Advances in Virus Research (ADV VIRUS RES )

Publisher: Elsevier

Description

  • Impact factor
    2.84
  • 5-year impact
    3.96
  • Cited half-life
    9.40
  • Immediacy index
    0.59
  • Eigenfactor
    0.00
  • Article influence
    1.46
  • Website
    Advances in Virus Research website
  • Other titles
    Advances in virus research
  • ISSN
    1557-8399
  • OCLC
    1461272
  • Material type
    Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Viruses are common agents of plant infectious diseases. During last decades, worldwide agriculture production has been compromised by a series of epidemics caused by new viruses that spilled over from reservoir species or by new variants of classic viruses that show new pathogenic and epidemiological properties. Virus emergence has been generally associated with ecological change or with intensive agronomical practices. However, the complete picture is much more complex since the viral populations constantly evolve and adapt to their new hosts and vectors. This chapter puts emergence of plant viruses into the framework of evolutionary ecology, genetics, and epidemiology. We will stress that viral emergence begins with the stochastic transmission of preexisting genetic variants from the reservoir to the new host, whose fate depends on their fitness on each hosts, followed by adaptation to new hosts or vectors, and finalizes with an efficient epidemiological spread.
    Advances in Virus Research 01/2014; 88:161-91.
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    ABSTRACT: Bacteria Pseudomonas aeruginosa, being opportunistic pathogens, are the major cause of nosocomial infections and, in some cases, the primary cause of death. They are virtually untreatable with currently known antibiotics. Phage therapy is considered as one of the possible approaches to the treatment of P. aeruginosa infections. Difficulties in the implementation of phage therapy in medical practice are related, for example, to the insufficient number and diversity of virulent phages that are active against P. aeruginosa. Results of interaction of therapeutic phages with bacteria in different conditions and environments are studied insufficiently. A little is known about possible interactions of therapeutic phages with resident prophages and plasmids in clinical strains in the foci of infections. This chapter highlights the different approaches to solving these problems and possible ways to expand the diversity of therapeutic P. aeruginosa phages and organizational arrangements (as banks of phages) to ensure long-term use of phages in the treatment of P. aeruginosa infections.
    Advances in Virus Research 01/2014; 88:227-78.
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    ABSTRACT: As shrimp aquaculture has evolved from a subsistent farming activity to an economically important global industry, viral diseases have also become a serious threat to the sustainable growth and productivity of this industry. Parvoviruses represent an economically important group of viruses that has greatly affected shrimp aquaculture. In the early 1980s, an outbreak of a shrimp parvovirus, infectious hypodermal and hematopoietic necrosis virus (IHHNV), led to the collapse of penaeid shrimp farming in theAmericas. Since then, considerable progress has been made in characterizing the parvoviruses of shrimp and developing diagnostic methods aimed to preventing the spread of diseases caused by these viruses. To date, four parvoviruses are known that infect shrimp; these include IHHNV, hepatopancreatic parvovirus (HPV), spawner-isolated mortality virus (SMV), and lymphoid organ parvo-like virus. Due to the economic repercussions that IHHNV and HPV outbreaks have caused to shrimp farming over the years, studies have been focused mostly on these two pathogens, while information on SMV and LPV remains limited. IHHNV was the first shrimp virus to be sequenced and the first for which highly sensitive diagnostic methods were developed. IHHNV-resistant lines of shrimp were also developed to mitigate the losses caused by this virus. While the losses due to IHHNV have been largely contained in recent years, reports of HPV-induced mortalities in larval stages in hatchery and losses due to reduced growth have increased. This review presents a comprehensive account of the history and current knowledge on the biology, diagnostics methods, genomic features, mechanisms of evolution, and management strategies of shrimp parvoviruses. We also highlighted areas where research efforts should be focused in order to gain further insight on the mechanisms of parvoviral pathogenicity in shrimp that will help to prevent future losses caused by these viruses.
    Advances in Virus Research 01/2014; 89:85-139.
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    ABSTRACT: The objective of this chapter is to provide an updated and concise systematic review on taxonomy, history, arthropod vectors, vertebrate hosts, animal disease, and geographic distribution of all arboviruses known to date to cause disease in homeotherm (endotherm) vertebrates, except those affecting exclusively man. Fifty arboviruses pathogenic for animals have been documented worldwide, belonging to seven families: Togaviridae (mosquito-borne Eastern, Western, and Venezuelan equine encephalilitis viruses; Sindbis, Middelburg, Getah, and Semliki Forest viruses), Flaviviridae (mosquito-borne yellow fever, Japanese encephalitis, Murray Valley encephalitis, West Nile, Usutu, Israel turkey meningoencephalitis, Tembusu and Wesselsbron viruses; tick-borne encephalitis, louping ill, Omsk hemorrhagic fever, Kyasanur Forest disease, and Tyuleniy viruses), Bunyaviridae (tick-borne Nairobi sheep disease, Soldado, and Bhanja viruses; mosquito-borne Rift Valley fever, La Crosse, Snowshoe hare, and Cache Valley viruses; biting midges-borne Main Drain, Akabane, Aino, Shuni, and Schmallenberg viruses), Reoviridae (biting midges-borne African horse sickness, Kasba, bluetongue, epizootic hemorrhagic disease of deer, Ibaraki, equine encephalosis, Peruvian horse sickness, and Yunnan viruses), Rhabdoviridae (sandfly/mosquito-borne bovine ephemeral fever, vesicular stomatitis-Indiana, vesicular stomatitis-New Jersey, vesicular stomatitis-Alagoas, and Coccal viruses), Orthomyxoviridae (tick-borne Thogoto virus), and Asfarviridae (tick-borne African swine fever virus). They are transmitted to animals by five groups of hematophagous arthropods of the subphyllum Chelicerata (order Acarina, families Ixodidae and Argasidae-ticks) or members of the class Insecta: mosquitoes (family Culicidae); biting midges (family Ceratopogonidae); sandflies (subfamily Phlebotominae); and cimicid bugs (family Cimicidae). Arboviral diseases in endotherm animals may therefore be classified as: tick-borne (louping ill and tick-borne encephalitis, Omsk hemorrhagic fever, Kyasanur Forest disease, Tyuleniy fever, Nairobi sheep disease, Soldado fever, Bhanja fever, Thogoto fever, African swine fever), mosquito-borne (Eastern, Western, and Venezuelan equine encephalomyelitides, Highlands J disease, Getah disease, Semliki Forest disease, yellow fever, Japanese encephalitis, Murray Valley encephalitis, West Nile encephalitis, Usutu disease, Israel turkey meningoencephalitis, Tembusu disease/duck egg-drop syndrome, Wesselsbron disease, La Crosse encephalitis, Snowshoe hare encephalitis, Cache Valley disease, Main Drain disease, Rift Valley fever, Peruvian horse sickness, Yunnan disease), sandfly-borne (vesicular stomatitis-Indiana, New Jersey, and Alagoas, Cocal disease), midge-borne (Akabane disease, Aino disease, Schmallenberg disease, Shuni disease, African horse sickness, Kasba disease, bluetongue, epizootic hemorrhagic disease of deer, Ibaraki disease, equine encephalosis, bovine ephemeral fever, Kotonkan disease), and cimicid-borne (Buggy Creek disease). Animals infected with these arboviruses regularly develop a febrile disease accompanied by various nonspecific symptoms; however, additional severe syndromes may occur: neurological diseases (meningitis, encephalitis, encephalomyelitis); hemorrhagic symptoms; abortions and congenital disorders; or vesicular stomatitis. Certain arboviral diseases cause significant economic losses in domestic animals-for example, Eastern, Western and Venezuelan equine encephalitides, West Nile encephalitis, Nairobi sheep disease, Rift Valley fever, Akabane fever, Schmallenberg disease (emerged recently in Europe), African horse sickness, bluetongue, vesicular stomatitis, and African swine fever; all of these (except for Akabane and Schmallenberg diseases) are notifiable to the World Organisation for Animal Health (OIE, 2012).
    Advances in Virus Research 01/2014; 89:201-75.
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    ABSTRACT: Arthropod-borne viruses (arboviruses) are transmitted between vertebrate hosts and arthropod vectors. An inherently complex interaction among virus, vector, and the environment determines successful transmission of the virus. Once believed to be "flying syringes," recent advances in the field have demonstrated that mosquito genetics, microbiota, salivary components, and mosquito innate immune responses all play important roles in modulating arbovirus transmissibility. The literature on the interaction among virus, mosquito, and environment has expanded dramatically in the preceding decade and the utilization of next-generation sequencing and transgenic vector methodologies assuredly will increase the pace of knowledge acquisition in this field. This chapter outlines the interplay among the three factors in both direct physical and biochemical manners as well as indirectly through superinfection barriers and altered induction of innate immune responses in mosquito vectors. The culmination of the aforementioned interactions and the arms race between the mosquito innate immune response and the capacity of arboviruses to antagonize such a response ultimately results in the subjugation of mosquito cells for viral replication and subsequent transmission.
    Advances in Virus Research 01/2014; 89:39-83.
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    ABSTRACT: While the role of viral variants has long been known to play a key role in causing variation in disease severity, it is also clear that host genetic variation plays a critical role in determining virus-induced disease responses. However, a variety of factors, including confounding environmental variables, rare genetic variants requiring extremely large cohorts, the temporal dynamics of infections, and ethical limitation on human studies, have made the identification and dissection of variant host genes and pathways difficult within human populations. This difficulty has led to the development of a variety of experimental approaches used to identify host genetic contributions to disease responses. In this chapter, we describe the history of genetic associations within the human population, the development of experimentally tractable systems, and the insights these specific approaches provide. We conclude with a discussion of recent advances that allow for the investigation of the role of complex genetic networks that underlie host responses to infection, with the goal of drawing connections to human infections. In particular, we highlight the need for robust animal models with which to directly control and assess the role of host genetics on viral infection outcomes.
    Advances in Virus Research 01/2014; 88:193-225.
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    ABSTRACT: Dengue virus (DENV) is a significant cause of morbidity and mortality in tropical and subtropical regions, causing hundreds of millions of infections each year. Infections range from asymptomatic to a self-limited febrile illness, dengue fever (DF), to the life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). The expanding of the habitat of DENV-transmitting mosquitoes has resulted in dramatic increases in the number of cases over the past 50 years, and recent outbreaks have occurred in the United States. Developing a dengue vaccine is a global health priority. DENV vaccine development is challenging due to the existence of four serotypes of the virus (DENV1-4), which a vaccine must protect against. Additionally, the adaptive immune response to DENV may be both protective and pathogenic upon subsequent infection, and the precise features of protective versus pathogenic immune responses to DENV are unknown, complicating vaccine development. Numerous vaccine candidates, including live attenuated, inactivated, recombinant subunit, DNA, and viral vectored vaccines, are in various stages of clinical development, from preclinical to phase 3. This review will discuss the adaptive immune response to DENV, dengue vaccine challenges, animal models used to test dengue vaccine candidates, and historical and current dengue vaccine approaches.
    Advances in Virus Research 01/2014; 88:315-72.
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    ABSTRACT: Species of plant viruses within the Luteoviridae, Geminiviridae, and Nanoviridae are transmitted by phloem-feeding insects in a circulative, nonpropagative manner. The precise route of virus movement through the vector can differ across and within virus families, but these viruses all share many biological, biochemical, and ecological features. All share temporal and spatial constraints with respect to transmission efficiency. The viruses also induce physiological changes in their plant hosts resulting in behavioral changes in the insects that optimize the transmission of virus to new hosts. Virus proteins interact with insect, endosymbiont, and plant proteins to orchestrate, directly and indirectly, virus movement in insects and plants to facilitate transmission. Knowledge of these complex interactions allows for the development of new tools to reduce or prevent transmission, to quickly identify important vector populations, and to improve the management of these economically important viruses affecting agricultural and natural plant populations.
    Advances in Virus Research 01/2014; 89:141-99.
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    ABSTRACT: Dengue virus (DENV) is an emerging mosquito-borne human pathogen that affects millions of individuals each year by causing severe and potentially fatal syndromes. Despite intense research efforts, no approved vaccine or antiviral therapy is yet available. Overcoming this limitation requires detailed understanding of the intimate relationship between the virus and its host cell, providing the basis to devise optimal prophylactic and therapeutic treatment options. With the advent of novel high-throughput technologies including functional genomics, transcriptomics, proteomics, and lipidomics, new important insights into the DENV replication cycle and the interaction of this virus with its host cell have been obtained. In this chapter, we provide a comprehensive overview on the current status of the DENV research field, covering every step of the viral replication cycle with a particular focus on virus-host cell interaction. We will also review specific chemical inhibitors targeting cellular factors and processes of relevance for the DENV replication cycle and their possible exploitation for the development of next generation antivirals.
    Advances in Virus Research 01/2014; 88:1-109.
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    ABSTRACT: Epstein-Barr virus (EBV) is an oncogenic human herpesvirus in the γ-herpesvirinae subfamily that contains a 170-180kb double-stranded DNA genome. In vivo, EBV commonly infects B and epithelial cells and persists for the life of the host in a latent state in the memory B-cell compartment of the peripheral blood. EBV can be reactivated from its latent state, leading to increased expression of lytic genes that primarily encode for enzymes necessary to replicate the viral genome and structural components of the virion. Lytic cycle proteins also aid in immune evasion, inhibition of apoptosis, and the modulation of other host responses to infection. In vitro, EBV has the potential to infect primary human B cells and induce cellular proliferation to yield effectively immortalized lymphoblastoid cell lines, or LCLs. EBV immortalization of B cells in vitro serves as a model system for studying EBV-mediated lymphomagenesis. While much is known about the steady-state viral gene expression within EBV-immortalized LCLs and other EBV-positive cell lines, relatively little is known about the early events after primary B-cell infection. It was previously thought that upon latent infection, EBV only expressed the well-characterized latency-associated transcripts found in LCLs. However, recent work has characterized the early, but transient, expression of lytic genes necessary for efficient transformation and delayed responses in the known latency genes. This chapter summarizes these recent findings that show how dynamic and controlled expression of multiple EBV genes can control the activation of B cells, entry into the cell cycle, the inhibition of apoptosis, and innate and adaptive immune responses.
    Advances in Virus Research 01/2014; 88:279-313.
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    ABSTRACT: Kaposi's sarcoma-associated herpesvirus (KSHV; also known as human herpesvirus 8) is the etiologic agent of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. These cancers often occur in the context of immunosuppression, which has made KSHV-associated malignancies an increasing global health concern with the persistence of the AIDS epidemic. KSHV has also been linked to several acute inflammatory diseases. KSHV exists between a lytic and latent lifecycle, which allows the virus to transition between active replication and quiescent infection. KSHV encodes a number of proteins and small RNAs that are thought to inadvertently transform host cells while performing their functions of helping the virus persist in the infected host. KSHV also has an arsenal of components that aid the virus in evading the host immune response, which help the virus establish a successful lifelong infection. In this comprehensive chapter, we will discuss the diseases associated with KSHV infection, the biology of latent and lytic infection, and individual proteins and microRNAs that are known to contribute to host cell transformation and immune evasion.
    Advances in Virus Research 01/2014; 88:111-59.
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    ABSTRACT: Assembly of negative-strand RNA viruses occurs by budding from host plasma membranes. The budding process involves association of the viral core or nucleocapsid with a region of cellular membrane that will become the virus budding site, which contains the envelope glycoproteins and matrix protein. This region of membrane then buds out and pinches off to become the virus envelope. This review will address the questions of what are the mechanisms that bring the nucleocapsid and envelope glycoproteins together to form the virus budding site, and how does this lead to release of progeny virions? Recent evidence supports the idea that viral envelope glycoproteins and matrix proteins are organized into membrane microdomains that coalesce to form virus budding sites. There has also been substantial progress in understanding the last step in virus release, referred to as the "late budding function," which often involves host proteins of the vacuolar protein sorting apparatus. Key questions are raised as to the mechanism of the initial steps in formation of virus budding sites: How are membrane microdomains brought together and how are nucleocapsids selected for incorporation into these budding sites, particularly in the case of viruses for which genome RNA sequences are important for envelopment of nucleocapsids?
    Advances in Virus Research 01/2013; 85:57-90.
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    ABSTRACT: The recent discovery of giant viruses exhibiting double-stranded DNA genomes larger than a million base pairs, encoding more than a thousand proteins and packed in near micron-sized icosahedral particles, opened a new and unexpected chapter in virology. As of today, these giant viruses and their closest relatives of lesser dimensions infect unicellular eukaryotes found in aquatic environments, but belonging to a wide diversity of early branching phyla. This broad phylogenetic distribution of hosts is consistent with the hypothesis that giant viruses originated prior to the radiation of the eukaryotic domain and/or might have been involved in the partition of nuclear versus cytoplasmic functions in ancestral cells. The distinctive features of the known giant viruses, in particular the recurrent presence of components of the translation apparatus in their proteome, raise a number of fundamental questions about their origin, their mode of evolution, and the relationship they may entertain with other dsDNA viruses, the genome size of which exhibits the widest distribution among all biological entities, from less than 5kb to more than 1.25Mb (a ratio of 1:250). At a more conceptual level, the convergence between the discovery of increasingly reduced parasitic cellular organisms and that of giant viruses exhibiting a widening array of cellular-like functions may ultimately abolish the historical discontinuity between the viral and the cellular world.
    Advances in Virus Research 01/2013; 85:25-56.
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    ABSTRACT: The genus Dianthovirus is one of eight genera in the family Tombusviridae. All the genera have monopartite positive-stranded RNA genomes, except the dianthoviruses which have bipartite genomes. The dianthoviruses are distributed worldwide. Although they share common structural features with the other Tombusviridae viruses in their virions and the terminal structure of the genomic RNAs, the bipartite nature of the dianthovirus genome offers an ideal experimental system with which to study basic issues of virology. The two genomic RNAs seem to use distinct strategies to regulate their translation, transcription, genome replication, genome packaging, and cell-to-cell movement during infection. This review summarizes the current state of our knowledge of the dianthoviruses, with its main emphasis on the molecular biology of the virus, including the viral and host factors required for its infection of host plants. The epidemiology of the virus and the possible viral impacts on agriculture and the environment are also discussed.
    Advances in Virus Research 01/2013; 87C:37-74.
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    ABSTRACT: Many viruses cause disease within an infected host after spread from an initial portal of entry to sites of secondary replication. Viruses can disseminate via the bloodstream or through nerves. Mammalian orthoreoviruses (reoviruses) are neurotropic viruses that use both bloodborne and neural pathways to spread systemically within their hosts to cause disease. Using a robust mouse model and a dynamic reverse genetics system, we have identified a viral receptor and a viral nonstructural protein that are essential for hematogenous reovirus dissemination. Junctional adhesion molecule-A (JAM-A) is a member of the immunoglobulin superfamily expressed in tight junctions and on hematopoietic cells that serves as a receptor for all reovirus serotypes. Expression of JAM-A is required for infection of endothelial cells and development of viremia in mice, suggesting that release of virus into the bloodstream from infected endothelial cells requires JAM-A. Nonstructural protein σ1s is implicated in cell cycle arrest and apoptosis in reovirus-infected cells but is completely dispensable for reovirus replication in cultured cells. Surprisingly, a recombinant σ1s-null reovirus strain fails to spread hematogenously in infected mice, suggesting that σ1s facilitates apoptosis of reovirus-infected intestinal epithelial cells. It is possible that apoptotic bodies formed as a consequence of σ1s expression lead to reovirus uptake by dendritic cells for subsequent delivery to the mesenteric lymph node and the blood. Thus, both host and viral factors are required for efficient hematogenous dissemination of reovirus. Understanding mechanisms of reovirus bloodborne spread may shed light on how microbial pathogens invade the bloodstream to disseminate and cause disease in infected hosts.
    Advances in Virus Research 01/2013; 87C:1-35.
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    ABSTRACT: Saccharomyces cerevisiae has been a key experimental organism for the study of infectious diseases, including dsRNA viruses, ssRNA viruses, and prions. Studies of the mechanisms of virus and prion replication, virus structure, and structure of the amyloid filaments that are the basis of yeast prions have been at the forefront of such studies in these classes of infectious entities. Yeast has been particularly useful in defining the interactions of the infectious elements with cellular components: chromosomally encoded proteins necessary for blocking the propagation of the viruses and prions, and proteins involved in the expression of viral components. Here, we emphasize the L-A dsRNA virus and its killer-toxin-encoding satellites, the 20S and 23S ssRNA naked viruses, and the several infectious proteins (prions) of yeast.
    Advances in Virus Research 01/2013; 86:1-36.
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    ABSTRACT: In Potato virus X, a member of the genus Potexvirus, special sequences and structures at the 5' and 3' ends of the nontranslated region function as cis-acting elements for viral replication. These elements greatly affect interactions between viral RNAs and those between viral RNAs and host factors. The potexvirus genome encodes five open-reading frames. Viral replicase, which is required for the synthesis of viral RNA, binds viral RNA elements and host factors to form a viral replication complex at the host cellular membrane. The coat protein (CP) and three viral movement proteins (TGB1, TGB2, and TGB3) have critical roles in mediating cell-to-cell viral movement through plasmodesmata by virion formation or by nonvirion ribonucleoprotein (RNP) complex formation with viral movement proteins (TGBs). The RNP complex, like TGB1-CP-viral RNA, is associated with viral replicase and used for immediate reinitiation of viral replication in newly invaded cells. Higher plants have defense mechanisms against potexviruses such as Rx-mediated resistance and RNA silencing. The CP acts as an avirulence effector for plant defense mechanisms, while TGB1 functions as a viral suppressor of RNA silencing, which is the mechanism of innate immune resistance. Here, we describe recent findings concerning the involvement of viral and host factors in potexvirus replication and in antiviral responses to potexvirus infection.
    Advances in Virus Research 01/2013; 87C:75-112.
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    ABSTRACT: The idea that viruses can be used to control fungal diseases has been a driving force in mycovirus research since the earliest days. Viruses in the family Hypoviridae associated with reduced virulence (hypovirulence) of the chestnut blight fungus, Cryphonectria parasitica, have held a prominent place in this research. This has been due in part to the severity of the chestnut blight epidemics in North America and Europe and early reports of hypovirulence-mediated mitigation of disease in European forests and successful application for control of chestnut blight in chestnut orchards. A more recent contributing factor has been the development of a hypovirus/C. parasitica experimental system that has overcome many of the challenges associated with mycovirus research, stemming primarily from the exclusive intracellular lifestyle shared by all mycoviruses. This chapter will focus on hypovirus molecular biology with an emphasis on the development of the hypovirus/C. parasitica experimental system and its contributions to fundamental and practical advances in mycovirology and the broader understanding of virus-host interactions and fungal pathogenesis.
    Advances in Virus Research 01/2013; 86:109-47.
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    ABSTRACT: Phytophthora sp. is a genus in the oomycetes, which are similar to filamentous fungi in morphology and habitat, but phylogenetically more closely related to brown algae and diatoms and fall in the kingdom Stramenopila. In the past few years, several viruses have been characterized in Phytophthora species, including four viruses from Phytophthora infestans, the late blight pathogen, and an endornavirus from an unnamed Phytophthora species from Douglas fir. Studies on Phytophthora viruses have revealed several interesting systems. Phytophthora infestans RNA virus 1 (PiRV-1) and PiRV-2 are likely the first members of two new virus families; studies on PiRV-3 support the establishment of a new virus genus that is not affiliated with established virus families; PiRV-4 is a member of Narnaviridae, most likely in the genus Narnavirus; and Phytophthora endornavirus 1 (PEV1) was the first nonplant endornavirus at the time of reporting. Viral capsids have not been found in any of the above-mentioned viruses. PiRV-1 demonstrated a unique genome organization that requires further examination, and PiRV-2 may have played a role in late blight resurgence in 1980s-1990s.
    Advances in Virus Research 01/2013; 86:327-50.

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