Viruses

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Open AccessArticle

Recombination in Avian Gamma-Coronavirus Infectious Bronchitis Virus

by Sharmi W. Thor, Deborah A. Hilt, Jessica C. Kissinger, Andrew H. Paterson and Mark W. Jackwood

Viruses 2011, 3(9), 1777-1799; https://doi.org/10.3390/v3091777 - 23 Sep 2011

Cited by 97 | Viewed by 9784

Recombination in the family Coronaviridae has been well documented and is thought to be a contributing factor in the emergence and evolution of different coronaviral genotypes as well as different species of coronavirus. However, there are limited data available on the frequency and [...] Read more.

Recombination in the family Coronaviridae has been well documented and is thought to be a contributing factor in the emergence and evolution of different coronaviral genotypes as well as different species of coronavirus. However, there are limited data available on the frequency and extent of recombination in coronaviruses in nature and particularly for the avian gamma-coronaviruses where only recently the emergence of a turkey coronavirus has been attributed solely to recombination. In this study, the full-length genomes of eight avian gamma-coronavirus infectious bronchitis virus (IBV) isolates were sequenced and along with other full-length IBV genomes available from GenBank were analyzed for recombination. Evidence of recombination was found in every sequence analyzed and was distributed throughout the entire genome. Areas that have the highest occurrence of recombination are located in regions of the genome that code for nonstructural proteins 2, 3 and 16, and the structural spike glycoprotein. The extent of the recombination observed, suggests that this may be one of the principal mechanisms for generating genetic and antigenic diversity within IBV. These data indicate that reticulate evolutionary change due to recombination in IBV, likely plays a major role in the origin and adaptation of the virus leading to new genetic types and strains of the virus. Full article

(This article belongs to the Special Issue Recombination in Viruses)

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2443 KiB

Open AccessReview

How HIV-1 Takes Advantage of the Cytoskeleton during Replication and Cell-to-Cell Transmission

by Martin Lehmann, Damjan S. Nikolic and Vincent Piguet

Viruses 2011, 3(9), 1757-1776; https://doi.org/10.3390/v3091757 - 15 Sep 2011

Cited by 37 | Viewed by 6335

Abstract

Human immunodeficiency virus 1 (HIV-1) infects T cells, macrophages and dendritic cells and can manipulate their cytoskeleton structures at multiple steps during its replication cycle. Based on pharmacological and genetic targeting of cytoskeleton modulators, new imaging approaches and primary cell culture models, important [...] Read more.

Human immunodeficiency virus 1 (HIV-1) infects T cells, macrophages and dendritic cells and can manipulate their cytoskeleton structures at multiple steps during its replication cycle. Based on pharmacological and genetic targeting of cytoskeleton modulators, new imaging approaches and primary cell culture models, important roles for actin and microtubules during entry and cell-to-cell transfer have been established. Virological synapses and actin-containing membrane extensions can mediate HIV-1 transfer from dendritic cells or macrophage cells to T cells and between T cells. We will review the role of the cytoskeleton in HIV-1 entry, cellular trafficking and cell-to-cell transfer between primary cells. Full article

(This article belongs to the Special Issue Cytoskeleton in Viral Infections)

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Open AccessReview

Functional RNA Elements in the Dengue Virus Genome

by Leopoldo G. Gebhard, Claudia V. Filomatori and Andrea V. Gamarnik

Viruses 2011, 3(9), 1739-1756; https://doi.org/10.3390/v3091739 - 15 Sep 2011

Cited by 187 | Viewed by 12658

Abstract

Dengue virus (DENV) genome amplification is a process that involves the viral RNA, cellular and viral proteins, and a complex architecture of cellular membranes. The viral RNA is not a passive template during this process; it plays an active role providing RNA signals [...] Read more.

Dengue virus (DENV) genome amplification is a process that involves the viral RNA, cellular and viral proteins, and a complex architecture of cellular membranes. The viral RNA is not a passive template during this process; it plays an active role providing RNA signals that act as promoters, enhancers and/or silencers of the replication process. RNA elements that modulate RNA replication were found at the 5' and 3' UTRs and within the viral coding sequence. The promoter for DENV RNA synthesis is a large stem loop structure located at the 5' end of the genome. This structure specifically interacts with the viral polymerase NS5 and promotes RNA synthesis at the 3' end of a circularized genome. The circular conformation of the viral genome is mediated by long range RNA-RNA interactions that span thousands of nucleotides. Recent studies have provided new information about the requirement of alternative, mutually exclusive, structures in the viral RNA, highlighting the idea that the viral genome is flexible and exists in different conformations. In this article, we describe elements in the promoter SLA and other RNA signals involved in NS5 polymerase binding and activity, and provide new ideas of how dynamic secondary and tertiary structures of the viral RNA participate in the viral life cycle. Full article

(This article belongs to the Special Issue Recent Progress in Dengue Virus Research)

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3832 KiB

Open AccessReview

Recombination in Eukaryotic Single Stranded DNA Viruses

by Darren P. Martin, Philippe Biagini, Pierre Lefeuvre, Michael Golden, Philippe Roumagnac and Arvind Varsani

Viruses 2011, 3(9), 1699-1738; https://doi.org/10.3390/v3091699 - 13 Sep 2011

Cited by 174 | Viewed by 12593

Abstract

Although single stranded (ss) DNA viruses that infect humans and their domesticated animals do not generally cause major diseases, the arthropod borne ssDNA viruses of plants do, and as a result seriously constrain food production in most temperate regions of the world. Besides [...] Read more.

Although single stranded (ss) DNA viruses that infect humans and their domesticated animals do not generally cause major diseases, the arthropod borne ssDNA viruses of plants do, and as a result seriously constrain food production in most temperate regions of the world. Besides the well known plant and animal-infecting ssDNA viruses, it has recently become apparent through metagenomic surveys of ssDNA molecules that there also exist large numbers of other diverse ssDNA viruses within almost all terrestrial and aquatic environments. The host ranges of these viruses probably span the tree of life and they are likely to be important components of global ecosystems. Various lines of evidence suggest that a pivotal evolutionary process during the generation of this global ssDNA virus diversity has probably been genetic recombination. High rates of homologous recombination, non-homologous recombination and genome component reassortment are known to occur within and between various different ssDNA virus species and we look here at the various roles that these different types of recombination may play, both in the day-to-day biology, and in the longer term evolution, of these viruses. We specifically focus on the ecological, biochemical and selective factors underlying patterns of genetic exchange detectable amongst the ssDNA viruses and discuss how these should all be considered when assessing the adaptive value of recombination during ssDNA virus evolution. Full article

(This article belongs to the Special Issue Recombination in Viruses)

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Open AccessReview

Viral Determinants of FeLV Infection and Pathogenesis: Lessons Learned from Analysis of a Natural Cohort

by Lisa L. Bolin and Laura S. Levy

Viruses 2011, 3(9), 1681-1698; https://doi.org/10.3390/v3091681 - 9 Sep 2011

Cited by 21 | Viewed by 5681

Abstract

Detailed analysis has been performed over many years of a geographic and temporal cohort of cats naturally infected with feline leukemia virus (FeLV). Molecular analysis of FeLV present in the diseased tissues and application of those viruses to experimental systems has revealed unique [...] Read more.

Detailed analysis has been performed over many years of a geographic and temporal cohort of cats naturally infected with feline leukemia virus (FeLV). Molecular analysis of FeLV present in the diseased tissues and application of those viruses to experimental systems has revealed unique isolates with distinctive disease potential, previously uncharacterized virus-receptor interactions, information about the role of recombinant viruses in disease induction, and novel viral and cellular oncogenes implicated in pathogenesis, among other findings. The studies have contributed to an understanding of the selective forces that lead to predominance of distinctive FeLV isolates and disease outcomes in a natural population. Full article

(This article belongs to the Special Issue Feline Retroviruses)

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Open AccessReview

Mechanisms and Factors that Influence High Frequency Retroviral Recombination

by Krista Delviks-Frankenberry, Andrea Galli, Olga Nikolaitchik, Helene Mens, Vinay K. Pathak and Wei-Shau Hu

Viruses 2011, 3(9), 1650-1680; https://doi.org/10.3390/v3091650 - 9 Sep 2011

Cited by 63 | Viewed by 7569

Abstract

With constantly changing environmental selection pressures, retroviruses rely upon recombination to reassort polymorphisms in their genomes and increase genetic diversity, which improves the chances for the survival of their population. Recombination occurs during DNA synthesis, whereby reverse transcriptase undergoes template switching events between [...] Read more.

With constantly changing environmental selection pressures, retroviruses rely upon recombination to reassort polymorphisms in their genomes and increase genetic diversity, which improves the chances for the survival of their population. Recombination occurs during DNA synthesis, whereby reverse transcriptase undergoes template switching events between the two copackaged RNAs, resulting in a viral recombinant with portions of the genetic information from each parental RNA. This review summarizes our current understanding of the factors and mechanisms influencing retroviral recombination, fidelity of the recombination process, and evaluates the subsequent viral diversity and fitness of the progeny recombinant. Specifically, the high mutation rates and high recombination frequencies of HIV-1 will be analyzed for their roles in influencing HIV-1 global diversity, as well as HIV-1 diagnosis, drug treatment, and vaccine development. Full article

(This article belongs to the Special Issue Recombination in Viruses)

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642 KiB

Open AccessReview

Filoviral Immune Evasion Mechanisms

by Parameshwaran Ramanan, Reed S. Shabman, Craig S. Brown, Gaya K. Amarasinghe, Christopher F. Basler and Daisy W. Leung

Viruses 2011, 3(9), 1634-1649; https://doi.org/10.3390/v3091634 - 7 Sep 2011

Cited by 65 | Viewed by 12213

Abstract

The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render [...] Read more.

The Filoviridae family of viruses, which includes the genera Ebolavirus (EBOV) and Marburgvirus (MARV), causes severe and often times lethal hemorrhagic fever in humans. Filoviral infections are associated with ineffective innate antiviral responses as a result of virally encoded immune antagonists, which render the host incapable of mounting effective innate or adaptive immune responses. The Type I interferon (IFN) response is critical for establishing an antiviral state in the host cell and subsequent activation of the adaptive immune responses. Several filoviral encoded components target Type I IFN responses, and this innate immune suppression is important for viral replication and pathogenesis. For example, EBOV VP35 inhibits the phosphorylation of IRF-3/7 by the TBK-1/IKKε kinases in addition to sequestering viral RNA from detection by RIG-I like receptors. MARV VP40 inhibits STAT1/2 phosphorylation by inhibiting the JAK family kinases. EBOV VP24 inhibits nuclear translocation of activated STAT1 by karyopherin-α. The examples also represent distinct mechanisms utilized by filoviral proteins in order to counter immune responses, which results in limited IFN-α/β production and downstream signaling. Full article

(This article belongs to the Special Issue Pathogenesis of Emerging and Re-Emerging RNA Viruses)

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201 KiB

Open AccessCommentary

Restricted Access to Myeloid Cells Explained

by Vicente Planelles

Viruses 2011, 3(9), 1624-1633; https://doi.org/10.3390/v3091624 - 5 Sep 2011

Cited by 10 | Viewed by 4950

Abstract

The lentiviral accessory protein, Vpx, is known to counteract a restriction factor that is specific to myeloid cells, such as macrophages and dendritic cells. This review summarizes the findings in two seminal studies that identify SAMHD1 as the cellular protein that is responsible [...] Read more.

The lentiviral accessory protein, Vpx, is known to counteract a restriction factor that is specific to myeloid cells, such as macrophages and dendritic cells. This review summarizes the findings in two seminal studies that identify SAMHD1 as the cellular protein that is responsible for myeloid cell restriction, and establish the existence of other types of restriction in these cells. Full article

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Open AccessReview

Unconventional Use of LC3 by Coronaviruses through the Alleged Subversion of the ERAD Tuning Pathway

by Fulvio Reggiori, Cornelis A.M. De Haan and Maurizio Molinari

Viruses 2011, 3(9), 1610-1623; https://doi.org/10.3390/v3091610 - 5 Sep 2011

Cited by 20 | Viewed by 6105

Abstract

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens [...] Read more.

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking. Full article

(This article belongs to the Special Issue Autophagy and Viruses)

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Open AccessEditorial

Special Issue: Viruses Infecting Fish, Amphibians, and Reptiles

by V. Gregory Chinchar

Viruses 2011, 3(9), 1609; https://doi.org/10.3390/v3091609 - 2 Sep 2011

Cited by 1 | Viewed by 4711

Abstract

Although viruses infecting and affecting humans are the focus of considerable research effort, viruses that target other animal species, including cold-blooded vertebrates, are receiving increased attention. In part this reflects the interests of comparative virologists, but increasingly it is based on the impact [...] Read more.

Although viruses infecting and affecting humans are the focus of considerable research effort, viruses that target other animal species, including cold-blooded vertebrates, are receiving increased attention. In part this reflects the interests of comparative virologists, but increasingly it is based on the impact that many viruses have on ecologically and commercially important animals. Frogs and other amphibians are sentinels of environmental health and their disappearance following viral or fungal (chytrid) infection is a cause for alarm. Likewise, because aquaculture and mariculture are providing an increasingly large percentage of the “seafood” consumed by humans, viral agents that adversely impact the harvest of cultured fish and amphibians are of equal concern. [...] Full article

(This article belongs to the Special Issue Viruses Infecting Fish, Amphibians, and Reptiles)

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Open AccessReview

Dengue — Quo tu et quo vadis?

by Rubing Chen and Nikos Vasilakis

Viruses 2011, 3(9), 1562-1608; https://doi.org/10.3390/v3091562 - 1 Sep 2011

Cited by 201 | Viewed by 11707

Abstract

Dengue viruses (DENV) are by far the most important arboviral pathogens in the tropics around the world, putting at risk of infection nearly a third of the global human population. DENV are members of the genus Flavivirus in the Family Flaviviridae and comprise [...] Read more.

Dengue viruses (DENV) are by far the most important arboviral pathogens in the tropics around the world, putting at risk of infection nearly a third of the global human population. DENV are members of the genus Flavivirus in the Family Flaviviridae and comprise four antigenically distinct serotypes (DENV-1-4). Although they share almost identical epidemiological features, they are genetically distinct. Phylogenetic analyses have revealed valuable insights into the origins, epidemiology and the forces that shape DENV evolution in nature. In this review, we examine the current status of DENV evolution, including but not limited to rates of evolution, selection pressures, population sizes and evolutionary constraints, and we discuss how these factors influence transmission, pathogenesis and emergence. Full article

(This article belongs to the Special Issue Recent Progress in Dengue Virus Research)

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315 KiB

Open AccessReview

Picornavirus Subversion of the Autophagy Pathway

by Kathryn A. Klein and William T. Jackson

Viruses 2011, 3(9), 1549-1561; https://doi.org/10.3390/v3091549 - 26 Aug 2011

Cited by 25 | Viewed by 5859

Abstract

While autophagy has been shown to act as an anti-viral defense, the Picornaviridae avoid and, in many cases, subvert this pathway to promote their own replication. Evidence indicates that some picornaviruses hijack autophagy in order to induce autophagosome-like membrane structures for genomic RNA [...] Read more.

While autophagy has been shown to act as an anti-viral defense, the Picornaviridae avoid and, in many cases, subvert this pathway to promote their own replication. Evidence indicates that some picornaviruses hijack autophagy in order to induce autophagosome-like membrane structures for genomic RNA replication. Expression of picornavirus proteins can specifically induce the machinery of autophagy, although the mechanisms by which the viruses employ autophagy appear to differ. Many picornaviruses up-regulate autophagy in order to promote viral replication while some members of the family also inhibit degradation by autolysosomes. Here we explore the unusual relationship of this medically important family of viruses with a degradative mechanism of innate immunity. Full article

(This article belongs to the Special Issue Autophagy and Viruses)

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Open AccessReview

Human T-Lymphotropic Virus Type 1 (HTLV-1) and Regulatory T Cells in HTLV-1-Associated Neuroinflammatory Disease

by Natsumi Araya, Tomoo Sato, Naoko Yagishita, Hitoshi Ando, Atae Utsunomiya, Steven Jacobson and Yoshihisa Yamano

Viruses 2011, 3(9), 1532-1548; https://doi.org/10.3390/v3091532 - 25 Aug 2011

Cited by 46 | Viewed by 7441

Abstract

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that is the causative agent of adult T cell leukemia/lymphoma (ATL) and associated with multiorgan inflammatory disorders, including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and uveitis. HTLV-1-infected T cells have been hypothesized to contribute to [...] Read more.

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that is the causative agent of adult T cell leukemia/lymphoma (ATL) and associated with multiorgan inflammatory disorders, including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and uveitis. HTLV-1-infected T cells have been hypothesized to contribute to the development of these disorders, although the precise mechanisms are not well understood. HTLV-1 primarily infects CD4⁺ T helper (Th) cells that play a central role in adaptive immune responses. Based on their functions, patterns of cytokine secretion, and expression of specific transcription factors and chemokine receptors, Th cells that are differentiated from naïve CD4⁺ T cells are classified into four major lineages: Th1, Th2, Th17, and T regulatory (Treg) cells. The CD4⁺CD25⁺CCR4⁺ T cell population, which consists primarily of suppressive T cell subsets, such as the Treg and Th2 subsets in healthy individuals, is the predominant viral reservoir of HTLV-1 in both ATL and HAM/TSP patients. Interestingly, CD4⁺CD25⁺CCR4⁺ T cells become Th1-like cells in HAM/TSP patients, as evidenced by their overproduction of IFN-γ, suggesting that HTLV-1 may intracellularly induce T cell plasticity from Treg to IFN-γ⁺ T cells. This review examines the recent research into the association between HTLV-1 and Treg cells that has greatly enhanced understanding of the pathogenic mechanisms underlying immune dysregulation in HTLV-1-associated neuroinflammatory disease. Full article

(This article belongs to the Special Issue Recent Developments in HTLV Research)

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Viruses, Volume 3, Issue 9 (September 2011) – 13 articles , Pages 1532-1799

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