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Viruses, Volume 5, Issue 3 (March 2013), Pages 777-1022

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Research

Jump to: Review, Other

Open AccessArticle Mutation Distribution in the NSP4 Protein in Rotaviruses Isolated from Mexican Children with Moderate to Severe Gastroenteritis
Viruses 2013, 5(3), 792-805; doi:10.3390/v5030792
Received: 13 February 2013 / Revised: 4 March 2013 / Accepted: 5 March 2013 / Published: 11 March 2013
Cited by 3 | PDF Full-text (530 KB) | HTML Full-text | XML Full-text
Abstract
The NSP4 protein is a multifunctional protein that plays a role in the morphogenesis and pathogenesis of the rotavirus. Although NSP4 is considered an enterotoxin, the relationship between gastroenteritis severity and amino acid variations in NSP4 of the human rotavirus remains unclear. [...] Read more.
The NSP4 protein is a multifunctional protein that plays a role in the morphogenesis and pathogenesis of the rotavirus. Although NSP4 is considered an enterotoxin, the relationship between gastroenteritis severity and amino acid variations in NSP4 of the human rotavirus remains unclear. In this study, we analyzed the sequence diversity of NSP4 and the severity of gastroenteritis of children with moderate to severe gastroenteritis. The rotavirus-infected children were hospitalized before the rotavirus vaccine program in Mexico. All children had diarrhea within 1-4 days, 44 (88%) were vomiting and 35 (70%) had fevers. The severity analysis showed that 13 (26%) cases had mild gastroenteritis, 23 (46%) moderate gastroenteritis and 14 (28%) severe. NSP4 phylogenetic analysis showed three clusters within the genotype E1. Sequence analysis revealed similar mutations inside each cluster, and an uncommon variation in residue 144 was found in five of the Mexican NSP4 sequences. Most of the amino acid variations were located in the VP4 and VP6 binding site domains, with no relationship to different grades of gastroenteritis. This finding indicates that severe gastroenteritis caused by the rotavirus appears to be related to diverse viral or cellular factors instead of NSP4 activity as a unique pathogenic factor. Full article
Open AccessArticle Fragment Merger: An Online Tool to Merge Overlapping Long Sequence Fragments
Viruses 2013, 5(3), 824-833; doi:10.3390/v5030824
Received: 16 January 2013 / Revised: 26 February 2013 / Accepted: 26 February 2013 / Published: 12 March 2013
Cited by 4 | PDF Full-text (491 KB) | HTML Full-text | XML Full-text
Abstract
While PCR amplicons extend to a few thousand bases, the length of sequences from direct Sanger sequencing is limited to 500–800 nucleotides. Therefore, several fragments may be required to cover an amplicon, a gene or an entire genome. These fragments are typically [...] Read more.
While PCR amplicons extend to a few thousand bases, the length of sequences from direct Sanger sequencing is limited to 500–800 nucleotides. Therefore, several fragments may be required to cover an amplicon, a gene or an entire genome. These fragments are typically sequenced in an overlapping fashion and assembled by manually sliding and aligning the sequences visually. This is time-consuming, repetitive and error-prone, and further complicated by circular genomes. An online tool merging two to twelve long overlapping sequence fragments was developed. Either chromatograms or FASTA files are submitted to the tool, which trims poor quality ends of chromatograms according to user-specified parameters. Fragments are assembled into a single sequence by repeatedly calling the EMBOSS merger tool in a consecutive manner. Output includes the number of trimmed nucleotides, details of each merge, and an optional alignment to a reference sequence. The final merge sequence is displayed and can be downloaded in FASTA format. All output files can be downloaded as a ZIP archive. This tool allows for easy and automated assembly of overlapping sequences and is aimed at researchers without specialist computer skills. The tool is genome- and organism-agnostic and has been developed using hepatitis B virus sequence data. Full article
Open AccessArticle Lost in Transcription: Molecular Mechanisms that Control HIV Latency
Viruses 2013, 5(3), 902-927; doi:10.3390/v5030902
Received: 27 February 2013 / Revised: 15 March 2013 / Accepted: 18 March 2013 / Published: 21 March 2013
Cited by 22 | PDF Full-text (899 KB) | HTML Full-text | XML Full-text
Abstract
Highly active antiretroviral therapy (HAART) has limited the replication and spread of the human immunodeficiency virus (HIV). However, despite treatment, HIV infection persists in latently infected reservoirs, and once therapy is interrupted, viral replication rebounds quickly. Extensive efforts are being directed at [...] Read more.
Highly active antiretroviral therapy (HAART) has limited the replication and spread of the human immunodeficiency virus (HIV). However, despite treatment, HIV infection persists in latently infected reservoirs, and once therapy is interrupted, viral replication rebounds quickly. Extensive efforts are being directed at eliminating these cell reservoirs. This feat can be achieved by reactivating latent HIV while administering drugs that prevent new rounds of infection and allow the immune system to clear the virus. However, current approaches to HIV eradication have not been effective. Moreover, as HIV latency is multifactorial, the significance of each of its molecular mechanisms is still under debate. Among these, transcriptional repression as a result of reduced levels and activity of the positive transcription elongation factor b (P-TEFb: CDK9/cyclin T) plays a significant role. Therefore, increasing levels of P-TEFb expression and activity is an excellent strategy to stimulate viral gene expression. This review summarizes the multiple steps that cause HIV to enter into latency. It positions the interplay between transcriptionally active and inactive host transcriptional activators and their viral partner Tat as valid targets for the development of new strategies to reactivate latent viral gene expression and eradicate HIV. Full article
(This article belongs to the Special Issue HIV Latency)
Open AccessArticle Protective Effect of Surfactant Protein D in Pulmonary Vaccinia Virus Infection: Implication of A27 Viral Protein
Viruses 2013, 5(3), 928-953; doi:10.3390/v5030928
Received: 11 February 2013 / Revised: 11 March 2013 / Accepted: 12 March 2013 / Published: 21 March 2013
Cited by 2 | PDF Full-text (931 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Vaccinia virus (VACV) was used as a surrogate of variola virus (VARV) (genus Orthopoxvirus), the causative agent of smallpox, to study Orthopoxvirus infection. VARV is principally transmitted between humans by aerosol droplets. Once inhaled, VARV first infects the respiratory tract where [...] Read more.
Vaccinia virus (VACV) was used as a surrogate of variola virus (VARV) (genus Orthopoxvirus), the causative agent of smallpox, to study Orthopoxvirus infection. VARV is principally transmitted between humans by aerosol droplets. Once inhaled, VARV first infects the respiratory tract where it could encounter surfactant components, such as soluble pattern recognition receptors. Surfactant protein D (SP-D), constitutively present in the lining fluids of the respiratory tract, plays important roles in innate host defense against virus infection. We investigated the role of SP-D in VACV infection and studied the A27 viral protein involvement in the interaction with SP-D. Interaction between SP-D and VACV caused viral inhibition in a lung cell model. Interaction of SP-D with VACV was mediated by the A27 viral protein. Binding required Ca2+ and interactions were blocked in the presence of excess of SP-D saccharide ligands. A27, which lacks glycosylation, directly interacted with SP-D. The interaction between SP-D and the viral particle was also observed using electron microscopy. Infection of mice lacking SP-D (SP-D-/-) resulted in increased mortality compared to SP-D+/+ mice. Altogether, our data show that SP-D participates in host defense against the vaccinia virus infection and that the interaction occurs with the viral surface protein A27. Full article
(This article belongs to the Section Animal Viruses)
Open AccessArticle Correlation of Naturally Occurring HIV-1 Resistance to DEB025 with Capsid Amino Acid Polymorphisms
Viruses 2013, 5(3), 981-997; doi:10.3390/v5030981
Received: 1 March 2013 / Revised: 18 March 2013 / Accepted: 20 March 2013 / Published: 22 March 2013
Cited by 7 | PDF Full-text (407 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
DEB025 (alisporivir) is a synthetic cyclosporine with inhibitory activity against human immunodeficiency virus type-1 (HIV-1) and hepatitis C virus (HCV). It binds to cyclophilin A (CypA) and blocks essential functions of CypA in the viral replication cycles of both viruses. DEB025 inhibits [...] Read more.
DEB025 (alisporivir) is a synthetic cyclosporine with inhibitory activity against human immunodeficiency virus type-1 (HIV-1) and hepatitis C virus (HCV). It binds to cyclophilin A (CypA) and blocks essential functions of CypA in the viral replication cycles of both viruses. DEB025 inhibits clinical HIV-1 isolates in vitro and decreases HIV-1 virus load in the majority of patients. HIV-1 isolates being naturally resistant to DEB025 have been detected in vitro and in nonresponder patients. By sequence analysis of their capsid protein (CA) region, two amino acid polymorphisms that correlated with DEB025 resistance were identified: H87Q and I91N, both located in the CypA-binding loop of the CA protein of HIV-1. The H87Q change was by far more abundant than I91N. Additional polymorphisms in the CypA-binding loop (positions 86, 91 and 96), as well as in the N-terminal loop of CA were detected in resistant isolates and are assumed to contribute to the degree of resistance. These amino acid changes may modulate the conformation of the CypA-binding loop of CA in such a way that binding and/or isomerase function of CypA are no longer necessary for virus replication. The resistant HIV-1 isolates thus are CypA-independent. Full article
(This article belongs to the Special Issue Cyclophilins and Viruses)

Review

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Open AccessReview Th17 Lymphocytes in Respiratory Syncytial Virus Infection
Viruses 2013, 5(3), 777-791; doi:10.3390/v5030777
Received: 23 January 2013 / Revised: 22 February 2013 / Accepted: 25 February 2013 / Published: 5 March 2013
Cited by 17 | PDF Full-text (475 KB) | HTML Full-text | XML Full-text
Abstract
Infection by respiratory syncytial virus (RSV) affects approximately 33 million infants annually worldwide and is a major cause of hospitalizations. Helper T lymphocytes (Th) play a central role in the immune response during such infections. However, Th lymphocytes that produce interleukin 17 [...] Read more.
Infection by respiratory syncytial virus (RSV) affects approximately 33 million infants annually worldwide and is a major cause of hospitalizations. Helper T lymphocytes (Th) play a central role in the immune response during such infections. However, Th lymphocytes that produce interleukin 17 (IL-17), known as Th17 lymphocytes, in addition to been protective can also cause pathology that accompany this type of infection. The protective effects of Th17 is associated with better prognosis in most infected individuals but heightened Th17 responses causes inflammation and pathology in others. Studies employing animal models haves shown that activated Th17 lymphocytes recruit neutrophils and facilitate tertiary lymphoid structure development in infected lungs. However, IL-17 also inhibits the ability of CD8+ lymphocytes to clear viral particles and acts synergistically with the innate immune system to exacerbate inflammation. Furthermore, IL-17 enhances IL-13 production which, in turn, promotes the activation of Th2 lymphocytes and excessive mucus production. Studies of these animal models have also shown that a lack of, or inadequate, responses by the Th1 subset of T lymphocytes enhances Th17-mediated responses and that this is detrimental during RSV co-infection in experimental asthma. The available evidence, therefore, indicates that Th17 can play contradictory roles during RSV infections. The factors that determine the shift in the balance between beneficial and adverse Th17 mediated effects during RSV infection remains to be determined. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
Open AccessReview Understanding Bacteriophage Specificity in Natural Microbial Communities
Viruses 2013, 5(3), 806-823; doi:10.3390/v5030806
Received: 12 February 2013 / Revised: 1 March 2013 / Accepted: 6 March 2013 / Published: 11 March 2013
Cited by 33 | PDF Full-text (733 KB) | HTML Full-text | XML Full-text
Abstract
Studying the coevolutionary dynamics between bacteria and the bacteriophage viruses that infect them is critical to understanding both microbial diversity and ecosystem functioning. Phages can play a key role in shaping bacterial population dynamics and can significantly alter both intra- and inter-specific [...] Read more.
Studying the coevolutionary dynamics between bacteria and the bacteriophage viruses that infect them is critical to understanding both microbial diversity and ecosystem functioning. Phages can play a key role in shaping bacterial population dynamics and can significantly alter both intra- and inter-specific competition among bacterial hosts. Predicting how phages might influence community stability and apparent competition, however, requires an understanding of how bacteria-phage interaction networks evolve as a function of host diversity and community dynamics. Here, we first review the progress that has been made in understanding phage specificity, including the use of experimental evolution, we then introduce a new dataset on natural bacteriophages collected from the phyllosphere of horse chestnut trees, and finally we highlight that bacterial sensitivity to phage is rarely a binary trait and that this variation should be taken into account and reported. We emphasize that there is currently insufficient evidence to make broad generalizations about phage host range in natural populations, the limits of phage adaptation to novel hosts, or the implications of phage specificity in shaping microbial communities. However, the combination of experimental and genomic approaches with the study of natural communities will allow new insight to the evolution and impact of phage specificity within complex bacterial communities. Full article
(This article belongs to the Special Issue Recent Progress in Bacteriophage Research) Print Edition available
Open AccessReview Antiviral Type I and Type III Interferon Responses in the Central Nervous System
Viruses 2013, 5(3), 834-857; doi:10.3390/v5030834
Received: 4 February 2013 / Revised: 11 March 2013 / Accepted: 12 March 2013 / Published: 15 March 2013
Cited by 16 | PDF Full-text (1001 KB) | HTML Full-text | XML Full-text
Abstract
The central nervous system (CNS) harbors highly differentiated cells, such as neurons that are essential to coordinate the functions of complex organisms. This organ is partly protected by the blood-brain barrier (BBB) from toxic substances and pathogens carried in the bloodstream. Yet, [...] Read more.
The central nervous system (CNS) harbors highly differentiated cells, such as neurons that are essential to coordinate the functions of complex organisms. This organ is partly protected by the blood-brain barrier (BBB) from toxic substances and pathogens carried in the bloodstream. Yet, neurotropic viruses can reach the CNS either by crossing the BBB after viremia, or by exploiting motile infected cells as Trojan horses, or by using axonal transport. Type I and type III interferons (IFNs) are cytokines that are critical to control early steps of viral infections. Deficiencies in the IFN pathway have been associated with fatal viral encephalitis both in humans and mice. Therefore, the IFN system provides an essential protection of the CNS against viral infections. Yet, basal activity of the IFN system appears to be low within the CNS, likely owing to the toxicity of IFN to this organ. Moreover, after viral infection, neurons and oligodendrocytes were reported to be relatively poor IFN producers and appear to keep some susceptibility to neurotropic viruses, even in the presence of IFN. This review addresses some trends and recent developments concerning the role of type I and type III IFNs in: i) preventing neuroinvasion and infection of CNS cells; ii) the identity of IFN-producing cells in the CNS; iii) the antiviral activity of ISGs; and iv) the activity of viral proteins of neurotropic viruses that target the IFN pathway. Full article
(This article belongs to the Special Issue Viral Infections of the CNS)
Open AccessReview Deregulation of Epigenetic Mechanisms by the Hepatitis B Virus X Protein in Hepatocarcinogenesis
Viruses 2013, 5(3), 858-872; doi:10.3390/v5030858
Received: 4 February 2013 / Revised: 12 March 2013 / Accepted: 13 March 2013 / Published: 18 March 2013
Cited by 13 | PDF Full-text (233 KB) | HTML Full-text | XML Full-text
Abstract
This review focuses on the significance of deregulation of epigenetic mechanisms by the hepatitis B virus (HBV) X protein in hepatocarcinogenesis and HBV replication. Epigenetic mechanisms, DNA methylation, and specific histone modifications, e.g., trimethylation of H3 on lysine-27 or lysine-4, maintain ‘cellular [...] Read more.
This review focuses on the significance of deregulation of epigenetic mechanisms by the hepatitis B virus (HBV) X protein in hepatocarcinogenesis and HBV replication. Epigenetic mechanisms, DNA methylation, and specific histone modifications, e.g., trimethylation of H3 on lysine-27 or lysine-4, maintain ‘cellular memory’ by silencing expression of lineage-inducing factors in stem cells and conversely, of pluripotency factors in differentiated cells. The X protein has been reported to induce expression of DNA methyltransferases (DNMTs), likely promoting epigenetic changes during hepatocarcinogenesis. Furthermore, in cellular and animal models of X-mediated oncogenic transformation, protein levels of chromatin modifying proteins Suz12 and Znf198 are down-regulated. Suz12 is essential for the Polycomb Repressive Complex 2 (PRC2) mediating the repressive trimethylation of H3 on lysine-27 (H3K27me3). Znf198, stabilizes the LSD1-CoREST-HDAC complex that removes, via lysine demethylase1 (LSD1), the activating trimethylation of H3 on lysine-4 (H3K4me3). Down-regulation of Suz12 also occurs in liver tumors of woodchucks chronically infected by woodchuck hepatitis virus, an animal model recapitulating HBV-mediated hepatocarcinogenesis in humans. Significantly, subgroups of HBV-induced liver cancer re-express hepatoblast and fetal markers, and imprinted genes, suggesting hepatocyte reprogramming during oncogenic transformation. Lastly, down-regulation of Suz12 and Znf198 enhances HBV replication. Collectively, these observations suggest deregulation of epigenetic mechanisms by HBV X protein influences both the viral cycle and the host cell. Full article
(This article belongs to the Special Issue Chromatin Control of Viral Infection) Print Edition available
Open AccessReview RSV Fusion: Time for a New Model
Viruses 2013, 5(3), 873-885; doi:10.3390/v5030873
Received: 21 February 2013 / Revised: 11 March 2013 / Accepted: 15 March 2013 / Published: 19 March 2013
Cited by 12 | PDF Full-text (372 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
In this review we propose a partially hypothetical model of respiratory syncytial virus (RSV) binding and entry to the cell that includes the recently discovered RSV receptor nucleolin, in an attempt to stimulate further inquiry in this research area. RSV binding and [...] Read more.
In this review we propose a partially hypothetical model of respiratory syncytial virus (RSV) binding and entry to the cell that includes the recently discovered RSV receptor nucleolin, in an attempt to stimulate further inquiry in this research area. RSV binding and entry is likely to be a two-step process, the first involving the attachment of the virus to the cell membrane, which may be enhanced by electrostatic interactions with cellular glycoproteins/heparin and the viral G protein, and the second involving fusion to the cell membrane mediated by the viral F protein and a specific cellular fusion receptor. With our recent discovery of nucleolin as a functional fusion receptor for RSV, comes the possibility of a number of new approaches to the development of novel strategies for RSV prophylaxis and therapy, as well as raising some new questions concerning the pathobiology of RSV infection and tropism. Full article
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
Open AccessReview Foamy Virus Assembly with Emphasis on Pol Encapsidation
Viruses 2013, 5(3), 886-900; doi:10.3390/v5030886
Received: 31 January 2013 / Revised: 11 March 2013 / Accepted: 14 March 2013 / Published: 20 March 2013
Cited by 4 | PDF Full-text (306 KB) | HTML Full-text | XML Full-text
Abstract
Foamy viruses (FVs) differ from all other genera of retroviruses (orthoretroviruses) in many aspects of viral replication. In this review, we discuss FV assembly, with special emphasis on Pol incorporation. FV assembly takes place intracellularly, near the pericentriolar region, at a site [...] Read more.
Foamy viruses (FVs) differ from all other genera of retroviruses (orthoretroviruses) in many aspects of viral replication. In this review, we discuss FV assembly, with special emphasis on Pol incorporation. FV assembly takes place intracellularly, near the pericentriolar region, at a site similar to that used by betaretroviruses. The regions of Gag, Pol and genomic RNA required for viral assembly are described. In contrast to orthoretroviral Pol, which is synthesized as a Gag-Pol fusion protein and packaged through Gag-Gag interactions, FV Pol is synthesized from a spliced mRNA lacking all Gag sequences. Thus, encapsidation of FV Pol requires a different mechanism. We detail how WT Pol lacking Gag sequences is incorporated into virus particles. In addition, a mutant in which Pol is expressed as an orthoretroviral-like Gag-Pol fusion protein is discussed. We also discuss temporal regulation of the protease, reverse transcriptase and integrase activities of WT FV Pol. Full article
(This article belongs to the Special Issue Recent Progress in Foamy Virus (FV) Research)
Open AccessReview Hepatitis C Virus-Induced Mitochondrial Dysfunctions
Viruses 2013, 5(3), 954-980; doi:10.3390/v5030954
Received: 22 February 2013 / Revised: 15 March 2013 / Accepted: 20 March 2013 / Published: 21 March 2013
Cited by 17 | PDF Full-text (1631 KB) | HTML Full-text | XML Full-text
Abstract
Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including modification of [...] Read more.
Chronic hepatitis C is characterized by metabolic disorders and a microenvironment in the liver dominated by oxidative stress, inflammation and regeneration processes that lead in the long term to hepatocellular carcinoma. Many lines of evidence suggest that mitochondrial dysfunctions, including modification of metabolic fluxes, generation and elimination of oxidative stress, Ca2+ signaling and apoptosis, play a central role in these processes. However, how these dysfunctions are induced by the virus and whether they play a role in disease progression and neoplastic transformation remains to be determined. Most in vitro studies performed so far have shown that several of the hepatitis C virus (HCV) proteins localize to mitochondria, but the consequences of these interactions on mitochondrial functions remain contradictory, probably due to the use of artificial expression and replication systems. In vivo studies are hampered by the fact that innate and adaptive immune responses will overlay mitochondrial dysfunctions induced directly in the hepatocyte by HCV. Thus, the molecular aspects underlying HCV-induced mitochondrial dysfunctions and their roles in viral replication and the associated pathology need yet to be confirmed in the context of productively replicating virus and physiologically relevant in vitro and in vivo model systems. Full article
(This article belongs to the Special Issue Hepatitis C Pathology)
Open AccessReview Discovering Host Genes Involved in the Infection by the Tomato Yellow Leaf Curl Virus Complex and in the Establishment of Resistance to the Virus Using Tobacco Rattle Virus-based Post Transcriptional Gene Silencing
Viruses 2013, 5(3), 998-1022; doi:10.3390/v5030998
Received: 18 February 2013 / Revised: 20 March 2013 / Accepted: 21 March 2013 / Published: 22 March 2013
Cited by 12 | PDF Full-text (792 KB) | HTML Full-text | XML Full-text
Abstract
The development of high-throughput technologies allows for evaluating gene expression at the whole-genome level. Together with proteomic and metabolomic studies, these analyses have resulted in the identification of plant genes whose function or expression is altered as a consequence of pathogen attacks. [...] Read more.
The development of high-throughput technologies allows for evaluating gene expression at the whole-genome level. Together with proteomic and metabolomic studies, these analyses have resulted in the identification of plant genes whose function or expression is altered as a consequence of pathogen attacks. Members of the Tomato yellow leaf curl virus (TYLCV) complex are among the most important pathogens impairing production of agricultural crops worldwide. To understand how these geminiviruses subjugate plant defenses, and to devise counter-measures, it is essential to identify the host genes affected by infection and to determine their role in susceptible and resistant plants. We have used a reverse genetics approach based on Tobacco rattle virus-induced gene silencing (TRV-VIGS) to uncover genes involved in viral infection of susceptible plants, and to identify genes underlying virus resistance. To identify host genes with a role in geminivirus infection, we have engineered a Nicotiana benthamiana line, coined 2IRGFP, which over-expresses GFP upon virus infection. With this system, we have achieved an accurate description of the dynamics of virus replication in space and time. Upon silencing selected N. benthamiana genes previously shown to be related to host response to geminivirus infection, we have identified eighteen genes involved in a wide array of cellular processes. Plant genes involved in geminivirus resistance were studied by comparing two tomato lines: one resistant (R), the other susceptible (S) to the virus. Sixty-nine genes preferentially expressed in R tomatoes were identified by screening cDNA libraries from infected and uninfected R and S genotypes. Out of the 25 genes studied so far, the silencing of five led to the total collapse of resistance, suggesting their involvement in the resistance gene network. This review of our results indicates that TRV-VIGS is an exquisite reverse genetics tool that may provide new insights into the molecular mechanisms underlying plant infection and resistance to infection by begomoviruses. Full article
(This article belongs to the Special Issue Plant Viruses)

Other

Jump to: Research, Review

Open AccessCorrection Witwer, K.W.; et al. Correction: miRNA Profiles of Monocyte-Lineage Cells Are Consistent with Complicated Roles in HIV-1 Restriction. Viruses 2012, 4, 1844-1864.
Viruses 2013, 5(3), 901; doi:10.3390/v5030901
Received: 17 March 2013 / Accepted: 18 March 2013 / Published: 20 March 2013
PDF Full-text (11 KB) | HTML Full-text | XML Full-text
Abstract A funding designation in our 2012 Viruses publication, doi: 10.3390/v4101844 (Viruses 2012, 4, 1844-1864), contained an incorrect digit. On page 1860, (Acknowledgments), U19 support was incorrectly listed as AI076113. The correct designation is AI096113. [...] Full article

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