DOCSLIB.ORG

Variola Virus and Orthopoxviruses

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Variola Virus and Orthopoxviruses CHAPTER 2 VARIOLA VIRUS AND OTHER ORTHOPOXVIRUSES Contents Page Introduction 70 Classification and nomenclature 71 Development of knowledge of the structure of poxvirions 71 The nucleic acid of poxviruses 72 Classification of poxviruses 72 Chordopoxvirinae: the poxviruses of vertebrates 72 The genus Orthopoxvirus 73 Recognized species of Orthopoxvirus 73 Characteristics shared by all species of Orthopoxvirus 75 Morphology of the virion 75 Antigenic structure 76 Composition and structure of the viral DNA 79 Non-genetic reactivation 80 Characterization of orthopoxviruses by biological tests 81 Lesions in rabbit skin 81 Pocks on the chorioallantoic membrane 82 Ceiling temperature 82 Lethality for mice and chick embryos 83 Growth in cultured cells 83 Inclusion bodies 86 Comparison of biological characteristics of different species 86 Viral replication 86 Adsorption, penetration and uncoating 86 Assembly and maturation 86 Release 88 Cellular changes 89 Characterization of orthopoxviruses by chemical methods 90 Comparison of viral DNAs 90 Comparison of viral polypeptides 93 Summary: distinctions between orthopoxviruses 95 Variola virus 95 Isolation from natural sources 96 Variola major and variola minor 96 Laboratory investigations with variola virus 97 Pathogenicity for laboratory animals 97 Growth in cultured cells 98 Laboratory tests for virulence 99 Differences in the virulence of strains of variola major virus 101 Comparison of the DNAs of strains of variola virus 101 Differences between the DNAs of variola and monkey- pox viruses 103 69 70 SMALLPOX AND ITS ERADICATION Page Variola virus (cont.) Genetic studies 103 Species diagnosis 104 Vaccinia virus 104 Isolation from natural sources 105 The variability of strains and their pathogenicity 105 Variation within a strain 106 Genetic studies 107 Species diagnosis 108 Cowpox virus 108 Cowpox and horsepox in Europe 108 Genetic studies 108 Species diagnosis 109 Laboratory confirmation of smallpox diagnosis 109 Preparation of a guide for laboratory diagnosis 110 Methods of laboratory diagnosis 110 Comparison of different laboratory diagnostic methods 112 Tests for species-specific viral antibodies 114 Resistance to physical and chemical agents 114 Vaccinia virus 115 Variola virus 115 Speculations about the origins of variola virus 116 The diversity and specificity of viruses of man 117 Requirements for human-to-human transmission 117 Possible derivation of variola virus from another Orthopoxvirus 118 Variola virus as the descendant of an Orthopoxvirus of early man 119 Conclusions 119 INTRODUCTION diseases with which this book is less directly concerned, was delineated as early as any other Because of its distinctive clinical picture, viral genus as the “variola-vaccinia subgroup’’ described in the previous chapter, smallpox of the poxvirus group. has been recognized as a disease entity for This chapter outlines the historical devel- many centuries. Its control by deliberate opment and current state of knowledge of the intervention, at first by variolation, then by orthopoxviruses, based primarily on studies vaccination, began long before such measures with vaccinia virus. Much of the material were adopted for any other disease. Likewise, presented will be of special interest to bio- knowledge of the virus that produced the logists, but it includes topics of greater disease and those that were used to control it, complexity and of a more technical nature variola and cowpox or vaccinia viruses respec- than can be readily understood by the other- tively, is as old as the relatively new science of wise informed general reader. However, the virology. The particles that cause these two authors consider that it is important in this diseases were seen with the microscope, and book to endeavour to embrace the full scope then by electron microscopy, before any other of currently available knowledge of the ortho- viruses had been visualized, and their chemi- poxviruses. For the virologist the account will cal composition was analysed earlier than that appear unbalanced, since the intention is to of any other animal virus. The family to limit it to providing the virological back- which they belong, now called Poxviridae, ground that is necessary to understand how was correctly categorized before any other the body responds to infection with these viral family, and the genus Orthopoxvirus, viruses, how the clinical diagnosis can be whose members are the causative, agents of confirmed by laboratory studies, and what smallpox, vaccinia and the several related other related agents may pose threats to man, 2. VARIOLA VIRUS AND OTHER .ORTHOPOXVIRUSES 71 \ The Nature of Viruses in General and Poxviruses in Particular Viruses form a distinct group of agents, which differ fundamentally from cellular microorganisms. The infective particle, known as the virion, is inert; it proceeds to a dynamic phase only after it enters a susceptible cell and loses enough of its outer protective layers to allow its genetic material to be transcribed and translated. The inert poxvirion is the largest of all virions and its genetic material, a single molecule of double-stranded DNA, is among the largest of all viral genomes. Poxviruses differ from most other DNA viruses in that they replicate in the cytoplasm rather than in the nucleus of susceptible cells. To accomplish this, they have a battery of enzymes not found in other DNA viruses, including a viral DNA-dependent RNA polymerase which transcribes messenger RNA from the viral DNA. confuse the diagnosis or give rise to problems term “elementary bodies”, originally intro- in interpreting ecological data. To do this it duced by Chaveau (1868) and used until will be necessary to describe some features of recently to describe the virions. Paschen the orthopoxviruses, such as their structure, (1906) used a modified Loeffler’s flagellar the composition of their genetic material and stain and championed the belief that the their behaviour in experimental animals, in elementary bodies of vaccinia virus thus made some detail, but it is not necessary to provide a visible with the microscope were the infective detailed analysis of the complex events of the particles ;they were later also called “Paschen replication cycle, a feature which has always bodies” in recognition of Paschen’s extensive been of central interest to virologists. work in this field (Plate 2.1). Negri (1906) had shown that the infectivity of vaccine lymph would remain after the lymph had been CLASSIFICATION AND passed through a filter that held back bacteria, NOMENCLATURE but final proof that the elementary body was indeed the infectious entity was not provided The internationally accepted classification until Ledingham (1931) showed that antisera of viruses is based primarily on the morphol- produced against vaccinia or fowlpox viruses ogy of the viral particle (virion) and the would simultaneously and specifically agglu- nature and structure of the viral nucleic acid. tinate the particles and neutralize the infec- As the largest of all viruses, the virions of tivity of the homologous but not the heter- poxviruses were the first to be seen with the ologous virus. microscope. Development of Knowledge of the Structure of Poxvirions As early as 1886, Buist (see Gordon, 1937) reported that he had seen what must have been the virions of vaccinia virus in stained smears, although he regarded them as spores. Calmette & GuCrin (1901) used the rabbit to assay batches of vaccine lymph and in the course of this work they observed that the lymph contained numerous minute refractile particles which they suggested might be the “virulent elements”. These observations were Plate 2. I. “Elementary bodies” (virions) of vaccinia confirmed by Prowazek (1905), an expert virus. Bar = lpm. Imprint of a rabbit cornea infected microscopist, who found that they could be with vaccinia virus, prepared and stained by Paschen stained by Giemsa’s method, and revived the in 1906. 72 SMALLPOX AND ITS ERADICATION Further analysis of the structure of pox (caused by a herpesvirus) and “the great POX” virions has depended on the use of the (syphilis-caused by a spirochaete) in the electron microscope with virions treated in same category as smallpox. various ways. Enzymatic digestion was used By examining sections of poxvirus-infected to demonstrate the existence of a substructure tissues, pathologists came to recognize cyto- within the brick-shaped virions (Dawson & plasmic inclusion bodies as characteristic of McFarlane, 1948). In a series of classical poxvirus infection (Guarnieri, 1892), al- studies, Peters (1956), using enzymatic diges- though for many years they were regarded as tion with deoxyribonuclease and metal shad- protozoa. Gradually, however, the signifi- owing, demonstrated the major viral com- cance of the minute particles seen in stained ponents and designated them as the outer smears was appreciated, and by the 1920s membrane, the lateral bodies and the core. Aragiio (1 927) grouped together, as belong- Thin sections of infected cells have been ing to one family, the viruses of “myxoma, particularly valuable in elucidating the mor- smallpox, molluscum contagiosum, epithe- phogenesis of the virions of vaccinia virus. lioma of fowls, etc.”. Subsequently, Goodpas- Negative staining, combined with a variety of ture (1933) formally proposed that vaccinia- methods of degrading the virion, has been variola, fowlpox, horsepox, sheep-pox, goat- useful in analysing the substructure of vac- pox, swinepox and molluscum contagiosum
Load more

Recommended publications
  • Camelpox Virus Genesig Standard
    Primerdesign TM Ltd Camelpox virus A-type inclusion protein fragment (ATI) gene genesig® Standard Kit 150 tests For general laboratory and research use only Quantification of Camelpox virus genomes. 1 genesig Standard kit handbook HB10.04.10 Published Date: 09/11/2018 Introduction to Camelpox virus Camelpox is a disease of camels caused by a virus of the family Poxviridae. The virus is closely related to the Vaccinia virus that causes Smallpox and is part of the Orthopoxvirus genus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally milder. The infection may also spread to the hands of those that work closely with camels in rare cases. It is a brick-shaped, enveloped virus that ranges in size from 265-295 nm. The double-stranded, linear DNA genome consists of approximately 202,000 tightly packed base pairs encased in a viral core with the replication enzymes believed to be held in lateral bodies outside the core. The virus can be transmitted via direct contact where a camel becomes infected via contact with an infected camel. This is transmission method is also suspected of being the transmission route to humans as most of the human cases presented symptoms on their hands and fingers. The virus can also be transmitted via indirect contact where a camel may become infected after coming into contact with milk, saliva, ocular and nasal secretions from infected camels. The virus has the ability to remain virulent for up to 4 months without a host.
    [Show full text]
  • The Munich Outbreak of Cutaneous Cowpox Infection: Transmission by Infected Pet Rats
    Acta Derm Venereol 2012; 92: 126–131 INVESTIGATIVE REPORT The Munich Outbreak of Cutaneous Cowpox Infection: Transmission by Infected Pet Rats Sandra VOGEL1, Miklós SÁRDY1, Katharina GLOS2, Hans Christian KOrting1, Thomas RUZICKA1 and Andreas WOLLENBERG1 1Department of Dermatology and Allergology, Ludwig Maximilian University, Munich, and 2Department of Dermatology, Haas and Link Animal Clinic, Germering, Germany Cowpox virus infection of humans is an uncommon, another type of orthopoxvirus, from infected pet prairie potentially fatal, skin disease. It is largely confined to dogs have recently been described in the USA, making Europe, but is not found in Eire, or in the USA, Austral­ the medical community aware of the risk of transmission asia, or the Middle or Far East. Patients having contact of pox viruses from pets (3). with infected cows, cats, or small rodents sporadically Seven of 8 exposed patients living in the Munich contract the disease from these animals. We report here area contracted cowpox virus infection from an unusual clinical aspects of 8 patients from the Munich area who source: rats infected with cowpox virus bought from had purchased infected pet rats from a local supplier. Pet local pet shops and reputedly from the same supplier rats are a novel potential source of local outbreaks. The caused a clinically distinctive pattern of infection, which morphologically distinctive skin lesions are mostly res­ was mostly restricted to the patients’ neck and trunk. tricted to the patients’ necks, reflecting the infected ani­ We report here dermatologically relevant aspects of mals’ contact pattern. Individual lesions vaguely resem­ our patients in order to alert the medical community to ble orf or Milker’s nodule, but show marked surrounding the possible risk of a zoonotic orthopoxvirus outbreak erythema, firm induration and local adenopathy.
    [Show full text]
  • The Clinical Features of Smallpox
    CHAPTER 1 THE CLINICAL FEATURES OF SMALLPOX Contents Page Introduction 2 Varieties of smallpox 3 The classification of clinical types of variola major 4 Ordinary-type smallpox 5 The incubation period 5 Symptoms of the pre-eruptive stage 5 The eruptive stage 19 Clinical course 22 Grades of severity 22 Modified-type smallpox 22 Variola sine eruptione 27 Subclinical infection with variola major virus 30 Evidence from viral isolations 30 Evidence from serological studies 30 Flat-type smallpox 31 The rash 31 Clinical course 32 Haemorrhagic-type smallpox 32 General features 32 Early haemorrhagic-type smallpox 37 Late haemorrhagic-type smallpox 38 Variola minor 38 Clinical course 38 Variola sine eruptione and subclinical infection 40 Smallpox acquired by unusual routes of infection 40 Inoculation variola and variolation 40 Congenital smallpox 42 Effects of vaccination on the clinical course of smallpox 42 Effects of vaccination on toxaemia 43 Effects of vaccination on the number of lesions 43 Effects of vaccination on the character and evolution of the rash 43 Effects of vaccination in variola minor 44 Laboratory findings 44 Virological observations 44 Serological observations 45 Haematological observations 46 1 2 SMALLPOX AND ITS ERADICATION Page Complications 47 The skin 47 Ocular system 47 Joints and bones 47 Respiratory system 48 Gastrointestinal system 48 Genitourinary system 49 Central nervous system 49 Sequelae 49 Pockmarks 49 Blindness 50 Limb deformities 50 Prognosis of variola major 50 Calculation of case-fatality rates 50 Effects
    [Show full text]
  • Ectromelia Virus (Mousepox)
    technical sheet Ectromelia Virus (Mousepox) Classification the virus its name, ectromelia, or partial amputation of DNA virus, enveloped the limbs and tail. Family Diagnosis Poxviridae Mousepox should be suspected if animals with the above clinical signs are seen in the animal facility, or Affected species there is unexplained widespread mortality in susceptible strains. Serologic diagnosis through MFIA™/ELISA Laboratory mice, wild mice, and other wild rodents or IFA is possible; if animals recover, they produce protective antibodies. Lesions strongly suggestive of Frequency mousepox are noted on necropsy, including splenic Rare in laboratory mice, uncommon in wild mice. fibrosis in recovered animals, and liver, spleen, and skin lesions in ill animals. Histologically, intracytoplasmic Transmission inclusion bodies are seen in skin lesions. PCR of skin Ectromelia virus, which causes the disease mousepox, lesions can be used for confirmation. Vaccination with is transmitted by direct contact or by fomites. Although vaccinia virus as part of an experimental protocol may many routes of infection are possible experimentally, give false positive serology results. exposure to the virus via cutaneous trauma is the natural route of infection. Lesions appear 7-11 days Interference with Research after infection in susceptible strains, and virus is shed Overwhelming mortality (near 100%) in susceptible for 3 weeks. However, virus has been found in scabs strains may have a negative effect on research and feces for as long as 16 weeks post-infection. programs and animal facilities. Ectromelia virus infection Cage-to-cage transmission in mousepox infections is may modify the phagocytic response in resistant primarily through handling of infected mice.
    [Show full text]
  • 'Risk Factors for Candidemia: a Prospective Matched Case-Control
    Poissy et al. Critical Care (2020) 24:109 https://doi.org/10.1186/s13054-020-2766-1 RESEARCH Open Access Risk factors for candidemia: a prospective matched case-control study Julien Poissy1,2,3 , Lauro Damonti3,4, Anne Bignon5, Nina Khanna6, Matthias Von Kietzell7, Katia Boggian7, Dionysios Neofytos8, Fanny Vuotto9, Valérie Coiteux10, Florent Artru11, Stephan Zimmerli4, Jean-Luc Pagani12, Thierry Calandra3, Boualem Sendid2,13, Daniel Poulain2,13, Christian van Delden8, Frédéric Lamoth3,14, Oscar Marchetti3,15, Pierre-Yves Bochud3*, the FUNGINOS and Allfun French Study Groups Abstract Background: Candidemia is an opportunistic infection associated with high morbidity and mortality in patients hospitalized both inside and outside intensive care units (ICUs). Identification of patients at risk is crucial to ensure prompt antifungal therapy. We sought to assess risk factors for candidemia and death, both outside and inside ICUs. Methods: This prospective multicenter matched case-control study involved six teaching hospitals in Switzerland and France. Cases were defined by positive blood cultures for Candida sp. Controls were matched to cases using the following criteria: age, hospitalization ward, hospitalization duration, and, when applicable, type of surgery. One to three controls were enrolled by case. Risk factors were analyzed by univariate and multivariate conditional regression models, as a basis for a new scoring system to predict candidemia. Results: One hundred ninety-two candidemic patients and 411 matched controls were included. Forty-four percent of included patients were hospitalized in ICUs, and 56% were hospitalized outside ICUs. Independent risk factors for candidemia in the ICU population included total parenteral nutrition, acute kidney injury, heart disease, prior septic shock, and exposure to aminoglycoside antibiotics.
    [Show full text]
  • Review on Camel Pox: an Economically Overwhelming Disease of Pastorals
    Int. J. Adv. Res. Biol. Sci. (2018). 5(9): 65-73 International Journal of Advanced Research in Biological Sciences ISSN: 2348-8069 www.ijarbs.com DOI: 10.22192/ijarbs Coden: IJARQG(USA) Volume 5, Issue 9 - 2018 Review Article DOI: http://dx.doi.org/10.22192/ijarbs.2018.05.09.006 Review on Camel Pox: An Economically Overwhelming Disease of pastorals Tekalign Tadesse*, Endalu Mulatu and Amanuel Bekuma College of Agriculture and Forestry, Mettu University, P.O. Box 318, Bedele, Ethiopia *Corresponding Author: Tekalign Tadesse. E-mail: [email protected] Abstract Camelpox is an economically important, notifiable skin disease of camelids and could be used as a potential bio-warfare agent. The disease is caused by the camel pox virus, which belongs to the Orthopoxvirus genus of the Poxviridae family. Young calves and pregnant females are more susceptible. Tentative diagnosis of camel pox can be made based on clinical signs and pox lesion, but it may confuse with other viral diseases like contagious etyma and papillomatosis. Hence, specific, sensitive, rapid and cost- effective diagnostic techniques would be useful in identification, thereby early implementations of therapeutic and preventives measures to curb these diseases prevalence. Treatment is often directed to minimizing secondary infections by topical application or parenteral administration of broad-spectrum antibiotics and vitamins. The zoonotic importance of the disease should be further studied as humans today are highly susceptible to smallpox a very related and devastating virus eradicated from the globe. This review address an overview on the epidemiology, Zoonotic impacts, diagnostic approaches and the preventive measures on camel pox.
    [Show full text]
  • Where Do We Stand After Decades of Studying Human Cytomegalovirus?
    microorganisms Review Where do we Stand after Decades of Studying Human Cytomegalovirus? 1, 2, 1 1 Francesca Gugliesi y, Alessandra Coscia y, Gloria Griffante , Ganna Galitska , Selina Pasquero 1, Camilla Albano 1 and Matteo Biolatti 1,* 1 Laboratory of Pathogenesis of Viral Infections, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] (F.G.); gloria.griff[email protected] (G.G.); [email protected] (G.G.); [email protected] (S.P.); [email protected] (C.A.) 2 Complex Structure Neonatology Unit, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] * Correspondence: [email protected] These authors contributed equally to this work. y Received: 19 March 2020; Accepted: 5 May 2020; Published: 8 May 2020 Abstract: Human cytomegalovirus (HCMV), a linear double-stranded DNA betaherpesvirus belonging to the family of Herpesviridae, is characterized by widespread seroprevalence, ranging between 56% and 94%, strictly dependent on the socioeconomic background of the country being considered. Typically, HCMV causes asymptomatic infection in the immunocompetent population, while in immunocompromised individuals or when transmitted vertically from the mother to the fetus it leads to systemic disease with severe complications and high mortality rate. Following primary infection, HCMV establishes a state of latency primarily in myeloid cells, from which it can be reactivated by various inflammatory stimuli. Several studies have shown that HCMV, despite being a DNA virus, is highly prone to genetic variability that strongly influences its replication and dissemination rates as well as cellular tropism. In this scenario, the few currently available drugs for the treatment of HCMV infections are characterized by high toxicity, poor oral bioavailability, and emerging resistance.
    [Show full text]
  • Investigation of Poxvirus Host-Range and Gene Expression in Mammalian Cells
    ABSTRACT Title: INVESTIGATION OF POXVIRUS HOST-RANGE AND GENE EXPRESSION IN MAMMALIAN CELLS. Jorge David Méndez Ríos, Doctor of Philosophy, 2014. Directed By: Dr. Bernard Moss, Chief, Laboratory of Viral Diseases, NIAID, NIH; Adjunct Professor Department of Cell Biology and Molecular Genetics, University of Maryland; Members of the Poxviridae family have been known as human pathogens for centuries. Their impact in society included several epidemics that decimated the population. In the last few centuries, Smallpox was of great concern that led to the development of our modern vaccines. The systematic study of Poxvirus host-range and immunogenicity provided the knowledge to translate those observations into practice. After the global vaccination campaign by the World Health Organization, Smallpox was the first infectious disease to be eradicated. Nevertheless, diseases such as Monkeypox, Molluscum contagiosum, new bioterrorist threads, and the use of poxviruses as vaccines or vectors provided the necessity to further understand the host-range from a molecular level. Here, we take advantage of the newly developed technologies such as 454 pyrosequencing and RNA-Seq to address previously unresolved questions for the field. First, we were able to identify the Erytrhomelagia-related poxvirus (ERPV) 25 years after its isolation in Hubei, China. Whole-genome sequencing and bioinformatics identified ERPV as an Ectromelia strain closely related to the Ectromelia Naval strain. Second, by using RNA-Seq, the first MOCV in vivo and in vitro transcriptome was generated. New tools have been developed to support future research and for this human pathogen. Finally, deep-sequencing and comparative genomes of several recombinant MVAs (rMVAs) in conjunction with classical virology allowed us to confirm several genes (O1, F5, C17, F11) association to plaque formation in mammalian cell lines.
    [Show full text]
  • Fungal Sepsis: Optimizing Antifungal Therapy in the Critical Care Setting
    Fungal Sepsis: Optimizing Antifungal Therapy in the Critical Care Setting a b,c, Alexander Lepak, MD , David Andes, MD * KEYWORDS Invasive candidiasis Pharmacokinetics-pharmacodynamics Therapy Source control Invasive fungal infections (IFI) and fungal sepsis in the intensive care unit (ICU) are increasing and are associated with considerable morbidity and mortality. In this setting, IFI are predominantly caused by Candida species. Currently, candidemia represents the fourth most common health care–associated blood stream infection.1–3 With increasingly immunocompromised patient populations, other fungal species such as Aspergillus species, Pneumocystis jiroveci, Cryptococcus, Zygomycetes, Fusarium species, and Scedosporium species have emerged.4–9 However, this review focuses on invasive candidiasis (IC). Multiple retrospective studies have examined the crude mortality in patients with candidemia and identified rates ranging from 46% to 75%.3 In many instances, this is partly caused by severe underlying comorbidities. Carefully matched, retrospective cohort studies have been undertaken to estimate mortality attributable to candidemia and report rates ranging from 10% to 49%.10–15 Resource use associated with this infection is also significant. Estimates from numerous studies suggest the added hospital cost is as much as $40,000 per case.10–12,16–20 Overall attributable costs are difficult to calculate with precision, but have been estimated to be close to 1 billion dollars in the United States annually.21 a University of Wisconsin, MFCB, Room 5218, 1685 Highland Avenue, Madison, WI 53705-2281, USA b Department of Medicine, University of Wisconsin, MFCB, Room 5211, 1685 Highland Avenue, Madison, WI 53705-2281, USA c Department of Microbiology and Immunology, University of Wisconsin, MFCB, Room 5211, 1685 Highland Avenue, Madison, WI 53705-2281, USA * Corresponding author.
    [Show full text]
  • Comparison of Host Cell Gene Expression in Cowpox, Monkeypox Or Vaccinia Virus-Infected Cells Reveals Virus-Specific Regulation
    Bourquain et al. Virology Journal 2013, 10:61 http://www.virologyj.com/content/10/1/61 RESEARCH Open Access Comparison of host cell gene expression in cowpox, monkeypox or vaccinia virus-infected cells reveals virus-specific regulation of immune response genes Daniel Bourquain1†, Piotr Wojtek Dabrowski1,2† and Andreas Nitsche1* Abstract Background: Animal-borne orthopoxviruses, like monkeypox, vaccinia and the closely related cowpox virus, are all capable of causing zoonotic infections in humans, representing a potential threat to human health. The disease caused by each virus differs in terms of symptoms and severity, but little is yet know about the reasons for these varying phenotypes. They may be explained by the unique repertoire of immune and host cell modulating factors encoded by each virus. In this study, we analysed the specific modulation of the host cell’s gene expression profile by cowpox, monkeypox and vaccinia virus infection. We aimed to identify mechanisms that are either common to orthopoxvirus infection or specific to certain orthopoxvirus species, allowing a more detailed description of differences in virus-host cell interactions between individual orthopoxviruses. To this end, we analysed changes in host cell gene expression of HeLa cells in response to infection with cowpox, monkeypox and vaccinia virus, using whole-genome gene expression microarrays, and compared these to each other and to non-infected cells. Results: Despite a dominating non-responsiveness of cellular transcription towards orthopoxvirus infection, we could identify several clusters of infection-modulated genes. These clusters are either commonly regulated by orthopoxvirus infection or are uniquely regulated by infection with a specific orthopoxvirus, with major differences being observed in immune response genes.
    [Show full text]
  • Nih Guidelines for Research Involving Recombinant Or Synthetic Nucleic Acid Molecules (Nih Guidelines)
    NIH GUIDELINES FOR RESEARCH INVOLVING RECOMBINANT OR SYNTHETIC NUCLEIC ACID MOLECULES (NIH GUIDELINES) APRIL 2019 DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health ************************************************************************************************************************ Visit the NIH OSP Web site at: https://osp.od.nih.gov NIH OFFICE OF SCIENCE POLICY CONTACT INFORMATION: Office of Science Policy, National Institutes of Health, 6705 Rockledge Drive, Suite 750, MSC 7985, Bethesda, MD 20892-7985 (20817 for non-USPS mail), (301) 496-9838; (301) 496-9839 (fax). For inquiries, information requests, and report submissions: [email protected] These NIH Guidelines shall supersede all earlier versions until further notice. ************************************************************************************************************************ Page 2 - NIH Guidelines for Research Involving Recombinant or Synthetic Nucleic Acid Molecules (April 2019) FEDERAL REGISTER NOTICES Effective June 24, 1994, Published in Federal Register, July 5, 1994 (59 FR 34472) Amendment Effective July 28, 1994, Federal Register, August 5, 1994 (59 FR 40170) Amendment Effective April 17, 1995, Federal Register, April 27, 1995 (60 FR 20726) Amendment Effective December 14, 1995, Federal Register, January 19, 1996 (61 FR 1482) Amendment Effective March 1, 1996, Federal Register, March 12, 1996 (61 FR 10004) Amendment Effective January 23, 1997, Federal Register, January 31, 1997 (62 FR 4782) Amendment Effective September 30, 1997,
    [Show full text]
  • Diversity of Large DNA Viruses of Invertebrates ⇑ Trevor Williams A, Max Bergoin B, Monique M
    Journal of Invertebrate Pathology 147 (2017) 4–22 Contents lists available at ScienceDirect Journal of Invertebrate Pathology journal homepage: www.elsevier.com/locate/jip Diversity of large DNA viruses of invertebrates ⇑ Trevor Williams a, Max Bergoin b, Monique M. van Oers c, a Instituto de Ecología AC, Xalapa, Veracruz 91070, Mexico b Laboratoire de Pathologie Comparée, Faculté des Sciences, Université Montpellier, Place Eugène Bataillon, 34095 Montpellier, France c Laboratory of Virology, Wageningen University, Droevendaalsesteeg 1, 6708 PB Wageningen, The Netherlands article info abstract Article history: In this review we provide an overview of the diversity of large DNA viruses known to be pathogenic for Received 22 June 2016 invertebrates. We present their taxonomical classification and describe the evolutionary relationships Revised 3 August 2016 among various groups of invertebrate-infecting viruses. We also indicate the relationships of the Accepted 4 August 2016 invertebrate viruses to viruses infecting mammals or other vertebrates. The shared characteristics of Available online 31 August 2016 the viruses within the various families are described, including the structure of the virus particle, genome properties, and gene expression strategies. Finally, we explain the transmission and mode of infection of Keywords: the most important viruses in these families and indicate, which orders of invertebrates are susceptible to Entomopoxvirus these pathogens. Iridovirus Ó Ascovirus 2016 Elsevier Inc. All rights reserved. Nudivirus Hytrosavirus Filamentous viruses of hymenopterans Mollusk-infecting herpesviruses 1. Introduction in the cytoplasm. This group comprises viruses in the families Poxviridae (subfamily Entomopoxvirinae) and Iridoviridae. The Invertebrate DNA viruses span several virus families, some of viruses in the family Ascoviridae are also discussed as part of which also include members that infect vertebrates, whereas other this group as their replication starts in the nucleus, which families are restricted to invertebrates.
    [Show full text]