The tenuiviruses are non-enveloped plant viruses, whose name derives from the Latin 'tenuis' (thin, fine, weak) which refers to the thin filamentous shape of the viral particle. Their genome is multi-segmented and composed of single stranded RNAs (ssRNAs) that are of either negative or of ambisense polarity. An RNA-dependent RNA polymerase (RdRp) is associated with the viral particle. Large inclusions of a viral protein are formed in infected plant tissues. Some tenuiviruses synthesize their messenger RNAs (mRNAs) via cap-snatching. The tenuiviruses are persistently transmitted by a particular species of planthopper in a propagative manner. Tenuiviruses infect economically important crop plants that are members of the family Poaceae. Tenuiviruses and phleboviruses are group in the family Phenuiviridae.

In February 2019, following the annual taxon ratification vote, the order Bunyavirales was amended by creation of two new families, four new subfamilies, 11 new genera and 77 new species, merging of two species, and deletion of one species. This article presents the updated taxonomy of the order Bunyavirales now accepted by the International Committee on Taxonomy of Viruses (ICTV).

In October 2018, the order Bunyavirales was amended by inclusion of the family Arenaviridae, abolishment of three families, creation of three new families, 19 new genera, and 14 new species, and renaming of three genera and 22 species. This article presents the updated taxonomy of the order Bunyavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV).

In 2018, the family Arenaviridae was expanded by inclusion of 1 new genus and 5 novel species. At the same time, the recently established order Bunyavirales was expanded by 3 species. This article presents the updated taxonomy of the family Arenaviridae and the order Bunyavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV) and summarizes additional taxonomic proposals that may affect the order in the near future.

Background: Synergy exists between DNA and RNA viruses. It was found that the Human Immunodeficiency Viruses (HIV-1) are RNA viruses at the origin of Acquired Immune Deficiency Syndrome (AIDS). The DNA recurrent herpes diseases are associated to AIDS virus at the origin of Sub-Saharan cancer AIDS pandemic. Objective: It is speculated that a varicella virus (HHV-3) immune defect could originate HSV- 1/HSV-2 recurrent herpes diseases that can be cured by varicella vaccine (2012). Methods: At a Symposium held in Kampala, Uganda (1962), impressive Sub-Saharan cancer epidemics: Hodgkin lymphomas and Kaposi sarcomas have been reported since the onset of the 20th century and remained unexplained. Over one thousand publications related to these cancer epidemics were presented. For millenniums, Bantu populations have been living in tropical forests close to chimpanzees infected by Simian Immune Deficiency viruses (SIV). SIV became Human Immune Deficiency viruses (HIV-1). AIDS is a zoonosis. Results: The DNA and RNA viruses, herpes with HIV-1 viruses, are correlated to Sub- Saharan AIDS infections. They induce an extensive immune deficiency with other herpes viruses such as HHV-4 and HHV-8, which are linked to lymphomas and Kaposi sarcomas. It is postulated that a primary HHV-3 immune weakness could be linked to herpes partnership with AIDS pandemic. Conclusion: The Oka, anti-HHV-3, varicella vaccine is able to cure HSV1/HSV2 recurrent herpes diseases. It induces a specific increase of the varicella antibodies. Thus varicella vaccination could prevent herpes recurrences in Sub-Saharan Africa. One- child dose varicella vaccine could be proposed as the first step to overcome HHV-3 herpes deficiency in order to prevent AIDS pandemic.

The complex parasite-host relationship involves multiple mechanisms. Moreover, parasites infected by viruses modify this relationship adding more complexity to the system that now comprises three partners. Viruses infecting parasites were described several decades ago. However, until recently little was known about the viruses involved and their impact on the resulting disease caused to the hosts. To clarify this situation, we have concentrated on parasitic diseases caused to humans and on how virus-infected parasites could alter the symptoms inflicted on the human host. It is clear that the effect caused to the human host depends on the virus and on the parasite it has infected. Consequently, the review is divided as follows: Viruses with a possible effect on the virulence of the parasite. This section reviews pertinent articles showing that infection of parasites by viruses might increase the detrimental effect of the tandem virus-parasite on the human host (hypervirulence) or decrease virulence of the parasite (hypovirulence). Parasites as vectors affecting the transmission of viruses. In some cases, the virus-infected parasite might facilitate the transfer of the virus to the human host. Parasites harboring viruses with unidentified effects on their host. In spite of recently renewed interest in parasites in connection with their viruses, there still remains a number of cases in which the effect of the virus of a given parasite on the human host remains ambiguous. The triangular relationship between the virus, the parasite and the host, and the modulation of the pathogenicity and virulence of the parasites by viruses should be taken into account in the rationale of fighting against parasites.

A growing body of evidence has demonstrated the role of components of innate immunity, including Toll-like receptors (TLRs), the retinoic acid-inducible gene I/melanoma-differentiation factor 5 (RIG-I/MDA5) and microRNAs (miRNAs) in the recognition of dengue virus (DENV) or its components by infected cells. TLR3, TLR7/8 and RIG-I/MDA5 sense genomic RNA or dsRNA, the product of an intermediate step of DENV replication, activating intracellular pathways leading to the production of antiviral effectors, including interferon and pro-inflammatory cytokines. Recognition by TLR2 and TLR4 also promotes the activation of other intracellular pathways and alters viral replication in an interferon-independent manner. It was also recently demonstrated that cellular miRNAs, a class of post-transcriptional regulatory small RNAs, can affect replication. To accomplish this, miRNAs bind either directly to viral RNA, through base-pair complementarity affecting translation, or indirectly through virus-mediated changes in host protein expression in the viral life cycle. There is also evidence that certain miRNAs can recognize or be recognized by TLRs and RIG-I/MDA5, resulting in alteration of the innate immune response. In this review, we summarize our present knowledge of DENV-host factor interactions, emphasizing the role of TLRs, RIG-I/MDA5 and miRNAs and their possible connection with pathogenesis. Our discussion is based on recent reports suggesting how these different innate immune components might be activated to induce an antiviral response, and how DENV has developed mechanisms to manipulate or evade these antiviral activities.

INTRODUCTION:At the onset of the 20th century, ancient clinical observations of cancer epidemics in Bantu populations of Sub-Saharan Africa were discovered. They were reported from 1914 to 1960, but remained unexplained. In 1983, in San Francisco, Calif., USA, cancer epidemics were related to infections by the human immunodeficiency virus type 1 (HIV-1) known as AIDS disease. Yet since 1996, it is known that HIV-1 strains are not the only ones involved. In Sub-Saharan Africa, recurrent orobuccal herpes simplex virus type 1 (HSV-1) and genital recurrent herpes simplex virus type 2 (HSV-2) appeared many times prior to infection by HIV-1.CASE REPORTS:Data on these ancient medical observations regarding African cancer epidemics can today be referred to as the relationship between the unfortunate immune deficiency of herpes in Bantu populations and HIV-1 viral strains. For centuries, the Bantu populations dispersed in forests were living in close proximity to chimpanzees infected by simian immunodeficiency virus (SIV) and were exposed to SIV contamination which became HIV-1 in human beings. Presently, these unexplained Bantu cancer epidemics can be linked to the viral partnership of HSV-1/HSV-2 to HIV-1 strains.CONCLUSION:The key issue is now to prevent HSV-1/HSV-2 diseases related to HIV-1. An anti-herpes treatment administered early during childhood to Bantu populations will offer a mean of preventing herpes diseases related to HIV-1 infection and hence avoid cancer epidemics.

Top-levelled international football and rugby teams usually train in teams on other sports such as volleyball or handball. Sportsmen work on their flexibility, their quickness, and the group cohesion. The problem of the top-levelled sports teams consist in training altogether: quickness, efficiency, and coordination exercises in other special fields.

In 2012, a 50 year-old athletic male presented with weakness, pain and unilateral phrenic paralysis, followed by bilateral phrenic paralysis with deep dyspnea. In 2013, the Parsonage-Turner syndrome was diagnosed. When the patient was seen in September 2014 for the first time, he was facing phrenic neuromuscular failure, which led to the hypothesis of neurotropic herpes viruses. A control of the global serological anti-Herpes immunity to analyze his antibody (Ab) levels confirmed herpes immune genetic deficiency. An appropriate herpes chemotherapy treatment was proposed. Immediately, a spectacular recovery of the patient was observed, and after a few weeks, the respiratory function tests showed normal values. The hypothesis of the inductive role of viruses of the herpes family in the Parsonage-Turner syndrome was thus substantiated. The patient's immune deficiency covers the HSV2, HHV3, HHV4, HHV5 and HHV6 Ab levels. This led to the control of herpes in the family lineage: indeed, his daughter presented alterations of her serological herpes Ab levels.

The Nuclear Factor 90 (NF90) and its isoforms constitute a family of proteins that can interact with double-stranded (ds) RNA, through its dsRNA binding motifs. Due to various potential translational events such as alternative splicing, the human Interleukin enhancer binding factor 3 (ilf3) gene codes for multifunctional proteins that are NF90 and its isoforms, involved in transcription, translation, mRNA export and microRNA biogenesis. These proteins can act as cellular partners affecting viral replication and they are also implicated in host defense. As a result of these numerous functions, these protein isoforms have been given various names over the years, leading to confusion in determining their specific functions. In this review we focus on the role of the human NF90 protein isoforms in DNA and RNA virus replication.

Jacqueline Le Goaster1 Sylvie Gonzalo2 Patrice Bouree1 Frederic Tangy3 Anne-Lise Haenni4 1Department of Tropical Diseases, Centre Hospitalo-Universitaire (CHU), University of Paris XI, Le Kremlin Bicetre, 2Biomnis Laboratory, Ivry-sur-Seine, 3Retro-Virology, Centre National de Recherche Scientifique (CNRS), Pasteur Institute, Paris; 4Jacques Monod Institute, Centre National de Recherche Scientifique (CNRS), University of Paris VII, Paris, France

While a large number of negative-strand (-)RNA viruses infect animals and humans, a relative small number have plants as their primary host. Some of these have been classified within families together with animal/human infecting viruses due to similarities in particle morphology and genome organization, while others have just recently been/or are still classified in floating genera. In most cases, at least two striking differences can still be discerned between the animal/human-infecting viruses and their plant-infecting counterparts which for the latter relate to their adaptation to plants as hosts. The first one is the capacity to modify plasmodesmata to facilitate systemic spread of infectious viral entities throughout the plant host. The second one is the capacity to counteract RNA interference (RNAi, also referred to as RNA silencing), the innate antiviral defence system of plants and insects. In this review an overview will be presented on the negative-strand RNA plant viruses classified within the families Bunyaviridae, Rhabdoviridae, Ophioviridae and floating genera Tenuivirus and Varicosavirus. Genetic differences with the animal-infecting counterparts and their evolutionary descendants will be described in light of the above processes.

The development of techniques based on fluorescence has made it possible to create new types of assays that represent an advantageous alternative to old tests relying on radioactivity. Such a novel approach has been applied to develop a high-throughput assay to measure the helicase activity of the hepatitis C virus (HCV) NS3 protein and the inhibitory potential of several classes of compounds. The NS3 helicase is one of the most promising targets of anti-HCV-oriented screening of compounds due to the urgent need for more effective and tolerable drugs. The 96- or 384-well microplate assay that we developed is based on the use of a quenched double-stranded DNA substrate labeled with a fluorophore (Cy3 or FAM) and with a Black Hole Quencher 1 or 2. It allows for direct (real-time) measurements of substrate unwinding and inhibition of unwinding by anti-helicase compounds. After a few modifications of buffers and assay conditions this method can be applied to various variants of HCV helicase and other proteins with helicase activities.

Dengue is the most important cause of mosquito-borne virus diseases in tropical and subtropical regions in the world. Severe clinical outcomes such as dengue hemorrhagic fever and dengue shock syndrome are potentially fatal. The epidemiology of dengue has undergone profound changes in recent years, due to several factors such as expansion of the geographical distribution of the insect vector, increase in traveling, and demographic pressure. As a consequence, the incidence of dengue has increased dramatically. Since mosquito control has not been successful and since no vaccine or antiviral treatment is available, new approaches to this problem are needed. Consequently, an in-depth understanding of the molecular and cellular biology of the virus should be helpful to design efficient strategies for the control of dengue. Here, we review the recently acquired knowledge on the molecular and cell biology of the dengue virus life cycle based on newly developed molecular biology technologies.

Regulation of protein synthesis by viruses occurs at all levels of translation. Even prior to protein synthesis itself, the accessibility of the various open reading frames contained in the viral genome is precisely controlled. Eukaryotic viruses resort to a vast array of strategies to divert the translation machinery in their favor, in particular, at initiation of translation. These strategies are not only designed to circumvent strategies common to cell protein synthesis in eukaryotes, but as revealed more recently, they also aim at modifying or damaging cell factors, the virus having the capacity to multiply in the absence of these factors. In addition to unraveling mechanisms that may constitute new targets in view of controlling virus diseases, viruses constitute incomparably useful tools to gain in-depth knowledge on a multitude of cell pathways.

Virus‐like particles (VLPs), formed by the structural elements of viruses, have received considerable attention over the past two decades. The number of reports on newly obtained VLPs has grown proportionally with the systems developed for the expression of these particles. The chapter outlines the recent achievements in two important fields of research brought about by the availability of VLPs produced in a foreign host. These are: (1) The requirements for VLP assembly and (2) the use of VLPs as carriers for foreign epitopes. VLP technology is a rapidly advancing domain of molecular and structural biology. Extensive progress in VLP studies was achieved as the insect cell based protein production system was developed. This baculovirus expression system has many advantages for the synthesis of viral structural proteins resulting in the formation of VLPs. It allows production of large amounts of correctly folded proteins while also providing cell membranes that can serve as structural elements for enveloped viruses. These features give us the opportunity to gain insights into the interactions and requirements accompanying VLP formation that are similar to the assembly events occurring in mammalian cells. Other encouraging elements are the ability to easily scale up the system and the simplicity of purification of the assembled VLPs. The growing number of VLPs carrying foreign protein fragments on their surface and studies on the successful assembly of these chimeric molecules is a promising avenue towards the development of a new technology, in which the newly designed VLPs will be directed to particular mammalian cell types by exposing specific binding domains. The progress made in modeling the surface of VLPs makes them to date the best candidates for the design of delivery systems that can efficiently reach their targets.