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Viruses, Volume 5, Issue 1 (January 2013), Pages 1-422

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Research

Jump to: Review

Open AccessArticle Bacteriophage 434 Hex Protein Prevents RecA-Mediated Repressor Autocleavage
Viruses 2013, 5(1), 111-126; doi:10.3390/v5010111
Received: 16 November 2012 / Revised: 14 December 2012 / Accepted: 17 December 2012 / Published: 9 January 2013
Cited by 4 | PDF Full-text (636 KB) | HTML Full-text | XML Full-text
Abstract
In a λimm434 lysogen, two proteins are expressed from the integrated prophage. Both are encoded by the same mRNA whose transcription initiates at the PRM promoter. One protein is the 434 repressor, needed for the establishment and maintenance of lysogeny. [...] Read more.
In a λimm434 lysogen, two proteins are expressed from the integrated prophage. Both are encoded by the same mRNA whose transcription initiates at the PRM promoter. One protein is the 434 repressor, needed for the establishment and maintenance of lysogeny. The other is Hex which is translated from an open reading frame that apparently partially overlaps the 434 repressor coding region. In the wild type host, disruption of the gene encoding Hex destabilizes λimm434 lysogens. However, the hex mutation has no effect on lysogen stability in a recA host. These observations suggest that Hex functions by modulating the ability of RecA to stimulate 434 repressor autocleavage. We tested this hypothesis by identifying and purifying Hex to determine if this protein inhibited RecA‑stimulated autocleavage of 434 repressor in vitro. Our results show that in vitro a fragment of Hex prevents RecA-stimulated autocleavage of 434 repressor, as well as the repressors of the closely related phage P22. Surprisingly, Hex does not prevent RecA‑stimulated autocleavage of phage lambda repressor, nor the E. coli LexA repressor. Full article
(This article belongs to the Special Issue Recent Progress in Bacteriophage Research) Print Edition available
Open AccessCommunication Lysogenic Conversion and Phage Resistance Development in Phage Exposed Escherichia coli Biofilms
Viruses 2013, 5(1), 150-161; doi:10.3390/v5010150
Received: 11 December 2012 / Revised: 3 January 2013 / Accepted: 9 January 2013 / Published: 11 January 2013
Cited by 6 | PDF Full-text (378 KB) | HTML Full-text | XML Full-text
Abstract
In this study, three-day old mature biofilms of Escherichia coli were exposed once to either a temperate Shiga-toxin encoding phage (H-19B) or an obligatory lytic phage (T7), after which further dynamics in the biofilm were monitored. As such, it was found that [...] Read more.
In this study, three-day old mature biofilms of Escherichia coli were exposed once to either a temperate Shiga-toxin encoding phage (H-19B) or an obligatory lytic phage (T7), after which further dynamics in the biofilm were monitored. As such, it was found that a single dose of H-19B could rapidly lead to a near complete lysogenization of the biofilm, with a subsequent continuous release of infectious H-19B particles. On the other hand, a single dose of T7 rapidly led to resistance development in the biofilm population. Together, our data indicates a profound impact of phages on the dynamics within structured bacterial populations. Full article
(This article belongs to the Special Issue Recent Progress in Bacteriophage Research) Print Edition available
Open AccessArticle Base Composition and Translational Selection are Insufficient to Explain Codon Usage Bias in Plant Viruses
Viruses 2013, 5(1), 162-181; doi:10.3390/v5010162
Received: 13 December 2012 / Revised: 9 January 2013 / Accepted: 11 January 2013 / Published: 15 January 2013
Cited by 9 | PDF Full-text (647 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Viral codon usage bias may be the product of a number of synergistic or antagonistic factors, including genomic nucleotide composition, translational selection, genomic architecture, and mutational or repair biases. Most studies of viral codon bias evaluate only the relative importance of genomic [...] Read more.
Viral codon usage bias may be the product of a number of synergistic or antagonistic factors, including genomic nucleotide composition, translational selection, genomic architecture, and mutational or repair biases. Most studies of viral codon bias evaluate only the relative importance of genomic base composition and translational selection, ignoring other possible factors. We analyzed the codon preferences of ssRNA (luteoviruses and potyviruses) and ssDNA (geminiviruses) plant viruses that infect translationally distinct monocot and dicot hosts. We found that neither genomic base composition nor translational selection satisfactorily explains their codon usage biases. Furthermore, we observed a strong relationship between the codon preferences of viruses in the same family or genus, regardless of host or genomic nucleotide content. Our results suggest that analyzing codon bias as either due to base composition or translational selection is a false dichotomy that obscures the role of other factors. Constraints such as genomic architecture and secondary structure can and do influence codon usage in plant viruses, and likely in viruses of other hosts. Full article
(This article belongs to the Special Issue Plant Viruses)
Open AccessArticle Altering SARS Coronavirus Frameshift Efficiency Affects Genomic and Subgenomic RNA Production
Viruses 2013, 5(1), 279-294; doi:10.3390/v5010279
Received: 6 December 2012 / Revised: 14 January 2013 / Accepted: 15 January 2013 / Published: 18 January 2013
Cited by 5 | PDF Full-text (833 KB) | HTML Full-text | XML Full-text
Abstract
In previous studies, differences in the amount of genomic and subgenomic RNA produced by coronaviruses with mutations in the programmed ribosomal frameshift signal of ORF1a/b were observed. It was not clear if these differences were due to changes in genomic sequence, the [...] Read more.
In previous studies, differences in the amount of genomic and subgenomic RNA produced by coronaviruses with mutations in the programmed ribosomal frameshift signal of ORF1a/b were observed. It was not clear if these differences were due to changes in genomic sequence, the protein sequence or the frequency of frameshifting. Here, viruses with synonymous codon changes are shown to produce different ratios of genomic and subgenomic RNA. These findings demonstrate that the protein sequence is not the primary cause of altered genomic and subgenomic RNA production. The synonymous codon changes affect both the structure of the frameshift signal and frameshifting efficiency. Small differences in frameshifting efficiency result in dramatic differences in genomic RNA production and TCID50 suggesting that the frameshifting frequency must stay above a certain threshold for optimal virus production. The data suggest that either the RNA sequence or the ratio of viral proteins resulting from different levels of frameshifting affects viral replication. Full article
(This article belongs to the Special Issue Animal Arteriviruses and Coronaviruses)
Open AccessArticle Innate and Adaptive Immune Response to Pneumonia Virus of Mice in a Resistant and a Susceptible Mouse Strain
Viruses 2013, 5(1), 295-320; doi:10.3390/v5010295
Received: 31 December 2012 / Revised: 13 January 2013 / Accepted: 15 January 2013 / Published: 21 January 2013
Cited by 5 | PDF Full-text (907 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Respiratory syncytial virus (RSV) is the leading cause of infant bronchiolitis. The closely related pneumonia virus of mice (PVM) causes a similar immune-mediated disease in mice, which allows an analysis of host factors that lead to severe illness. This project was designed [...] Read more.
Respiratory syncytial virus (RSV) is the leading cause of infant bronchiolitis. The closely related pneumonia virus of mice (PVM) causes a similar immune-mediated disease in mice, which allows an analysis of host factors that lead to severe illness. This project was designed to compare the immune responses to lethal and sublethal doses of PVM strain 15 in Balb/c and C57Bl/6 mice. Balb/c mice responded to PVM infection with an earlier and stronger innate response that failed to control viral replication. Production of inflammatory cyto- and chemokines, as well as infiltration of neutrophils and IFN-γ secreting natural killer cells into the lungs, was more predominant in Balb/c mice. In contrast, C57Bl/6 mice were capable of suppressing both viral replication and innate inflammatory responses. After a sublethal infection, PVM-induced IFN-γ production by splenocytes was stronger early during infection and weaker at late time points in C57Bl/6 mice when compared to Balb/c mice. Furthermore, although the IgG levels were similar and the mucosal IgA titres lower, the virus neutralizing antibody titres were higher in C57Bl/6 mice than in Balb/c mice. Overall, the difference in susceptibility of these two strains appeared to be related not to an inherent T helper bias, but to the capacity of the C57Bl/6 mice to control both viral replication and the immune response elicited by PVM. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
Open AccessArticle A Genotype of Modified Vaccinia Ankara (MVA) that Facilitates Replication in Suspension Cultures in Chemically Defined Medium
Viruses 2013, 5(1), 321-339; doi:10.3390/v5010321
Received: 19 December 2012 / Revised: 11 January 2013 / Accepted: 17 January 2013 / Published: 21 January 2013
Cited by 4 | PDF Full-text (5288 KB) | HTML Full-text | XML Full-text
Abstract
While vectored vaccines, based on hyperattenuated viruses, may lead to new treatment options against infectious diseases and certain cancers, they are also complex products and sometimes difficult to provide in sufficient amount and purity. To facilitate vaccine programs utilizing host-restricted poxviruses, we [...] Read more.
While vectored vaccines, based on hyperattenuated viruses, may lead to new treatment options against infectious diseases and certain cancers, they are also complex products and sometimes difficult to provide in sufficient amount and purity. To facilitate vaccine programs utilizing host-restricted poxviruses, we established avian suspension cell lines (CR and CR.pIX) and developed a robust, chemically defined, culturing process for production of this class of vectors. For one prominent member, modified vaccinia Ankara (MVA), we now describe a new strain that appears to replicate to greater yields of infectious units, especially in the cell-free supernatant of cultures in chemically defined media. The new strain was obtained by repeated passaging in CR suspension cultures and, consistent with reports on the exceptional genetic stability of MVA, sequencing of 135 kb of the viral genomic DNA revealed that only three structural proteins (A3L, A9L and A34R) each carry a single amino acid exchange (H639Y, K75E and D86Y, respectively). Host restriction in a plaque-purified isolate of the new genotype appears to be maintained in cell culture. Processing towards an injectable vaccine preparation may be simplified with this strain as a complete lysate, containing the main burden of host cell contaminants, may not be required anymore to obtain adequate yields. Full article
(This article belongs to the Section Antivirals & Vaccines)

Review

Jump to: Research

Open AccessReview Molecular Mechanisms of HIV Immune Evasion of the Innate Immune Response in Myeloid Cells
Viruses 2013, 5(1), 1-14; doi:10.3390/v5010001
Received: 7 November 2012 / Revised: 19 December 2012 / Accepted: 19 December 2012 / Published: 21 December 2012
Cited by 6 | PDF Full-text (352 KB) | HTML Full-text | XML Full-text
Abstract
The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of [...] Read more.
The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of virally encoded proteins that are necessary to infect myeloid cells, a better understanding of cellular intrinsic antiviral strategies has now been achieved. Recent findings have provided insight into how the lentiviral accessory proteins, Vpx, Vpr and Vif counteract antiviral factors found in myeloid cells including SAMHD1, APOBEC3G, APOBEC3A, UNG2 and uracil. Here we review our current understanding of the molecular basis of how cellular antiviral factors function and the viral countermeasures that antagonize them to promote viral transmission and spread. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview A Genetic Approach to the Development of New Therapeutic Phages to Fight Pseudomonas Aeruginosa in Wound Infections
Viruses 2013, 5(1), 15-53; doi:10.3390/v5010015
Received: 10 November 2012 / Revised: 3 December 2012 / Accepted: 12 December 2012 / Published: 21 December 2012
Cited by 18 | PDF Full-text (679 KB) | HTML Full-text | XML Full-text
Abstract
Pseudomonas aeruginosa is a frequent participant in wound infections. Emergence of multiple antibiotic resistant strains has created significant problems in the treatment of infected wounds. Phage therapy (PT) has been proposed as a possible alternative approach. Infected wounds are the perfect place [...] Read more.
Pseudomonas aeruginosa is a frequent participant in wound infections. Emergence of multiple antibiotic resistant strains has created significant problems in the treatment of infected wounds. Phage therapy (PT) has been proposed as a possible alternative approach. Infected wounds are the perfect place for PT applications, since the basic condition for PT is ensured; namely, the direct contact of bacteria and their viruses. Plenty of virulent (“lytic”) and temperate (“lysogenic”) bacteriophages are known in P. aeruginosa. However, the number of virulent phage species acceptable for PT and their mutability are limited. Besides, there are different deviations in the behavior of virulent (and temperate) phages from their expected canonical models of development. We consider some examples of non-canonical phage-bacterium interactions and the possibility of their use in PT. In addition, some optimal approaches to the development of phage therapy will be discussed from the point of view of a biologist, considering the danger of phage-assisted horizontal gene transfer (HGT), and from the point of view of a surgeon who has accepted the Hippocrates Oath to cure patients by all possible means. It is also time now to discuss the possible approaches in international cooperation for the development of PT. We think it would be advantageous to make phage therapy a kind of personalized medicine. Full article
(This article belongs to the Special Issue Recent Progress in Bacteriophage Research) Print Edition available
Open AccessReview Utility of the Bacteriophage RB69 Polymerase gp43 as a Surrogate Enzyme for Herpesvirus Orthologs
Viruses 2013, 5(1), 54-86; doi:10.3390/v5010054
Received: 1 December 2012 / Revised: 16 December 2012 / Accepted: 17 December 2012 / Published: 8 January 2013
Cited by 5 | PDF Full-text (7738 KB) | HTML Full-text | XML Full-text
Abstract
Viral polymerases are important targets in drug discovery and development efforts. Most antiviral compounds that are currently approved for treatment of infection with members of the herpesviridae family were shown to inhibit the viral DNA polymerase. However, biochemical studies that shed light [...] Read more.
Viral polymerases are important targets in drug discovery and development efforts. Most antiviral compounds that are currently approved for treatment of infection with members of the herpesviridae family were shown to inhibit the viral DNA polymerase. However, biochemical studies that shed light on mechanisms of drug action and resistance are hampered primarily due to technical problems associated with enzyme expression and purification. In contrast, the orthologous bacteriophage RB69 polymerase gp43 has been crystallized in various forms and therefore serves as a model system that provides a better understanding of structure–function relationships of polymerases that belong the type B family. This review aims to discuss strengths, limitations, and opportunities of the phage surrogate with emphasis placed on its utility in the discovery and development of anti-herpetic drugs. Full article
(This article belongs to the Special Issue Recent Progress in Bacteriophage Research) Print Edition available
Open AccessReview Human Metapneumovirus in Adults
Viruses 2013, 5(1), 87-110; doi:10.3390/v5010087
Received: 30 November 2012 / Revised: 17 December 2012 / Accepted: 19 December 2012 / Published: 8 January 2013
Cited by 12 | PDF Full-text (246 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Human metapneumovirus (HMPV) is a relative newly described virus. It was first isolated in 2001 and currently appears to be one of the most significant and common human viral infections. Retrospective serologic studies demonstrated the presence of HMPV antibodies in humans more [...] Read more.
Human metapneumovirus (HMPV) is a relative newly described virus. It was first isolated in 2001 and currently appears to be one of the most significant and common human viral infections. Retrospective serologic studies demonstrated the presence of HMPV antibodies in humans more than 50 years earlier. Although the virus was primarily known as causative agent of respiratory tract infections in children, HMPV is an important cause of respiratory infections in adults as well. Almost all children are infected by HMPV below the age of five; the repeated infections throughout life indicate transient immunity. HMPV infections usually are mild and self-limiting, but in the frail elderly and the immunocompromised patients, the clinical course can be complicated. Since culturing the virus is relatively difficult, diagnosis is mostly based on a nucleic acid amplification test, such as reverse transcriptase polymerase chain reaction. To date, no vaccine is available and treatment is supportive. However, ongoing research shows encouraging results. The aim of this paper is to review the current literature concerning HMPV infections in adults, and discuss recent development in treatment and vaccination. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
Open AccessReview Approaches for Identification of HIV-1 Entry Inhibitors Targeting gp41 Pocket
Viruses 2013, 5(1), 127-149; doi:10.3390/v5010127
Received: 3 December 2012 / Revised: 3 January 2013 / Accepted: 3 January 2013 / Published: 11 January 2013
Cited by 11 | PDF Full-text (600 KB) | HTML Full-text | XML Full-text
Abstract
The hydrophobic pocket in the HIV-1 gp41 N-terminal heptad repeat (NHR) domain plays an important role in viral fusion and entry into the host cell, and serves as an attractive target for development of HIV-1 fusion/entry inhibitors. The peptide anti-HIV drug targeting [...] Read more.
The hydrophobic pocket in the HIV-1 gp41 N-terminal heptad repeat (NHR) domain plays an important role in viral fusion and entry into the host cell, and serves as an attractive target for development of HIV-1 fusion/entry inhibitors. The peptide anti-HIV drug targeting gp41 NHR, T-20 (generic name: enfuvirtide; brand name: Fuzeon), was approved by the U.S. FDA in 2003 as the first HIV fusion/entry inhibitor for treatment of HIV/AIDS patients who fail to respond to the current antiretroviral drugs. However, because T20 lacks the pocket-binding domain (PBD), it exhibits low anti-HIV-1 activity and short half-life. Therefore, several next-generation HIV fusion inhibitory peptides with PBD have been developed. They possess longer half-life and more potent antiviral activity against a broad spectrum of HIV-1 strains, including the T-20-resistant variants. Nonetheless, the clinical application of these peptides is still limited by the lack of oral availability and the high cost of production. Thus, development of small molecule compounds targeting the gp41 pocket with oral availability has been promoted. This review describes the main approaches for identification of HIV fusion/entry inhibitors targeting the gp41 pocket and summarizes the latest progress in developing these inhibitors as a new class of anti-HIV drugs. Full article
(This article belongs to the Special Issue Viral Entry Inhibitors)
Open AccessReview Insights into the Roles of Cyclophilin A During Influenza Virus Infection
Viruses 2013, 5(1), 182-191; doi:10.3390/v5010182
Received: 22 November 2012 / Revised: 22 December 2012 / Accepted: 9 January 2013 / Published: 15 January 2013
Cited by 9 | PDF Full-text (274 KB) | HTML Full-text | XML Full-text
Abstract
Cyclophilin A (CypA) is the main member of the immunophilin superfamily that has peptidyl-prolyl cis-trans isomerase activity. CypA participates in protein folding, cell signaling, inflammation and tumorigenesis. Further, CypA plays critical roles in the replication of several viruses. Upon influenza virus infection, [...] Read more.
Cyclophilin A (CypA) is the main member of the immunophilin superfamily that has peptidyl-prolyl cis-trans isomerase activity. CypA participates in protein folding, cell signaling, inflammation and tumorigenesis. Further, CypA plays critical roles in the replication of several viruses. Upon influenza virus infection, CypA inhibits viral replication by interacting with the M1 protein. In addition, CypA is incorporated into the influenza virus virions. Finally, Cyclosporin A (CsA), the main inhibitor of CypA, inhibits influenza virus replication through CypA-dependent and -independent pathways. This review briefly summarizes recent advances in understanding the roles of CypA during influenza virus infection. Full article
(This article belongs to the Special Issue Cyclophilins and Viruses)
Open AccessReview Breaking In: Human Metapneumovirus Fusion and Entry
Viruses 2013, 5(1), 192-210; doi:10.3390/v5010192
Received: 14 December 2012 / Revised: 9 January 2013 / Accepted: 10 January 2013 / Published: 16 January 2013
Cited by 5 | PDF Full-text (465 KB) | HTML Full-text | XML Full-text
Abstract
Human metapneumovirus (HMPV) is a leading cause of respiratory infection that causes upper airway and severe lower respiratory tract infections. HMPV infection is initiated by viral surface glycoproteins that attach to cellular receptors and mediate virus membrane fusion with cellular membranes. Most [...] Read more.
Human metapneumovirus (HMPV) is a leading cause of respiratory infection that causes upper airway and severe lower respiratory tract infections. HMPV infection is initiated by viral surface glycoproteins that attach to cellular receptors and mediate virus membrane fusion with cellular membranes. Most paramyxoviruses use two viral glycoproteins to facilitate virus entry—an attachment protein and a fusion (F) protein. However, membrane fusion for the human paramyxoviruses in the Pneumovirus subfamily, HMPV and respiratory syncytial virus (hRSV), is unique in that the F protein drives fusion in the absence of a separate viral attachment protein. Thus, pneumovirus F proteins can perform the necessary functions for virus entry, i.e., attachment and fusion. In this review, we discuss recent advances in the understanding of how HMPV F mediates both attachment and fusion. We review the requirements for HMPV viral surface glycoproteins during entry and infection, and review the identification of cellular receptors for HMPV F. We also review our current understanding of how HMPV F mediates fusion, concentrating on structural regions of the protein that appear to be critical for membrane fusion activity. Finally, we illuminate key unanswered questions and suggest how further studies can elucidate how this clinically important paramyxovirus fusion protein may have evolved to initiate infection by a unique mechanism. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
Open AccessReview Respiratory Syncytial Virus Entry Inhibitors Targeting the F Protein
Viruses 2013, 5(1), 211-225; doi:10.3390/v5010211
Received: 7 December 2012 / Revised: 17 December 2012 / Accepted: 11 January 2013 / Published: 16 January 2013
Cited by 18 | PDF Full-text (1058 KB) | HTML Full-text | XML Full-text
Abstract
Human respiratory syncytial virus (RSV) is the main viral cause of respiratory tract infection in infants as well as some elderly and high-risk adults with chronic pulmonary disease and the severely immunocompromised. So far, no specific anti-RSV therapeutics or effective anti-RSV [...] Read more.
Human respiratory syncytial virus (RSV) is the main viral cause of respiratory tract infection in infants as well as some elderly and high-risk adults with chronic pulmonary disease and the severely immunocompromised. So far, no specific anti-RSV therapeutics or effective anti-RSV vaccines have been reported. Only one humanized monoclonal antibody, Palivizumab, has been approved for use in high-risk infants to prevent RSV infection. Ribavirin is the only drug licensed for therapy of RSV infection, but its clinical use is limited by its nonspecific anti-RSV activity, toxic effect, and relatively high cost. Therefore, development of novel effective anti-RSV therapeutics is urgently needed. The RSV envelope glycoprotein F plays an important role in RSV fusion with, and entry into, the host cell and, consequently, serves as an attractive target for developing RSV entry inhibitors. This article reviews advances made in studies of the structure and function of the F protein and the development of RSV entry inhibitors targeting it. Full article
(This article belongs to the Special Issue Viral Entry Inhibitors)
Open AccessReview Potential Cellular Functions of Epstein-Barr Nuclear Antigen 1 (EBNA1) of Epstein-Barr Virus
Viruses 2013, 5(1), 226-240; doi:10.3390/v5010226
Received: 5 December 2012 / Revised: 23 December 2012 / Accepted: 11 January 2013 / Published: 16 January 2013
Cited by 16 | PDF Full-text (260 KB) | HTML Full-text | XML Full-text
Abstract
Epstein-Barr Nuclear Antigen 1 (EBNA1) is a multifunctional protein encoded by EBV. EBNA1’s role in maintaining EBV in latently proliferating cells, by mediating EBV genome synthesis and nonrandom partitioning to daughter cells, as well as regulating viral gene transcription, is well characterized. [...] Read more.
Epstein-Barr Nuclear Antigen 1 (EBNA1) is a multifunctional protein encoded by EBV. EBNA1’s role in maintaining EBV in latently proliferating cells, by mediating EBV genome synthesis and nonrandom partitioning to daughter cells, as well as regulating viral gene transcription, is well characterized. Less understood are the roles of EBNA1 in affecting the host cell to provide selective advantages to those cells that harbor EBV. In this review we will focus on the interactions between EBNA1 and the host cell that may provide EBV-infected cells selective advantages beyond the maintenance of EBV. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)
Open AccessReview Arenavirus Variations Due to Host-Specific Adaptation
Viruses 2013, 5(1), 241-278; doi:10.3390/v5010241
Received: 12 December 2012 / Revised: 11 January 2013 / Accepted: 14 January 2013 / Published: 17 January 2013
Cited by 11 | PDF Full-text (862 KB) | HTML Full-text | XML Full-text
Abstract
Arenavirus particles are enveloped and contain two single-strand RNA genomic segments with ambisense coding. Genetic plasticity of the arenaviruses comes from transcription errors, segment reassortment, and permissive genomic packaging, and results in their remarkable ability, as a group, to infect a wide [...] Read more.
Arenavirus particles are enveloped and contain two single-strand RNA genomic segments with ambisense coding. Genetic plasticity of the arenaviruses comes from transcription errors, segment reassortment, and permissive genomic packaging, and results in their remarkable ability, as a group, to infect a wide variety of hosts. In this review, we discuss some in vitro studies of virus genetic and phenotypic variation after exposure to selective pressures such as high viral dose, mutagens and antivirals. Additionally, we discuss the variation in vivo of selected isolates of Old World arenaviruses, particularly after infection of different animal species. We also discuss the recent emergence of new arenaviruses in the context of our observations of sequence variations that appear to be host-specific. Full article
(This article belongs to the Special Issue Arenaviruses)
Open AccessReview Pathogenic Mechanisms Involved in the Hematological Alterations of Arenavirus-induced Hemorrhagic Fevers
Viruses 2013, 5(1), 340-351; doi:10.3390/v5010340
Received: 22 December 2012 / Revised: 17 January 2013 / Accepted: 18 January 2013 / Published: 21 January 2013
Cited by 6 | PDF Full-text (476 KB) | HTML Full-text | XML Full-text
Abstract
Viral hemorrhagic fevers (VHFs) caused by arenaviruses are acute diseases characterized by fever, headache, general malaise, impaired cellular immunity, eventual neurologic involvement, and hemostatic alterations that may ultimately lead to shock and death. The causes of the bleeding are still poorly understood. [...] Read more.
Viral hemorrhagic fevers (VHFs) caused by arenaviruses are acute diseases characterized by fever, headache, general malaise, impaired cellular immunity, eventual neurologic involvement, and hemostatic alterations that may ultimately lead to shock and death. The causes of the bleeding are still poorly understood. However, it is generally accepted that these causes are associated to some degree with impaired hemostasis, endothelial cell dysfunction and low platelet counts or function. In this article, we present the current knowledge about the hematological alterations present in VHF induced by arenaviruses, including new aspects on the underlying pathogenic mechanisms. Full article
(This article belongs to the Special Issue Arenaviruses)
Open AccessReview Influenza A Virus Entry Inhibitors Targeting the Hemagglutinin
Viruses 2013, 5(1), 352-373; doi:10.3390/v5010352
Received: 14 December 2012 / Revised: 17 January 2013 / Accepted: 21 January 2013 / Published: 22 January 2013
Cited by 27 | PDF Full-text (365 KB) | HTML Full-text | XML Full-text
Abstract
Influenza A virus (IAV) has caused seasonal influenza epidemics and influenza pandemics, which resulted in serious threat to public health and socioeconomic impacts. Until now, only 5 drugs belong to two categories are used for prophylaxis and treatment of IAV infection. Hemagglutinin [...] Read more.
Influenza A virus (IAV) has caused seasonal influenza epidemics and influenza pandemics, which resulted in serious threat to public health and socioeconomic impacts. Until now, only 5 drugs belong to two categories are used for prophylaxis and treatment of IAV infection. Hemagglutinin (HA), the envelope glycoprotein of IAV, plays a critical role in viral binding, fusion and entry. Therefore, HA is an attractive target for developing anti‑IAV drugs to block the entry step of IAV infection. Here we reviewed the recent progress in the study of conformational changes of HA during viral fusion process and the development of HA-based IAV entry inhibitors, which may provide a new choice for controlling future influenza pandemics. Full article
(This article belongs to the Special Issue Viral Entry Inhibitors)
Open AccessReview Cellular Aspects of Prion Replication In Vitro
Viruses 2013, 5(1), 374-405; doi:10.3390/v5010374
Received: 12 December 2012 / Revised: 7 January 2013 / Accepted: 16 January 2013 / Published: 22 January 2013
Cited by 12 | PDF Full-text (753 KB) | HTML Full-text | XML Full-text
Abstract
Prion diseases or transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative disorders in mammals that are caused by unconventional agents predominantly composed of aggregated misfolded prion protein (PrP). Prions self-propagate by recruitment of host-encoded PrP into highly ordered b-sheet rich aggregates. Prion [...] Read more.
Prion diseases or transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative disorders in mammals that are caused by unconventional agents predominantly composed of aggregated misfolded prion protein (PrP). Prions self-propagate by recruitment of host-encoded PrP into highly ordered b-sheet rich aggregates. Prion strains differ in their clinical, pathological and biochemical characteristics and are likely to be the consequence of distinct abnormal prion protein conformers that stably replicate their alternate states in the host cell. Understanding prion cell biology is fundamental for identifying potential drug targets for disease intervention. The development of permissive cell culture models has greatly enhanced our knowledge on entry, propagation and dissemination of TSE agents. However, despite extensive research, the precise mechanism of prion infection and potential strain effects remain enigmatic. This review summarizes our current knowledge of the cell biology and propagation of prions derived from cell culture experiments. We discuss recent findings on the trafficking of cellular and pathologic PrP, the potential sites of abnormal prion protein synthesis and potential co-factors involved in prion entry and propagation. Full article
(This article belongs to the Special Issue Recent Developments in the Prion Field)
Open AccessReview Apoptosis in Pneumovirus Infection
Viruses 2013, 5(1), 406-422; doi:10.3390/v5010406
Received: 30 November 2012 / Revised: 15 January 2013 / Accepted: 18 January 2013 / Published: 23 January 2013
Cited by 3 | PDF Full-text (882 KB) | HTML Full-text | XML Full-text
Abstract
Pneumovirus infections cause a wide spectrum of respiratory disease in humans and animals. The airway epithelium is the major site of pneumovirus replication. Apoptosis or regulated cell death, may contribute to the host anti-viral response by limiting viral replication. However, apoptosis of [...] Read more.
Pneumovirus infections cause a wide spectrum of respiratory disease in humans and animals. The airway epithelium is the major site of pneumovirus replication. Apoptosis or regulated cell death, may contribute to the host anti-viral response by limiting viral replication. However, apoptosis of lung epithelial cells may also exacerbate lung injury, depending on the extent, the timing and specific location in the lungs. Differential apoptotic responses of epithelial cells versus innate immune cells (e.g., neutrophils, macrophages) during pneumovirus infection can further contribute to the complex and delicate balance between host defense and disease pathogenesis. The purpose of this manuscript is to give an overview of the role of apoptosis in pneumovirus infection. We will examine clinical and experimental data concerning the various pro-apoptotic stimuli and the roles of apoptotic epithelial and innate immune cells during pneumovirus disease. Finally, we will discuss potential therapeutic interventions targeting apoptosis in the lungs. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)

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