response by functioning as a pattern recognition receptor [1]. This unique function of TRIM5 is dependent on its association with the E2 ubiquitin-conjugating enzyme complex UBC13-UEV1A and subsequent activation of the TAK1 kinase complex and downstream genes involved in innate immune responses. These 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. Here we discuss the significance of these new findings in understanding TRIM5-mediated HIV restriction. Full article
(This article belongs to the Section Editorial)
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