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Viruses, Volume 4, Issue 2 (February 2012), Pages 200-324

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Editorial

Jump to: Research, Review

Open AccessEditorial A Plea for Caution: Huge Risks Associated with Lab-bred Flu
Viruses 2012, 4(2), 276-279; doi:10.3390/v4020276
Received: 3 February 2012 / Accepted: 3 February 2012 / Published: 7 February 2012
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Abstract I wish to express concern about the maintenance of laboratory strains of H5N1 influenza viruses that might be adapted for transmission among humans. Full article
(This article belongs to the Section Editorial)

Research

Jump to: Editorial, Review

Open AccessArticle Clinical Characteristics and Genetic Variability of Human Rhinovirus in Mexico
Viruses 2012, 4(2), 200-210; doi:10.3390/v4020200
Received: 15 November 2011 / Revised: 17 January 2012 / Accepted: 17 January 2012 / Published: 25 January 2012
Cited by 8 | PDF Full-text (514 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Human rhinovirus (HRV) is a leading cause of acute respiratory infection (ARI) in young children and infants worldwide and has a high impact on morbidity and mortality in this population. Initially, HRV was classified into two species: HRV-A and HRV-B. Recently, a [...] Read more.
Human rhinovirus (HRV) is a leading cause of acute respiratory infection (ARI) in young children and infants worldwide and has a high impact on morbidity and mortality in this population. Initially, HRV was classified into two species: HRV-A and HRV-B. Recently, a species called HRV-C and possibly another species, HRV-D, were identified. In Mexico, there is little information about the role of HRV as a cause of ARI, and the presence and importance of species such as HRV-C are not known. The aim of this study was to determine the clinical characteristics and genetic variability of HRV in Mexican children. Genetic characterization was carried out by phylogenetic analysis of the 5′-nontranslated region (5′-NTR) of the HRV genome. The results show that the newly identified HRV-C is circulating in Mexican children more frequently than HRV-B but not as frequently as HRV-A, which was the most frequent species. Most of the cases of the three species of HRV were in children under 2 years of age, and all species were associated with very mild and moderate ARI. Full article

Review

Jump to: Editorial, Research

Open AccessReview Back to BAC: The Use of Infectious Clone Technologies for Viral Mutagenesis
Viruses 2012, 4(2), 211-235; doi:10.3390/v4020211
Received: 20 December 2011 / Revised: 26 January 2012 / Accepted: 30 January 2012 / Published: 3 February 2012
Cited by 12 | PDF Full-text (924 KB) | HTML Full-text | XML Full-text
Abstract
Bacterial artificial chromosome (BAC) vectors were first developed to facilitate the propagation and manipulation of large DNA fragments in molecular biology studies for uses such as genome sequencing projects and genetic disease models. To facilitate these studies, methodologies have been developed to [...] Read more.
Bacterial artificial chromosome (BAC) vectors were first developed to facilitate the propagation and manipulation of large DNA fragments in molecular biology studies for uses such as genome sequencing projects and genetic disease models. To facilitate these studies, methodologies have been developed to introduce specific mutations that can be directly applied to the mutagenesis of infectious clones (icBAC) using BAC technologies. This has resulted in rapid identification of gene function and expression at unprecedented rates. Here we review the major developments in BAC mutagenesis in vitro. This review summarises the technologies used to construct and introduce mutations into herpesvirus icBAC. It also explores developing technologies likely to provide the next leap in understanding these important viruses. Full article
Open AccessReview Emerging Viruses in the Felidae: Shifting Paradigms
Viruses 2012, 4(2), 236-257; doi:10.3390/v4020236
Received: 1 December 2011 / Revised: 21 December 2011 / Accepted: 11 January 2012 / Published: 7 February 2012
Cited by 13 | PDF Full-text (1016 KB) | HTML Full-text | XML Full-text
Abstract
The domestic cat is afflicted with multiple viruses that serve as powerful models for human disease including cancers, SARS and HIV/AIDS. Cat viruses that cause these diseases have been studied for decades revealing detailed insight concerning transmission, virulence, origins and pathogenesis. Here we [...] Read more.
The domestic cat is afflicted with multiple viruses that serve as powerful models for human disease including cancers, SARS and HIV/AIDS. Cat viruses that cause these diseases have been studied for decades revealing detailed insight concerning transmission, virulence, origins and pathogenesis. Here we review recent genetic advances that have questioned traditional wisdom regarding the origins of virulent Feline infectious peritonitis (FIP) diseases, the pathogenic potential of Feline Immunodeficiency Virus (FIV) in wild non-domestic Felidae species, and the restriction of Feline Leukemia Virus (FeLV) mediated immune impairment to domestic cats rather than other Felidae species. The most recent interpretations indicate important new evolutionary conclusions implicating these deadly infectious agents in domestic and non-domestic felids. Full article
(This article belongs to the Special Issue Feline Retroviruses)
Open AccessReview Filovirus Entry: A Novelty in the Viral Fusion World
Viruses 2012, 4(2), 258-275; doi:10.3390/v4020258
Received: 23 December 2011 / Revised: 24 January 2012 / Accepted: 30 January 2012 / Published: 7 February 2012
Cited by 30 | PDF Full-text (1888 KB) | HTML Full-text | XML Full-text
Abstract
Ebolavirus (EBOV) and Marburgvirus (MARV) that compose the filovirus family of negative strand RNA viruses infect a broad range of mammalian cells. Recent studies indicate that cellular entry of this family of viruses requires a series of cellular protein interactions and molecular [...] Read more.
Ebolavirus (EBOV) and Marburgvirus (MARV) that compose the filovirus family of negative strand RNA viruses infect a broad range of mammalian cells. Recent studies indicate that cellular entry of this family of viruses requires a series of cellular protein interactions and molecular mechanisms, some of which are unique to filoviruses and others are commonly used by all viral glycoproteins. Details of this entry pathway are highlighted here. Virus entry into cells is initiated by the interaction of the viral glycoprotein1 subunit (GP1) with both adherence factors and one or more receptors on the surface of host cells. On epithelial cells, we recently demonstrated that TIM-1 serves as a receptor for this family of viruses, but the cell surface receptors in other cell types remain unidentified. Upon receptor binding, the virus is internalized into endosomes primarily via macropinocytosis, but perhaps by other mechanisms as well. Within the acidified endosome, the heavily glycosylated GP1 is cleaved to a smaller form by the low pH-dependent cellular proteases Cathepsin L and B, exposing residues in the receptor binding site (RBS). Details of the molecular events following cathepsin-dependent trimming of GP1 are currently incomplete; however, the processed GP1 specifically interacts with endosomal/lysosomal membranes that contain the Niemann Pick C1 (NPC1) protein and expression of NPC1 is required for productive infection, suggesting that GP/NPC1 interactions may be an important late step in the entry process. Additional events such as further GP1 processing and/or reducing events may also be required to generate a fusion-ready form of the glycoprotein. Once this has been achieved, sequences in the filovirus GP2 subunit mediate viral/cellular membrane fusion via mechanisms similar to those previously described for other enveloped viruses. This multi-step entry pathway highlights the complex and highly orchestrated path of internalization and fusion that appears unique for filoviruses. Full article
(This article belongs to the Special Issue Virus-Induced Membrane Fusion)
Open AccessReview Henipavirus Mediated Membrane Fusion, Virus Entry and Targeted Therapeutics
Viruses 2012, 4(2), 280-308; doi:10.3390/v4020280
Received: 30 December 2011 / Revised: 30 January 2012 / Accepted: 30 January 2012 / Published: 13 February 2012
Cited by 18 | PDF Full-text (2277 KB) | HTML Full-text | XML Full-text
Abstract
The Paramyxoviridae genus Henipavirus is presently represented by the type species Hendra and Nipah viruses which are both recently emerged zoonotic viral pathogens responsible for repeated outbreaks associated with high morbidity and mortality in Australia, Southeast Asia, India and Bangladesh. These enveloped [...] Read more.
The Paramyxoviridae genus Henipavirus is presently represented by the type species Hendra and Nipah viruses which are both recently emerged zoonotic viral pathogens responsible for repeated outbreaks associated with high morbidity and mortality in Australia, Southeast Asia, India and Bangladesh. These enveloped viruses bind and enter host target cells through the coordinated activities of their attachment (G) and class I fusion (F) envelope glycoproteins. The henipavirus G glycoprotein interacts with host cellular B class ephrins, triggering conformational alterations in G that lead to the activation of the F glycoprotein, which facilitates the membrane fusion process. Using the recently published structures of HeV-G and NiV-G and other paramyxovirus glycoproteins, we review the features of the henipavirus envelope glycoproteins that appear essential for mediating the viral fusion process, including receptor binding, G-F interaction, F activation, with an emphasis on G and the mutations that disrupt viral infectivity. Finally, recent candidate therapeutics for henipavirus-mediated disease are summarized in light of their ability to inhibit HeV and NiV entry by targeting their G and F glycoproteins. Full article
(This article belongs to the Special Issue Virus-Induced Membrane Fusion)
Open AccessReview Novel Approaches to Inhibit HIV Entry
Viruses 2012, 4(2), 309-324; doi:10.3390/v4020309
Received: 16 December 2011 / Revised: 17 January 2012 / Accepted: 7 February 2012 / Published: 21 February 2012
Cited by 29 | PDF Full-text (913 KB) | HTML Full-text | XML Full-text
Abstract
Human Immunodeficiency Virus (HIV) entry into target cells is a multi-step process involving binding of the viral glycoprotein, Env, to its receptor CD4 and a coreceptor—either CCR5 or CXCR4. Understanding the means by which HIV enters cells has led to the identification [...] Read more.
Human Immunodeficiency Virus (HIV) entry into target cells is a multi-step process involving binding of the viral glycoprotein, Env, to its receptor CD4 and a coreceptor—either CCR5 or CXCR4. Understanding the means by which HIV enters cells has led to the identification of genetic polymorphisms, such as the 32 base-pair deletion in the ccr5 gene (ccr5∆32) that confers resistance to infection in homozygous individuals, and has also resulted in the development of entry inhibitors—small molecule antagonists that block infection at the entry step. The recent demonstration of long-term control of HIV infection in a leukemic patient following a hematopoietic stem cell transplant using cells from a ccr5∆32 homozygous donor highlights the important role of the HIV entry in maintaining an established infection and has led to a number of attempts to treat HIV infection by genetically modifying the ccr5 gene. In this review, we describe the HIV entry process and provide an overview of the different classes of approved HIV entry inhibitors while highlighting novel genetic strategies aimed at blocking HIV infection at the level of entry. Full article
(This article belongs to the Special Issue Virus-Induced Membrane Fusion)

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