Next Issue
Previous Issue

E-Mail Alert

Add your e-mail address to receive forthcoming issues of this journal:

Journal Browser

Journal Browser

Table of Contents

Viruses, Volume 1, Issue 2 (September 2009), Pages 84-334

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
View options order results:
result details:
Displaying articles 1-14
Export citation of selected articles as:

Research

Jump to: Review

Open AccessArticle Molecular Characterization of Viruses from Clinical Respiratory Samples Producing Unidentified Cytopathic Effects in Cell Culture
Viruses 2009, 1(2), 84-90; doi:10.3390/v1020084
Received: 1 July 2009 / Revised: 14 July 2009 / Accepted: 16 July 2009 / Published: 17 July 2009
Cited by 4 | PDF Full-text (42 KB) | HTML Full-text | XML Full-text
Abstract
The sequence-independent single primer amplification (SISPA) method was performed to identify a virus in 17 clinical respiratory samples producing uncharacterized cytopathic effects in LLC-MK2 cells. Sequence analysis of 600-1600 bp amplicons allowed the identification of six viruses (one influenza C, two parechovirus-3 [...] Read more.
The sequence-independent single primer amplification (SISPA) method was performed to identify a virus in 17 clinical respiratory samples producing uncharacterized cytopathic effects in LLC-MK2 cells. Sequence analysis of 600-1600 bp amplicons allowed the identification of six viruses (one influenza C, two parechovirus-3 and three cardioviruses). Genomic sequences of the cardioviruses showed similarities with those of the recently-described Saffold virus strain although significant variation was present in the viral surface EF and CD loops. These results demonstrate the usefulness of SISPA for identifying emerging viruses and also known viruses not easily identified by standard virological methods. Full article
(This article belongs to the Special Issue Newly Identified Respiratory Viruses)
Open AccessArticle Significance of Coronavirus Mutants in Feces and Diseased Tissues of Cats Suffering from Feline Infectious Peritonitis
Viruses 2009, 1(2), 166-184; doi:10.3390/v1020166
Received: 17 July 2009 / Revised: 10 August 2009 / Accepted: 11 August 2009 / Published: 26 August 2009
Cited by 42 | PDF Full-text (157 KB) | HTML Full-text | XML Full-text
Abstract
The internal FECV→FIPV mutation theory and three of its correlates were tested in four sibs/half-sib kittens, a healthy contact cat, and in four unrelated cats that died of FIP at geographically disparate regions. Coronavirus from feces and extraintestinal FIP lesions from the [...] Read more.
The internal FECV→FIPV mutation theory and three of its correlates were tested in four sibs/half-sib kittens, a healthy contact cat, and in four unrelated cats that died of FIP at geographically disparate regions. Coronavirus from feces and extraintestinal FIP lesions from the same cat were always >99% related in accessory and structural gene sequences. SNPs and deletions causing a truncation of the 3c gene product were found in almost all isolates from the diseased tissues of the eight cats suffering from FIP, whereas most, but not all fecal isolates from these same cats had intact 3c genes. Other accessory and structural genes appeared normal in both fecal and lesional viruses. Deliterious mutations in the 3c gene were unique to each cat, indicating that they did not originate in one cat and were subsequently passed horizontally to the others. Compartmentalization of the parental and mutant forms was not absolute; virus of lesional type was sometimes found in feces of affected cats and virus identical to fecal type was occasionally identified in diseased tissues. Although 3c gene mutants in this study were not horizontally transmitted, the parental fecal virus was readily transmitted by contact from a cat that died of FIP to its housemate. There was a high rate of mutability in all structural and accessory genes both within and between cats, leading to minor genetic variants. More than one variant could be identified in both diseased tissues and feces of the same cat. Laboratory cats inoculated with a mixture of two closely related variants from the same FIP cat developed disease from one or the other variant, but not both. Significant genetic drift existed between isolates from geographically distinct regions of the Western US. Full article

Review

Jump to: Research

Open AccessReview HBV-Specific Adaptive Immunity
Viruses 2009, 1(2), 91-103; doi:10.3390/v1020091
Received: 9 June 2009 / Revised: 8 July 2009 / Accepted: 16 July 2009 / Published: 27 July 2009
Cited by 12 | PDF Full-text (196 KB) | HTML Full-text | XML Full-text
Abstract
The successful control of HBV infection requires an efficient expansion of distinct elements of the adaptive immune system (B cells, helper and cytotoxic T cells) that, due to the hepatotropic nature of HBV, need to operate in the liver parenchyma. In this [...] Read more.
The successful control of HBV infection requires an efficient expansion of distinct elements of the adaptive immune system (B cells, helper and cytotoxic T cells) that, due to the hepatotropic nature of HBV, need to operate in the liver parenchyma. In this respect, we will discuss broad features of HBV immunity in patients with resolved or chronic HBV infection and analyze how the liver environment can directly modulate HBV-immunity. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Role of Host Genetic Factors in the Outcome of Hepatitis C Virus Infection
Viruses 2009, 1(2), 104-125; doi:10.3390/v1020104
Received: 16 June 2009 / Revised: 23 July 2009 / Accepted: 28 July 2009 / Published: 5 August 2009
Cited by 12 | PDF Full-text (585 KB) | HTML Full-text | XML Full-text
Abstract
The natural history of hepatitis C virus (HCV) infection is determined by a complex interplay between host genetic, immunological and viral factors. This review highlights genes involved in innate and adaptive immune responses associated with different outcomes of HCV infection. For example, [...] Read more.
The natural history of hepatitis C virus (HCV) infection is determined by a complex interplay between host genetic, immunological and viral factors. This review highlights genes involved in innate and adaptive immune responses associated with different outcomes of HCV infection. For example, an association of HCV clearance with certain HLA alleles has been demonstrated. The mechanisms responsible for these associations have been linked to specific T cell responses for some particular alleles (e.g., HLA-B27). Genetic associations involved in T cell regulation and function further underline the role of the adaptive immune response in the natural history of HCV infection. In addition, some genes involved in innate NK cell responses demonstrate the complex interplay between components of the immune system necessary for a successful host response to HCV infection. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Hepatitis C Virus Infection: Molecular Pathways to Steatosis, Insulin Resistance and Oxidative Stress
Viruses 2009, 1(2), 126-143; doi:10.3390/v1020126
Received: 14 June 2009 / Revised: 27 July 2009 / Accepted: 29 July 2009 / Published: 11 August 2009
Cited by 30 | PDF Full-text (462 KB) | HTML Full-text | XML Full-text
Abstract
The persistent infection with hepatitis C virus is a major cause of chronic liver disease worldwide. However, the morbidity associated with hepatitis C virus widely varies and depends on several host-related cofactors, such as age, gender, alcohol consumption, body weight, and co-infections. [...] Read more.
The persistent infection with hepatitis C virus is a major cause of chronic liver disease worldwide. However, the morbidity associated with hepatitis C virus widely varies and depends on several host-related cofactors, such as age, gender, alcohol consumption, body weight, and co-infections. The objective of this review is to discuss three of these cofactors: steatosis, insulin resistance and oxidative stress. Although all may occur independently of HCV, a direct role of HCV infection in their pathogenesis has been reported. This review summarizes the current understanding and potential molecular pathways by which HCV contributes to their development. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Prophylactic and Therapeutic Vaccination against Hepatitis C Virus (HCV): Developments and Future Perspectives
Viruses 2009, 1(2), 144-165; doi:10.3390/v1020144
Received: 3 June 2009 / Revised: 25 July 2009 / Accepted: 11 August 2009 / Published: 12 August 2009
Cited by 7 | PDF Full-text (291 KB) | HTML Full-text | XML Full-text
Abstract
Studies in patients and chimpanzees that spontaneously clear Hepatitis C Virus (HCV) have demonstrated that natural immunity to the virus is induced during primary infections and that this immunity can be cross protective. These discoveries led to optimism regarding prophylactic HCV vaccines [...] Read more.
Studies in patients and chimpanzees that spontaneously clear Hepatitis C Virus (HCV) have demonstrated that natural immunity to the virus is induced during primary infections and that this immunity can be cross protective. These discoveries led to optimism regarding prophylactic HCV vaccines and a number of studies in the chimpanzee model have been performed, all of which resulted in modified infections after challenge but did not always prevent persistence of the virus. Therapeutic vaccine strategies have also been pursued in an effort to reduce the costs and side effects associated with anti-viral drug treatment. This review summarizes the studies performed thus far in both patients and chimpanzees for prophylactic and therapeutic vaccination, assesses the progress made and future perspectives. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview HBV Life Cycle: Entry and Morphogenesis
Viruses 2009, 1(2), 185-209; doi:10.3390/v1020185
Received: 13 June 2009 / Revised: 31 July 2009 / Accepted: 13 August 2009 / Published: 1 September 2009
Cited by 21 | PDF Full-text (323 KB) | HTML Full-text | XML Full-text
Abstract
Hepatitis B virus (HBV) is a major cause of liver disease. HBV primarily infects hepatocytes by a still poorly understood mechanism. After an endocytotic process, the nucleocapsids are released into the cytoplasm and the relaxed circular rcDNA genome is transported towards the [...] Read more.
Hepatitis B virus (HBV) is a major cause of liver disease. HBV primarily infects hepatocytes by a still poorly understood mechanism. After an endocytotic process, the nucleocapsids are released into the cytoplasm and the relaxed circular rcDNA genome is transported towards the nucleus where it is converted into covalently closed circular cccDNA. Replication of the viral genome occurs via an RNA pregenome (pgRNA) that binds to HBV polymerase (P). P initiates pgRNA encapsidation and reverse transcription inside the capsid. Matured, rcDNA containing nucleocapsids can re-deliver the RC-DNA to the nucleus, or be secreted via interaction with the envelope proteins as progeny virions. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Viroid Intercellular Trafficking: RNA Motifs, Cellular Factors and Broad Impacts
Viruses 2009, 1(2), 210-221; doi:10.3390/v1020210
Received: 29 July 2009 / Revised: 31 August 2009 / Accepted: 1 September 2009 / Published: 1 September 2009
Cited by 9 | PDF Full-text (179 KB) | HTML Full-text | XML Full-text
Abstract
Viroids are noncoding RNAs that infect plants. In order to establish systemic infection, these RNAs must traffic from an initially infected host cell into neighboring cells and ultimately throughout a whole plant. Recent studies have identified structural motifs in a viroid that [...] Read more.
Viroids are noncoding RNAs that infect plants. In order to establish systemic infection, these RNAs must traffic from an initially infected host cell into neighboring cells and ultimately throughout a whole plant. Recent studies have identified structural motifs in a viroid that are required for trafficking, enabling further studies on the mechanisms of their function. Some cellular proteins interact with viroids in vivo and may play a role in viroid trafficking, which can now be directly tested by using a virus-induced gene silencing system that functions efficiently in plant species from which these factors were identified. This review discusses these recent advances, unanswered questions and the use of viroid infection as an highly productive model to elucidate mechanisms of RNA trafficking that is of broad biological significance. Full article
(This article belongs to the Special Issue Subviral RNAs)
Open AccessReview HCV Animal Models: A Journey of More than 30 Years
Viruses 2009, 1(2), 222-240; doi:10.3390/v1020222
Received: 12 June 2009 / Revised: 5 August 2009 / Accepted: 18 August 2009 / Published: 2 September 2009
Cited by 9 | PDF Full-text (218 KB) | HTML Full-text | XML Full-text
Abstract
In the 1970s and 1980s it became increasingly clear that blood transfusions could induce a form of chronic hepatitis that could not be ascribed to any of the viruses known to cause liver inflammation. In 1989, the hepatitis C virus (HCV) was [...] Read more.
In the 1970s and 1980s it became increasingly clear that blood transfusions could induce a form of chronic hepatitis that could not be ascribed to any of the viruses known to cause liver inflammation. In 1989, the hepatitis C virus (HCV) was discovered and found to be the major causative agent of these infections. Because of its narrow ropism, the in vivo study of this virus was, especially in the early days, limited to the chimpanzee. In the past decade, several alternative animal models have been created. In this review we review these novel animal models and their contribution to our current understanding of the biology of HCV. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Evolutionary Constraints to Viroid Evolution
Viruses 2009, 1(2), 241-254; doi:10.3390/v1020241
Received: 10 July 2009 / Revised: 27 August 2009 / Accepted: 27 August 2009 / Published: 2 September 2009
Cited by 7 | PDF Full-text (355 KB) | HTML Full-text | XML Full-text
Abstract
We suggest that viroids are trapped into adaptive peaks as the result of adaptive constraints. The first one is imposed by the necessity to fold into packed structures to escape from RNA silencing. This creates antagonistic epistases, which make future adaptive trajectories [...] Read more.
We suggest that viroids are trapped into adaptive peaks as the result of adaptive constraints. The first one is imposed by the necessity to fold into packed structures to escape from RNA silencing. This creates antagonistic epistases, which make future adaptive trajectories contingent upon the first mutation and slow down the rate of adaptation. This second constraint can only be surpassed by increasing genetic redundancy or by recombination. Eigen’s paradox imposes a limit to the increase in genome complexity in the absence of mechanisms reducing mutation rate. Therefore, recombination appears as the only possible route to evolutionary innovation in viroids. Full article
(This article belongs to the Special Issue Subviral RNAs)
Open AccessReview Regulation of Innate Immune Responses by Bovine Herpesvirus 1 and Infected Cell Protein 0 (bICP0)
Viruses 2009, 1(2), 255-275; doi:10.3390/v1020255
Received: 15 July 2009 / Revised: 24 August 2009 / Accepted: 2 September 2009 / Published: 7 September 2009
Cited by 23 | PDF Full-text (264 KB) | HTML Full-text | XML Full-text
Abstract
Bovine herpesvirus 1 (BoHV-1) infected cell protein 0 (bICP0) is an important transcriptional regulatory protein that stimulates productive infection. In transient transfection assays, bICP0 also inhibits interferon dependent transcription. bICP0 can induce degradation of interferon stimulatory factor 3 (IRF3), a cellular transcription [...] Read more.
Bovine herpesvirus 1 (BoHV-1) infected cell protein 0 (bICP0) is an important transcriptional regulatory protein that stimulates productive infection. In transient transfection assays, bICP0 also inhibits interferon dependent transcription. bICP0 can induce degradation of interferon stimulatory factor 3 (IRF3), a cellular transcription factor that is crucial for activating beta interferon (IFN-β) promoter activity. Recent studies also concluded that interactions between bICP0 and IRF7 inhibit trans-activation of IFN-β promoter activity. The C3HC4 zinc RING (really important new gene) finger located near the amino terminus of bICP0 is important for all known functions of bICP0. A recombinant virus that contains a single amino acid change in a well conserved cysteine residue of the C3HC4 zinc RING finger of bICP0 grows poorly in cultured cells, and does not reactivate from latency in cattle confirming that the C3HC4 zinc RING finger is crucial for viral growth and pathogenesis. A bICP0 deletion mutant does not induce plaques in permissive cells, but induces autophagy in a cell type dependent manner. In summary, the ability of bICP0 to stimulate productive infection, and repress IFN dependent transcription plays a crucial role in the BoHV-1 infection cycle. Full article
(This article belongs to the Special Issue Antiviral Responses to Herpes Viruses)
Open AccessReview Adaptive Immunity to Hepatitis C Virus
Viruses 2009, 1(2), 276-297; doi:10.3390/v1020276
Received: 3 July 2009 / Revised: 14 August 2009 / Accepted: 25 August 2009 / Published: 8 September 2009
PDF Full-text (230 KB) | HTML Full-text | XML Full-text
Abstract
The precise role of adaptive immune responses in the clinical outcome of HCV infection is still only partially defined. Recent studies suggest that viral-host cell interactions during the acute phase of infection are essential for viral clearance or progression into chronic HCV [...] Read more.
The precise role of adaptive immune responses in the clinical outcome of HCV infection is still only partially defined. Recent studies suggest that viral-host cell interactions during the acute phase of infection are essential for viral clearance or progression into chronic HCV infection. This review focuses on different aspects of the adaptive immune responses as determinants of the different outcomes of HCV infection, clearance or persistent infection, and outlines current concepts of HCV evasion strategies. Unravelling these important mechanisms of virus-host interaction will contribute to the development of novel strategies to prevent and control HCV infection. Full article
(This article belongs to the Special Issue Hepatitis Viruses)
Open AccessReview Viroid Pathogenicity: One Process, Many Faces
Viruses 2009, 1(2), 298-316; doi:10.3390/v1020298
Received: 14 July 2009 / Revised: 31 August 2009 / Accepted: 1 September 2009 / Published: 10 September 2009
Cited by 25 | PDF Full-text (357 KB) | HTML Full-text | XML Full-text
Abstract
Despite the non-coding nature of their small RNA genomes, the visible symptoms of viroid infection resemble those associated with many plant virus diseases. Recent evidence indicates that viroid-derived small RNAs acting through host RNA silencing pathways play a key role in viroid [...] Read more.
Despite the non-coding nature of their small RNA genomes, the visible symptoms of viroid infection resemble those associated with many plant virus diseases. Recent evidence indicates that viroid-derived small RNAs acting through host RNA silencing pathways play a key role in viroid pathogenicity. Host responses to viroid infection are complex, involving signaling cascades containing host-encoded protein kinases and crosstalk between hormonal and defense-signaling pathways. Studies of viroid-host interaction in the context of entire biochemical or developmental pathways are just beginning, and many working hypotheses have yet to be critically tested. Full article
(This article belongs to the Special Issue Subviral RNAs)
Open AccessReview Viroid Replication: Rolling-Circles, Enzymes and Ribozymes
Viruses 2009, 1(2), 317-334; doi:10.3390/v1020317
Received: 6 July 2009 / Revised: 9 September 2009 / Accepted: 9 September 2009 / Published: 14 September 2009
Cited by 22 | PDF Full-text (427 KB) | HTML Full-text | XML Full-text
Abstract
Viroids, due to their small size and lack of protein-coding capacity, must rely essentially on their hosts for replication. Intriguingly, viroids have evolved the ability to replicate in two cellular organella, the nucleus (family Pospiviroidae) and the chloroplast (family Avsunviroidae). [...] Read more.
Viroids, due to their small size and lack of protein-coding capacity, must rely essentially on their hosts for replication. Intriguingly, viroids have evolved the ability to replicate in two cellular organella, the nucleus (family Pospiviroidae) and the chloroplast (family Avsunviroidae). Viroid replication proceeds through an RNA-based rolling-circle mechanism with three steps that, with some variations, operate in both polarity strands: i) synthesis of longer-than-unit strands catalyzed by either the nuclear RNA polymerase II or a nuclear-encoded chloroplastic RNA polymerase, in both instances redirected to transcribe RNA templates, ii) cleavage to unit-length, which in the family Avsunviroidae is mediated by hammerhead ribozymes embedded in both polarity strands, while in the family Pospiviroidae the oligomeric RNAs provide the proper conformation but not the catalytic activity, and iii) circularization. The host RNA polymerases, most likely assisted by additional host proteins, start transcription from specific sites, thus implying the existence of viroid promoters. Cleavage and ligation in the family Pospiviroidae is probably catalyzed by an RNase III-like enzyme and an RNA ligase able to circularize the resulting 5’ and 3’ termini. Whether a chloroplastic RNA ligase mediates circularization in the family Avsunviroidae, or this reaction is autocatalytic, remains an open issue. Full article
(This article belongs to the Special Issue Subviral RNAs)

Journal Contact

MDPI AG
Viruses Editorial Office
St. Alban-Anlage 66, 4052 Basel, Switzerland
viruses@mdpi.com
Tel. +41 61 683 77 34
Fax: +41 61 302 89 18
Editorial Board
Contact Details Submit to Viruses
Back to Top