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Viruses Infecting Reptiles  [PDF]
Rachel E. Marschang
Viruses , 2011, DOI: 10.3390/v3112087
Abstract: A large number of viruses have been described in many different reptiles. These viruses include arboviruses that primarily infect mammals or birds as well as viruses that are specific for reptiles. Interest in arboviruses infecting reptiles has mainly focused on the role reptiles may play in the epidemiology of these viruses, especially over winter. Interest in reptile specific viruses has concentrated on both their importance for reptile medicine as well as virus taxonomy and evolution. The impact of many viral infections on reptile health is not known. Koch’s postulates have only been fulfilled for a limited number of reptilian viruses. As diagnostic testing becomes more sensitive, multiple infections with various viruses and other infectious agents are also being detected. In most cases the interactions between these different agents are not known. This review provides an update on viruses described in reptiles, the animal species in which they have been detected, and what is known about their taxonomic positions.
Whole-Genome Analysis of Human Influenza A Virus Reveals Multiple Persistent Lineages and Reassortment among Recent H3N2 Viruses  [PDF]
Edward C. Holmes,Elodie Ghedin,Naomi Miller,Jill Taylor,Yiming Bao,Kirsten St George,Bryan T. Grenfell,Steven L. Salzberg,Claire M. Fraser,David J. Lipman,Jeffery K. Taubenberger
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0030300
Abstract: Understanding the evolution of influenza A viruses in humans is important for surveillance and vaccine strain selection. We performed a phylogenetic analysis of 156 complete genomes of human H3N2 influenza A viruses collected between 1999 and 2004 from New York State, United States, and observed multiple co-circulating clades with different population frequencies. Strikingly, phylogenies inferred for individual gene segments revealed that multiple reassortment events had occurred among these clades, such that one clade of H3N2 viruses present at least since 2000 had provided the hemagglutinin gene for all those H3N2 viruses sampled after the 2002–2003 influenza season. This reassortment event was the likely progenitor of the antigenically variant influenza strains that caused the A/Fujian/411/2002-like epidemic of the 2003–2004 influenza season. However, despite sharing the same hemagglutinin, these phylogenetically distinct lineages of viruses continue to co-circulate in the same population. These data, derived from the first large-scale analysis of H3N2 viruses, convincingly demonstrate that multiple lineages can co-circulate, persist, and reassort in epidemiologically significant ways, and underscore the importance of genomic analyses for future influenza surveillance.
Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses.
Holmes Edward C,Ghedin Elodie,Miller Naomi,Taylor Jill
PLOS Biology , 2005,
Abstract: Understanding the evolution of influenza A viruses in humans is important for surveillance and vaccine strain selection. We performed a phylogenetic analysis of 156 complete genomes of human H3N2 influenza A viruses collected between 1999 and 2004 from New York State, United States, and observed multiple co-circulating clades with different population frequencies. Strikingly, phylogenies inferred for individual gene segments revealed that multiple reassortment events had occurred among these clades, such that one clade of H3N2 viruses present at least since 2000 had provided the hemagglutinin gene for all those H3N2 viruses sampled after the 2002-2003 influenza season. This reassortment event was the likely progenitor of the antigenically variant influenza strains that caused the A/Fujian/411/2002-like epidemic of the 2003-2004 influenza season. However, despite sharing the same hemagglutinin, these phylogenetically distinct lineages of viruses continue to co-circulate in the same population. These data, derived from the first large-scale analysis of H3N2 viruses, convincingly demonstrate that multiple lineages can co-circulate, persist, and reassort in epidemiologically significant ways, and underscore the importance of genomic analyses for future influenza surveillance.
Whole-Genome Analysis of Human Influenza A Virus Reveals Multiple Persistent Lineages and Reassortment among Recent H3N2 Viruses  [PDF]
Edward C Holmes,Elodie Ghedin,Naomi Miller,Jill Taylor,Yiming Bao,Kirsten St George,Bryan T Grenfell,Steven L Salzberg,Claire M Fraser,David J Lipman ,Jeffery K Taubenberger
PLOS Biology , 2005, DOI: 10.1371/journal.pbio.0030300
Abstract: Understanding the evolution of influenza A viruses in humans is important for surveillance and vaccine strain selection. We performed a phylogenetic analysis of 156 complete genomes of human H3N2 influenza A viruses collected between 1999 and 2004 from New York State, United States, and observed multiple co-circulating clades with different population frequencies. Strikingly, phylogenies inferred for individual gene segments revealed that multiple reassortment events had occurred among these clades, such that one clade of H3N2 viruses present at least since 2000 had provided the hemagglutinin gene for all those H3N2 viruses sampled after the 2002–2003 influenza season. This reassortment event was the likely progenitor of the antigenically variant influenza strains that caused the A/Fujian/411/2002-like epidemic of the 2003–2004 influenza season. However, despite sharing the same hemagglutinin, these phylogenetically distinct lineages of viruses continue to co-circulate in the same population. These data, derived from the first large-scale analysis of H3N2 viruses, convincingly demonstrate that multiple lineages can co-circulate, persist, and reassort in epidemiologically significant ways, and underscore the importance of genomic analyses for future influenza surveillance.
Viruses and Lipids  [PDF]
Akira Ono
Viruses , 2010, DOI: 10.3390/v2051236
Abstract: As obligatory intracellular pathogens, viruses exploit various cellular molecules and structures, such as cellular membranes, for their propagation. Enveloped viruses acquire lipid membranes as their outer coat through interactions with cellular membranes during morphogenesis within, and egress from, infected cells. In contrast, non-enveloped viruses typically exit cells by cell lysis, and lipid membranes are not part of the released virions. However, non-enveloped viruses also interact with lipid membranes at least during entry into target cells. Therefore, lipids, as part of cellular membranes, inevitably play some roles in life cycle of viruses. [...]
Oncogenic viruses and their role in tumor formation
?upi? Maja,Lazarevi? Ivana,Kulji?-Kapulica Nada
Srpski Arhiv za Celokupno Lekarstvo , 2005, DOI: 10.2298/sarh0508384c
Abstract: Oncogenic viruses trigger persistent infections, which can stimulate uncontrolled cell growth by inducing cell transformation. Different oncogenic viruses use different mechanisms for infecting cells. Most oncogenic DNA viruses integrate transforming sets of genes into the host chromosome and encode proteins that bind and inactivate cell growth regulatory proteins, such as p53 and retinoblastoma gene product. Tumorous RNA viruses use different oncogenic mechanisms. Some of them encode oncogenic proteins that are almost identical to the cellular proteins involved in the control of cellular growth. The overproduction or altered function of these oncogenic materials stimulates cell growth. These RNA viruses can cause tumors rapidly. The second group of oncoviruses integrates their promoter sequences and viral enhancers near to the cellular growth-stimulating gene, initiating the transformation of the cell. The third group of RNA tumor viruses encodes a protein tax that transactivates the expression of cellular genes. Virus-induced malignant transformation of the cell represents the first step in the complex process of oncogenesis.
Towards the Epidemiological Modeling of Computer Viruses  [PDF]
Xiaofan Yang,Lu-Xing Yang
Discrete Dynamics in Nature and Society , 2012, DOI: 10.1155/2012/259671
Abstract: Epidemic dynamics of computer viruses is an emerging discipline aiming to understand the way that computer viruses spread on networks. This paper is intended to establish a series of rational epidemic models of computer viruses. First, a close inspection of some common characteristics shared by all typical computer viruses clearly reveals the flaws of previous models. Then, a generic epidemic model of viruses, which is named as the SLBS model, is proposed. Finally, diverse generalizations of the SLBS model are suggested. We believe this work opens a door to the full understanding of how computer viruses prevail on the Internet. 1. Introduction As a technical term coined by Cohen, a computer virus is a malicious program that can replicate itself and spread from computer to computer. Once breaking out, a virus can perform devastating operations such as modifying data, deleting data, deleting files, encrypting files, and formatting disks [1]. In the past, massive outbreaks of computer viruses have brought about huge financial losses. With the advent of the era of cloud computing and the Internet of Things, the threat from viruses would become increasingly serious, even leading to a havoc [2]. As we all know, antivirus software is the major means of defending against viruses. With the continual emergence of new variants of existing viruses as well as new types of virus strains, the struggle waged by human being against viruses is doomed to be endless, arduous, and devious; indeed, the development of new types of antivirus software always lags behind the emergence of new types of viruses. As thus, antivirus technique cannot predict the evolution trend of viruses and, hence, cannot provide global suggestions for their prevention and control. Inspired by the intriguing analogies between computer viruses and their biological counterparts, Cohen [3] and Murray [4] inventively suggested that the techniques developed in the epidemic dynamics of infectious diseases should be exploited to study the spread of computer viruses. Later, Kephart and White [5] borrowed a biological epidemic model (the SIS model) to investigate the way that computer viruses spread on the Internet. The researches in this field have since been made mainly in the following two different directions. (i) The finding that the autonomous system level topological structure of the Internet follows diverse power law distributions [6–8] has stimulated the interest in the spreading behavior of viruses on complex networks. Previous work in this direction focused on the existence and estimation of the
Viruses in and out
Mariam Andrawiss
Genome Biology , 2002, DOI: 10.1186/gb-2002-3-10-reports4033
Abstract: Microbes are the smallest forms of life on earth. Some microbes are deadly, most are harmless, and some are extremely beneficial. They can be found anywhere - in air, water, plants, animals and humans - and fall into four major categories: fungi, protozoa, bacteria (including Archaea, in this context), and viruses, which are the smallest of all. The international meeting 'The world of microbes' was divided into congresses on mycology (on fungi), bacteriology and applied microbiology, and virology; I will focus on the latter here.Viruses are replicating microorganisms that are heavily dependent on the structural and metabolic components of the host cell. Viruses can infect bacteria, fungi, plants, invertebrates and vertebrates. Whatever the host, virus particles (or virions) must penetrate the cell and uncoat their structure to allow transcription and translation of their genomes by the viral and the host machinery. Once the viruses have replicated, new virions are released from the infected cells. Even though most viral infections result in no symptoms, many viruses can cause virulent disorders, such as acquired immune-deficiency syndrome (AIDS), hemorrhagic fever, yellow fever, rabies or poliomyelitis. Viruses are classified in different taxonomic groups on the basis of their structural, physicochemical and replicative characteristics, and the meeting sessions were organized along these lines; I will focus on the sessions on the movement of plant viruses and the structure, assembly and entry of some enveloped viruses that infect vertebrates.In contrast to animal viruses, which penetrate the cell after specific binding of a virion protein to a receptor on the cell surface, plant viruses enter cells in the first instance by passive diffusion through breaches in the cell wall. This is later followed by spreading of the virus from cell to cell in the plant through plasmodesmata, cytoplasmic connections through channels in the cell wall that provide communication betwee
Viruses in reptiles
Ellen Ariel
Veterinary Research , 2011, DOI: 10.1186/1297-9716-42-100
Abstract: 1. Introduction2. Methods for working with reptilian viruses3. Reptilian viruses described by virus families3.1. Herpesviridae3.2. Iridoviridae3.2.1 Ranavirus3.2.2 Erythrocytic virus3.2.3 Iridovirus3.3. Poxviridae3.4. Adenoviridae3.5. Papillomaviridae3.6. Parvoviridae3.7. Reoviridae3.8. Retroviridae and inclusion body disease of Boid snakes3.9. Arboviruses3.9.1. Flaviviridae3.9.2. Togaviridae3.10. Caliciviridae3.11. Picornaviridae3.12. Paramyxoviridae4. Summary5. Acknowledgements6. Competing interests7. ReferencesThe etiology of reptilian viral diseases can be attributed to a wide range of viruses occurring across different genera and families. Thirty to forty years ago, studies of viruses in reptiles focused mainly on the zoonotic potential of arboviruses in reptiles and much effort went into surveys and challenge trials of a range of reptiles with eastern and western equine encephalitis as well as Japanese encephalitis viruses [1-3]. In the past decade, outbreaks of infection with West Nile virus in human populations and in farmed alligators in the USA have seen the research emphasis placed on the issue of reptiles, particularly crocodiles and alligators, being susceptible to, and reservoirs for, this serious zoonotic disease [4-7]. Although there are many recognised reptilian viruses, the evidence for those being primary pathogens is relatively limited. Transmission studies establishing pathogenicity and cofactors are likewise scarce, possibly due to the relatively low commercial importance of reptiles, difficulties with the availability of animals and permits for statistically sound experiments, difficulties with housing of reptiles in an experimental setting or the inability to propagate some viruses in cell culture to sufficient titres for transmission studies. Viruses as causes of direct loss of threatened species, such as the chelonid fibropapilloma associated herpesvirus and ranaviruses in farmed and wild tortoises and turtles, have re-focused attention bac
Persistent Erythema Multiforme  [PDF]
Dilek,Aysun,Kür?at Demir,Burcu
Turkderm , 2011,
Abstract: Erythema multiforme (EM) is a mucocutaneous disease characterized by the typical target-like erythematous papules and plaques especially localized on the acral regions. It is classified clinically into three subgroups as classical, recurrent and persistent type. Persistent EM (PEM) is a rare variant of EM characterized by the continuous appearance of typical EM lesions and atypical cutaneous or mucosal lesions such as erythematous papules-plaques, targetoid lesions, blistering and necrotic lesions. PEM can be induced by viruses or some malignant and inflammatory underlying diseases although there are some idiopathic cases. Here, we report a 30-year-old woman who was diagnosed as PEM and responded well to treatment with acyclovir. In addition, our case is the first reported case with PEM in Turkey. (Turk-derm 2011; 45: 210-12)
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