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Viruses, Volume 2, Issue 5 (May 2010) – 13 articles , Pages 1050-1260

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Open AccessReview
HIV-1 Virological Synapse is not Simply a Copycat of the Immunological Synapse
Viruses 2010, 2(5), 1239-1260; https://doi.org/10.3390/v2051239 - 21 May 2010
Cited by 41 | Viewed by 7714
Abstract
The virological synapse (VS) is a tight adhesive junction between an HIV-infected cell and an uninfected target cell, across which virus can be efficiently transferred from cell to cell in the absence of cell-cell fusion. The VS has been postulated to resemble, in [...] Read more.
The virological synapse (VS) is a tight adhesive junction between an HIV-infected cell and an uninfected target cell, across which virus can be efficiently transferred from cell to cell in the absence of cell-cell fusion. The VS has been postulated to resemble, in its morphology, the well-studied immunological synapse (IS). This review article discusses the structural similarities between IS and VS and the shared T cell receptor (TCR) signaling components that are found in the VS. However, the IS and the VS display distinct kinetics in disassembly and intracellular signaling events, possibly leading to different biological outcomes. Hence, HIV-1 exploits molecular components of IS and TCR signaling machinery to trigger unique changes in cellular morphology, migration, and activation that facilitate its transmission and cell-to-cell spread. Full article
(This article belongs to the Special Issue Transmission of Retroviruses across Virological Synapses)
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Open AccessEditorial
Viruses and Lipids
Viruses 2010, 2(5), 1236-1238; https://doi.org/10.3390/v2051236 - 20 May 2010
Cited by 4 | Viewed by 5383
Abstract
As obligatory intracellular pathogens, viruses exploit various cellular molecules and structures, such as cellular membranes, for their propagation. Enveloped viruses acquire lipid membranes as their outer coat through interactions with cellular membranes during morphogenesis within, and egress from, infected cells. In contrast, non-enveloped [...] Read more.
As obligatory intracellular pathogens, viruses exploit various cellular molecules and structures, such as cellular membranes, for their propagation. Enveloped viruses acquire lipid membranes as their outer coat through interactions with cellular membranes during morphogenesis within, and egress from, infected cells. In contrast, non-enveloped viruses typically exit cells by cell lysis, and lipid membranes are not part of the released virions. However, non-enveloped viruses also interact with lipid membranes at least during entry into target cells. Therefore, lipids, as part of cellular membranes, inevitably play some roles in life cycle of viruses. [...] Full article
(This article belongs to the Special Issue Role of Lipids in Virus Replication)
Open AccessReview
Role of Lipids on Entry and Exit of Bluetongue Virus, a Complex Non-Enveloped Virus
Viruses 2010, 2(5), 1218-1235; https://doi.org/10.3390/v2051218 - 18 May 2010
Cited by 18 | Viewed by 6610
Abstract
Non-enveloped viruses such as members of Picornaviridae and Reoviridae are assembled in the cytoplasm and are generally released by cell lysis. However, recent evidence suggests that some non-enveloped viruses exit from infected cells without lysis, indicating that these viruses may also utilize alternate [...] Read more.
Non-enveloped viruses such as members of Picornaviridae and Reoviridae are assembled in the cytoplasm and are generally released by cell lysis. However, recent evidence suggests that some non-enveloped viruses exit from infected cells without lysis, indicating that these viruses may also utilize alternate means for egress. Moreover, it appears that complex, non-enveloped viruses such as bluetongue virus (BTV) and rotavirus interact with lipids during their entry process as well as with lipid rafts during the trafficking of newly synthesized progeny viruses. This review will discuss the role of lipids in the entry, maturation and release of non-enveloped viruses, focusing mainly on BTV. Full article
(This article belongs to the Special Issue Role of Lipids in Virus Replication)
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Open AccessReview
Lipid Metabolism and HCV Infection
Viruses 2010, 2(5), 1195-1217; https://doi.org/10.3390/v2051195 - 11 May 2010
Cited by 25 | Viewed by 11220
Abstract
Chronic infection by hepatitis C virus (HCV) can lead to severe liver disease and is a global healthcare problem. The liver is highly metabolically active and one of its key functions is to control the balance of lipid throughout the body. A number [...] Read more.
Chronic infection by hepatitis C virus (HCV) can lead to severe liver disease and is a global healthcare problem. The liver is highly metabolically active and one of its key functions is to control the balance of lipid throughout the body. A number of pathologies have been linked to the impact of HCV infection on liver metabolism. However, there is also growing evidence that hepatic metabolic processes contribute to the HCV life cycle. This review summarizes the relationship between lipid metabolism and key stages in the production of infectious HCV. Full article
(This article belongs to the Special Issue Role of Lipids in Virus Replication)
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Open AccessCommentary
HIV Nuclear Entry: Clearing the Fog
Viruses 2010, 2(5), 1190-1194; https://doi.org/10.3390/v2051190 - 11 May 2010
Cited by 4 | Viewed by 7276
Abstract
HIV-1 and other lentiviruses have the unusual capability of infecting nondividing cells, but the mechanism by which they cross an intact nuclear membrane is mysterious. Recent work, including a new study (Lee, K.; Ambrose, Z.; Martin, T.D.; Oztop, I.; Mulky, A.; Julias, J.G.; [...] Read more.
HIV-1 and other lentiviruses have the unusual capability of infecting nondividing cells, but the mechanism by which they cross an intact nuclear membrane is mysterious. Recent work, including a new study (Lee, K.; Ambrose, Z.; Martin, T.D.; Oztop, I.; Mulky, A.; Julias, J.G.; Vandergraaff, N.; Baumann, J.G.; Wang, R.; Yuen, W. et al. Flexible use of nuclear import pathways by HIV-1. Cell Host Microbe 2010,7, 221-233) confirms that the viral capsid plays a key role in HIV-1 nuclear entry in both dividing and nondividing cells. The identification of mutations in the viral capsid that alter the virus’s dependence on host cell nucleoporins represents an important advance in this poorly understood stage of the virus life cycle. Full article
(This article belongs to the Section Editorial)
Open AccessCommentary
Retrovirus Integrase-DNA Structure Elucidates Concerted Integration Mechanisms
Viruses 2010, 2(5), 1185-1189; https://doi.org/10.3390/v2051185 - 10 May 2010
Cited by 5 | Viewed by 4871
Abstract
Commentary on Hare, S.; Gupta, S.S.; Valkov, E.; Engelman, A.; Cherepanov, P. Retroviral intasome assembly and inhibition of DNA strand transfer. Nature 2010, 464, 232-236. Full article
(This article belongs to the Section Editorial)
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Open AccessEditorial
Special Issue: Retroviral Enzymes
Viruses 2010, 2(5), 1181-1184; https://doi.org/10.3390/v2051181 - 07 May 2010
Cited by 3 | Viewed by 5243
Abstract
The retroviral RNA genome encodes for three enzymes essential for virus replication: (i) the viral protease (PR), that converts the immature virion into a mature virus through the cleavage of precursor polypeptides; (ii) the reverse transcriptase (RT), responsible for the conversion of the [...] Read more.
The retroviral RNA genome encodes for three enzymes essential for virus replication: (i) the viral protease (PR), that converts the immature virion into a mature virus through the cleavage of precursor polypeptides; (ii) the reverse transcriptase (RT), responsible for the conversion of the single-stranded genomic RNA into double-stranded proviral DNA; and (iii) the integrase (IN) that inserts the proviral DNA into the host cell genome. All of them are important targets for therapeutic intervention. This Special Issue provides authoritative reviews on the most recent research towards a better understanding of structure-function relationships in retroviral enzymes. The Issue includes three reviews on retroviral PRs, seven on RT and reverse transcription, and four dedicated to viral integration. [...] Full article
(This article belongs to the Special Issue Retroviral Enzymes)
Open AccessReview
The Role of Lipids in Retrovirus Replication
Viruses 2010, 2(5), 1146-1180; https://doi.org/10.3390/v2051146 - 06 May 2010
Cited by 62 | Viewed by 8007
Abstract
Retroviruses undergo several critical steps to complete a replication cycle. These include the complex processes of virus entry, assembly, and budding that often take place at the plasma membrane of the host cell. Both virus entry and release involve membrane fusion/fission reactions between [...] Read more.
Retroviruses undergo several critical steps to complete a replication cycle. These include the complex processes of virus entry, assembly, and budding that often take place at the plasma membrane of the host cell. Both virus entry and release involve membrane fusion/fission reactions between the viral envelopes and host cell membranes. Accumulating evidence indicates important roles for lipids and lipid microdomains in virus entry and egress. In this review, we outline the current understanding of the role of lipids and membrane microdomains in retroviral replication. Full article
(This article belongs to the Special Issue Role of Lipids in Virus Replication)
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Open AccessReview
Interactions of Host Proteins with the Murine Leukemia Virus Integrase
Viruses 2010, 2(5), 1110-1145; https://doi.org/10.3390/v2051110 - 05 May 2010
Cited by 10 | Viewed by 6819
Abstract
Retroviral infections cause a variety of cancers in animals and a number of diverse diseases in humans such as leukemia and acquired immune deficiency syndrome. Productive and efficient proviral integration is critical for retroviral function and is the key step in establishing a [...] Read more.
Retroviral infections cause a variety of cancers in animals and a number of diverse diseases in humans such as leukemia and acquired immune deficiency syndrome. Productive and efficient proviral integration is critical for retroviral function and is the key step in establishing a stable and productive infection, as well as the mechanism by which host genes are activated in leukemogenesis. Host factors are widely anticipated to be involved in all stages of the retroviral life cycle, and the identification of integrase interacting factors has the potential to increase our understanding of mechanisms by which the incoming virus might appropriate cellular proteins to target and capture host DNA sequences. Identification of MoMLV integrase interacting host factors may be key to designing efficient and benign retroviral-based gene therapy vectors; key to understanding the basic mechanism of integration; and key in designing efficient integrase inhibitors. In this review, we discuss current progress in the field of MoMLV integrase interacting proteins and possible roles for these proteins in integration. Full article
(This article belongs to the Special Issue Retroviral Enzymes)
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Open AccessCommentary
A Potent, Broad-Spectrum Antiviral Agent that Targets Viral Membranes
Viruses 2010, 2(5), 1106-1109; https://doi.org/10.3390/v2051106 - 04 May 2010
Cited by 14 | Viewed by 7100
Abstract
Commentary on Wolf, M.C.; Freiberg, A.N.; Zhang, T.; Akyol-Ataman, Z.; Grock, A.; Hong, P.W.; Li, J.; Watson, N.F.; Fang, A.Q.; Aguilar, H.C.; et al. A broad-spectrum antiviral targeting entry of enveloped viruses. Proc. Natl. Acad. Sci. U. S. A. 2010, 107, 3157-3162. Full article
(This article belongs to the Section Editorial)
Open AccessReview
HIV-1 Entry, Inhibitors, and Resistance
Viruses 2010, 2(5), 1069-1105; https://doi.org/10.3390/v2051069 - 29 Apr 2010
Cited by 42 | Viewed by 8287
Abstract
Entry inhibitors represent a new class of antiretroviral agents for the treatment of infection with HIV-1. While resistance to other HIV drug classes has been well described, resistance to this new class is still ill defined despite considerable clinical use. Several potential mechanisms [...] Read more.
Entry inhibitors represent a new class of antiretroviral agents for the treatment of infection with HIV-1. While resistance to other HIV drug classes has been well described, resistance to this new class is still ill defined despite considerable clinical use. Several potential mechanisms have been proposed: tropism switching (utilization of CXCR4 instead of CCR5 for entry), increased affinity for the coreceptor, increased rate of virus entry into host cells, and utilization of inhibitor-bound receptor for entry. In this review we will address the development of attachment, fusion, and coreceptor entry inhibitors and explore recent studies describing potential mechanisms of resistance. Full article
(This article belongs to the Special Issue HIV Drug Resistance 2010)
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Open AccessReview
Role of Cellular Lipids in Positive-Sense RNA Virus Replication Complex Assembly and Function
Viruses 2010, 2(5), 1055-1068; https://doi.org/10.3390/v2051055 - 29 Apr 2010
Cited by 32 | Viewed by 9259
Abstract
Positive-sense RNA viruses are responsible for frequent and often devastating diseases in humans, animals, and plants. However, the development of effective vaccines and anti-viral therapies targeted towards these pathogens has been hindered by an incomplete understanding of the molecular mechanisms involved in viral [...] Read more.
Positive-sense RNA viruses are responsible for frequent and often devastating diseases in humans, animals, and plants. However, the development of effective vaccines and anti-viral therapies targeted towards these pathogens has been hindered by an incomplete understanding of the molecular mechanisms involved in viral replication. One common feature of all positive-sense RNA viruses is the manipulation of host intracellular membranes for the assembly of functional viral RNA replication complexes. This review will discuss the interplay between cellular membranes and positive-sense RNA virus replication, and will focus specifically on the potential structural and functional roles for cellular lipids in this process. Full article
(This article belongs to the Special Issue Role of Lipids in Virus Replication)
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Open AccessCommentary
Surf and Turf: Mechanism of Enhanced Virus Spread During Poxvirus Infection
Viruses 2010, 2(5), 1050-1054; https://doi.org/10.3390/v2051050 - 28 Apr 2010
Cited by 4 | Viewed by 5627
Abstract
Commentary on Doceul, V.; Hollinshead, M.; van der Linden, L.; Smith, G.L. Repulsion of superinfecting virions: a mechanism for rapid virus spread. Science 2010, 327, 873-876. Full article
(This article belongs to the Section Editorial)
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