DOCSLIB.ORG

Investigation of Poxvirus Host-Range and Gene Expression in Mammalian Cells

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read 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. We also provided additional evidence that plaque formation and virus replication can be independent. More importantly, we identified vgf as the first gene outside MVA’s deletion that explains its host-restriction. Replacement of this region with a vgf cassette derived from a replication-competent virus demonstrated to be sufficient to increase viral yield in all mammalian cell lines tested. Several research and clinical applications can be envisioned derived from this work. INVESTIGATION OF POXVIRUS HOST-RANGE AND GENE EXPRESSION IN MAMMALIAN CELLS. By Jorge David Méndez Ríos Dissertation submitted to the Faculty of the Graduate School of the University of Maryland, College Park, in partial fulfillment of the requirements for the degree of Doctor of Philosophy 2014 Advisory Committee: Dr. Jeffrey DeStefano, Chair Dr. Bernard Moss, Vice-chair Dr. James Culver, Dean’s Representative Dr. Kim Green Dr. Alison McBride Dr. Donald Nuss © Copyright by Jorge David Mendez Rios 2014 Dedication To my wife, parents, grandparents and mentors which all contributed as the building blocks for my success. To the All Mighty, who keeps bringing new surprises to my life. Aby and Ann, study hard. ii Acknowledgment I want to acknowledge my mentor Dr. Bernard Moss for sharing his knowledge and experience in science and virology. Wisdom and ingenious are two things worth imitating from him. I thank Linda Wyatt for teaching me the basic assays in virology. I also want to acknowledge technical support by Zhilong Yang for the plasmids provided; and Karl Erlandson and Andrea Weisberg for the Electron microscopy done for this work. Thanks also to all the post-docs in the lab from 2009 to 2014 for sharing with me all the little tricks that only experience provides. Thanks to my country, Panama, for all the support provided through SENACYT & IFARHU. iii Table of Contents Dedication ........................................................................................................................... ii Acknowledgment ............................................................................................................... iii List of Tables ................................................................................................................... viii List of Figures .................................................................................................................... ix List of Abbreviations ......................................................................................................... xi Chapter 1: Review of Literature ......................................................................................... 1 The Poxviridae ............................................................................................................................. 1 History and epidemiology ....................................................................................................... 1 Virion structure and morphologies .......................................................................................... 4 Genome structure .................................................................................................................... 4 Viral entry ............................................................................................................................... 7 Gene expression ...................................................................................................................... 7 DNA replication .................................................................................................................... 11 Morphogenesis and egress .................................................................................................... 14 Host-range determinants for VACV ...................................................................................... 14 Plaque formation phenotype and its determinants................................................................. 20 Chapter 2: Whole-genome sequencing and identification of the Erythromelalgia-related poxvirus............................................................................................................................. 23 Summary .................................................................................................................................... 23 Introduction ............................................................................................................................... 23 Materials and Methods .............................................................................................................. 24 Cells and virus growth ........................................................................................................... 24 Virus purification and DNA extraction ................................................................................. 24 Library preparation and pyrosequencing ............................................................................... 25 Assembly and completion of the genome sequence .............................................................. 25 Genome annotation and ORF comparison ............................................................................ 28 Genome alignment and comparison of ERPV to closest sequences. .................................... 28 Phylogenetic tree of ERPV and other poxviruses. ................................................................ 29 iv Results ....................................................................................................................................... 29 ERPV genome sequence ....................................................................................................... 29 Comparison of ERPV with ECTV genomes ......................................................................... 30 Phylogeny of ERPV and other orthopoxviruses .................................................................... 35 Discussion .................................................................................................................................. 36 Conclusions ............................................................................................................................... 37 Chapter 3: Generation of MOCV transcriptome profile from in vitro and in vivo samples. ........................................................................................................................................... 38 Summary .................................................................................................................................... 38 Introduction ............................................................................................................................... 38 Materials and Methods .............................................................................................................. 39 Virus stock preparation ......................................................................................................... 39 Cell culturing and infection ................................................................................................... 40 Electron microscopy evaluation ............................................................................................ 40 Cytopathic effect evaluation .................................................................................................. 41 Plasmids and expression constructs ...................................................................................... 41 RNA extraction and RNASeq library preparation................................................................. 42 Sequencing and quality
Load more

Recommended publications
  • Evaluation of the Tetracore Orthopox Biothreat® Antigen Detection Assay
    Journal of Virological Methods 187 (2013) 37–42 Contents lists available at SciVerse ScienceDirect Journal of Virological Methods jou rnal homepage: www.elsevier.com/locate/jviromet ® Evaluation of the Tetracore Orthopox BioThreat antigen detection assay using laboratory grown orthopoxviruses and rash illness clinical specimens a,∗ b a a a Michael B. Townsend , Adam MacNeil , Mary G. Reynolds , Christine M. Hughes , Victoria A. Olson , a a Inger K. Damon , Kevin L. Karem a Centers for Disease Control and Prevention, Division of High-Consequence Pathogens and Pathology, Poxvirus and Rabies Branch, 1600 Clifton Road NE, Mailstop G-06, Atlanta, GA 30333, United States b Centers for Disease Control and Prevention, Global Immunization Division, CGH, 1600 Clifton Road NE, Mailstop G-06, Atlanta, GA 30333, United States a b s t r a c t ® Article history: The commercially available Orthopox BioThreat Alert assay for orthopoxvirus (OPV) detection is piloted. Received 5 December 2011 This antibody-based lateral-flow assay labels and captures OPV viral agents to detect their presence. Serial Received in revised form 23 August 2012 dilutions of cultured Vaccinia virus (VACV) and Monkeypox virus (MPXV) were used to evaluate the sensi- Accepted 30 August 2012 tivity of the Tetracore assay by visual and quantitative determinations; specificity was assessed using a Available online 5 September 2012 small but diverse set of diagnostically relevant blinded samples from viral lesions submitted for routine ® OPV diagnostic testing. The BioThreat Alert assay reproducibly detected samples at concentrations of Keywords: 7 6 10 pfu/ml for VACV and MPXV and positively identified samples containing 10 pfu/ml in 4 of 7 inde- Monkeypox Orthopoxvirus pendent experiments.
    [Show full text]
  • Seroprevalence of TORCH Infections in Children
    Chattagram Maa-O-Shishu Hospital Medical College Journal Volume 17, Issue 1, January 2018 Original Article Seroprevalence of TORCH Infections in Children Sanjoy Kanti Biswas1* Abstract 2 Md. Badruddoza Background : The acronym “TORCH” was introduced to highlight a group of Nahid Sultana1 pathogens that cause a congenital and perinatal infections: Toxoplasma gondi, rubella virus, Cytomegalovirus (CMV) and Herpes Simplex Virus (HSV). These pathogens are often associated with congenital anomalies. Congenital malformations 1 Department of Microbiology have a direct impact on the family. This study was undertaken to detect the Chattagram Maa-O-Shishu Hospital Medical College Chittagong, Bangladesh. serological evidence of TORCH infections in children, by establishing the presence of specific IgM antibodies. Methods: During the period 1st June 2016 to 30th May 2 Department of Paediatrics 2017, 58 suspected TORCH infection cases were included from Paediatrics Chattagram Maa-O-Shishu Hospital Medical College Chittagong, Bangladesh. Department of CMOSH for TORCH antibody detection. The children were in the age of 0 day to 1 year with an average age of 3.3±2.59 months. The serum samples were tested forIgM and IgG antibodies against TORCH agents by using enzyme linked immunoassay method (ELISA). Results: Among the 58 children, seropositivity was found in 55 (94.82%) cases. Of the 55 seropositive cases serological evidence for combination of IgM and IgG with any one of the TORCH agents was detected in 25 (43.10%) and IgG alone was detected in 30 (51.72%) children. IgM/IgG antibody positivity to Toxoplasma, Rubella, CMV and HSV was 21(36.21%), 50(86.21%), 52(89.66%) and 8(13.79%) respectively.
    [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]
  • Control of Lymphocytic Choriomeningitis Virus Infection in Granzyme B Deficient Mice
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Virology 305, 1–9 (2003) doi:10.1006/viro.2002.1754 Control of Lymphocytic Choriomeningitis Virus Infection in Granzyme B Deficient Mice Allan J. Zajac,*,† John M. Dye,* and Daniel G. Quinn*,1 *Department of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois 60153; and †Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 Received July 11, 2001; returned to author for revision October 5, 2001; accepted August 30, 2002 We have investigated whether granzyme B (GzmB)is required for effective cytotoxic T lymphocyte (CTL)mediated control of lymphocytic choriomeningitis virus (LCMV)infection. Clearance of LCMV from tissues of GzmB-deficient (GzmB Ϫ)mice following intraperitoneal infection with LCMV was impaired compared with control mice; however, the virus was ultimately eliminated. The impaired clearance of LCMV in GzmBϪ mice was not due to a deficiency in the generation of LCMV-specific T cells. In addition, CTL from LCMV-infected GzmBϪ mice efficiently lysed virus-infected cells in vitro, but were deficient in their ability to induce rapid DNA fragmentation in target cells. We examined whether the development of protective immunity against intracranial (i.c.)rechallenge with LCMV was compromised in GzmB Ϫ mice. We found that clearance of LCMV from the brain following secondary i.c. infection also was slower in the absence of GzmB; however, the virus was ultimately eliminated and the mice survived. Our data indicate that clearance of LCMV is delayed in the absence of GzmB expression, but that other CTL effector molecules can compensate for the absence of this granule constituent in vivo.
    [Show full text]
  • Rubella ! PROTOCOL CHECKLIST
    Rubella ! PROTOCOL CHECKLIST Enter available information into Merlin upon receipt of initial report, ideally by the next business day Review background on disease, case definition, and laboratory testing Contact health care provider Contact reporting laboratory and request that specimens be sent to the Bureau of Public Health Laboratories (BPHL) for testing Interview patient or guardian Review disease facts Modes of transmission Incubation period Symptoms Ask about exposure to relevant risk factors Immunization history Travel Contact with a known infected or symptomatic person(s) Recent visit to a healthcare setting Identify settings where exposures may have occurred and all known contacts (Sections 6 and 7) Determine evidence of immunity to rubella for contacts Recommend health care provider consultation for exposed women who are pregnant or trying to become pregnant. Monitor contacts for the duration of the incubation period Determine whether patient, symptomatic contacts, or susceptible contacts have exposures in sensitive situation (e.g., school, child care, college dormitory, military, other congregate living settings, health care workers, etc.) Ensure isolation of symptomatic contacts Identify those at-risk with unknown immune status (susceptible persons) for vaccination as indicated Provide education on prevention through vaccination Address patient’s questions or concerns Follow-up on special situations, including persons in sensitive situations and pregnant women Enter additional data obtained from interview into Merlin Rubella Guide to Surveillance and Investigation Rubella 1. DISEASE REPORTING A. Purpose of reporting and surveillance 1. To prevent congenital rubella syndrome (CRS). 2. To assure that children with suspected CRS are tested to confirm or rule out the diagnosis in a timely manner, to assure prompt treatment, and prevent spread of the disease.
    [Show full text]
  • A System Based-Approach to Examine Cytokine Response in Poxvirus-Infected Macrophages
    viruses Article A System Based-Approach to Examine Cytokine Response in Poxvirus-Infected Macrophages Pui-San Wong 1,†, Richard Sutejo 2,†,‡, Hui Chen 2,§ , Sock-Hoon Ng 1, Richard J. Sugrue 2 and Boon-Huan Tan 1,3,* 1 Defence Medical and Environmental Research Institute, DSO National Labs, Singapore 117510, Singapore; [email protected] (P.-S.W.); [email protected] (S.-H.N.) 2 School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore; [email protected] (R.S.); [email protected] (H.C.); [email protected] (R.J.S.) 3 Infection and Immunity, LKC School of Medicine, Nanyang Technological University, Singapore 308232, Singapore * Correspondence: [email protected]; Tel: +65-64857238 † These authors contributed equally to this work. ‡ Current address: International Institute for life Sciences, Jakarta Timur 13210, Indonesia. Received: 9 October 2018; Accepted: 30 November 2018; Published: 5 December 2018 Abstract: The poxviruses are large, linear, double-stranded DNA viruses about 130 to 230 kbp, that have an animal origin and evolved to infect a wide host range. Variola virus (VARV), the causative agent of smallpox, is a poxvirus that infects only humans, but other poxviruses such as monkey poxvirus and cowpox virus (CPXV) have crossed over from animals to infect humans. Therefore understanding the biology of poxviruses can devise antiviral strategies to prevent these human infections. In this study we used a system-based approach to examine the host responses to three orthopoxviruses, CPXV, vaccinia virus (VACV), and ectromelia virus (ECTV) in the murine macrophage RAW 264.7 cell line.
    [Show full text]
  • German Measles
    Rubella (German Measles) Summary Rubella is an infectious viral disease characterized by mild clinical disease, where cases are often subclinical, when symptomatic individuals may present with an erythematous maculopapular rash, lymphadenopathy and a low-grade fever. Infection with the rubella virus causes two distinct illnesses: congenital rubella syndrome (CRS) and postnatal rubella. Rubella virus occurs worldwide. It is most prevalent in winter and spring. In the United States, rubella has been largely controlled after the advent of immunization. The incidence of rubella in the U.S. has decreased by approximately 99% from the pre-vaccine era. Epidemic rubella in the U.S. last occurred in 1964. Agent Rubella virus is in the Togaviridae family, genus Rubivirus. Transmission Reservoir: Humans. Mode of transmission: For postnatal rubella, direct or droplet contact with nasopharyngeal secretions of infected persons. Infants with CRS may shed virus in nasopharyngeal secretions and urine for one year or more and can transmit infection to susceptible contacts. Period of communicability: A few days to 7 days after the onset of rash. Infants with CRS may shed virus in nasopharyngeal secretions and urine for one year or more and can transmit infection to susceptible contacts. Clinical Disease Incubation period: For postnatally acquired rubella, usually 16-18 days; range 14-21 days. Illness: Postnatal rubella is usually a mild disease with diffuse erythematous maculopapular rash, lymphademopathy (commonly sub-occipital, postauricular and cervical) and fever. Adults sometimes have a prodromal illness of headache, malaise, coryza, and conjunctivitis. Arthralgias and arthritis can frequently complicate postnatal rubella, especially in females. Leukopenia and thrombocytopenia can occur, but hemorrhagic complications are rare.
    [Show full text]
  • Enhanced Resistance in STAT6-Deficient Mice to Infection with Ectromelia Virus
    Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus Surendran Mahalingam*†, Gunasegaran Karupiah‡, Kiyoshi Takeda§, Shizuo Akira¶, Klaus I. Matthaei*, and Paul S. Foster* *Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University, Canberra ACT 2601, Australia; ‡Department of Pathology, Division of Faculty of Medicine, Blackburn Building, D06, University of Sydney, Sydney NSW 2006, Australia; §Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Suita-shi, Osaka 565-0871, Japan; and ¶Department of Biochemistry, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan Communicated by Frank J. Fenner, Australian National University, Canberra, Australia, March 27, 2001 (received for review January 25, 2001) -We inoculated BALB͞c mice deficient in STAT6 (STAT6؊/؊) and their characterized in Leishmania major infection. Studies have indi wild-type (wt) littermates (STAT6؉/؉) with the natural mouse cated that control of lesion growth induced by L. major in pathogen, ectromelia virus (EV). STAT6؊/؊ mice exhibited in- genetically resistant mice (C57BL͞6) is associated with the creased resistance to generalized infection with EV when com- expansion of CD4ϩ T helper 1 (Th1) cells and the production of ؉ ؉ pared with STAT6 / mice. In the spleens and lymph nodes of cytokines such as IL-12, IFN-␥, and IL-2 (13, 14). By contrast, ؊ ؊ STAT6 / mice, T helper 1 (Th1) cytokines were induced at earlier nonhealing responses in susceptible mice (BALB͞c) have been time points and at higher levels postinfection when compared with related to the expansion of CD4ϩ Th2 cells and the production ؉ ؉ those in STAT6 / mice.
    [Show full text]
  • Ectromelia Virus Disease Characterization in the BALB/C Mouse: a Surrogate Model for Assessment of Smallpox Medical Countermeasures
    viruses Article Ectromelia Virus Disease Characterization in the BALB/c Mouse: A Surrogate Model for Assessment of Smallpox Medical Countermeasures Jennifer Garver 1,*, Lauren Weber 1, Eric M. Vela 2, Mike Anderson 1, Richard Warren 3, Michael Merchlinsky 3, Christopher Houchens 3 and James V. Rogers 1 1 Battelle Biomedical Research Center, West Jefferson, OH 43162, USA; [email protected] (L.W.); [email protected] (M.A.); [email protected] (J.V.R.) 2 Vaccine and Gene Therapy Institute, Oregon Health and Science University, Portland, OR 97239, USA; [email protected] 3 Biomedical Advanced Research and Development Authority, US Department of Health and Human Services, Washington, DC 20201, USA; [email protected] (R.W.); [email protected] (M.M.); [email protected] (C.H.) * Correspondence: [email protected]; Tel.: +1-614-424-3984; Fax: +1-614-458-3984 Academic Editor: Curt Hagedorn Received: 22 June 2016; Accepted: 19 July 2016; Published: 22 July 2016 Abstract: In 2007, the United States’ Food and Drug Administration (FDA) issued guidance concerning animal models for testing the efficacy of medical countermeasures against variola virus (VARV), the etiologic agent for smallpox. Ectromelia virus (ECTV) is naturally-occurring and responsible for severe mortality and morbidity as a result of mousepox disease in the murine model, displaying similarities to variola infection in humans. Due to the increased need of acceptable surrogate animal models for poxvirus disease, we have characterized ECTV infection in the BALB/c mouse. Mice were inoculated intranasally with a high lethal dose (125 PFU) of ECTV, resulting in complete mortality 10 days after infection.
    [Show full text]
  • Measles, Mumps, Rubella, Varicella Jul 2020
    Measles, Mumps, Rubella, Varicella Jul 2020 Health Care Professional Programs Measles, mumps, rubella and varicella are vaccine-preventable diseases. The efficacy of two doses of vaccine (one for rubella) is close to 100% for measles, 76-95% for mumps, 95% for rubella, and 98-100% for varicella. If born before 1970, you may be immune to measles, mumps and rubella due to naturally acquired infection; after 1970 you most likely received one or two vaccines. You may be immune to varicella due to naturally acquired infection or you may have received one or two vaccines (vaccine introduced in Canada in 1999). If you are unable to locate your vaccination records, revaccination is safe unless you are pregnant or immunocompromised. Measles: Measles is one of the most highly communicable infectious diseases with greater than 90% secondary attack rates among susceptible persons. Symptoms include fever, cough, runny nose, red eyes, Koplik spots (white spots on the inner lining of the mouth), followed by a rash that begins on the face, advances to the trunk and then to the arms and legs. The virus is transmitted by the airborne route, respiratory droplets, or direct contact with nasal or throat secretions of infected persons. The incubation period is 7 to 18 days. Cases are infectious from 4 days before the beginning of the prodromal period to 4 days after rash onset. Mumps: Mumps virus is highly contagious and is transmitted primarily by droplet spread, as well as by direct contact with saliva of an infected person. Symptoms of mumps virus infection include fever, headache and muscle aches followed by swelling in one or more salivary glands (usually parotid gland).
    [Show full text]
  • Sequential Activation of Two Pathogen-Sensing Pathways Required for Type I Interferon Expression and Resistance to an Acute DNA Virus Infection
    Article Sequential Activation of Two Pathogen-Sensing Pathways Required for Type I Interferon Expression and Resistance to an Acute DNA Virus Infection Highlights Authors d TLR9, MyD88, STING, and IRF7 are required for IFN-I Ren-Huan Xu, Eric B. Wong, Daniel expression in the dLN Rubio, ..., Shinu John, Mark Shlomchik, Luis J. Sigal d Inflammatory monocytes are the major producers of IFN-I in the dLN Correspondence + [email protected] d TLR9, MyD88, and IRF7 are required in CD11c cells for iMo recruitment to dLNs In Brief d STING-IRF7 are required in iMos for IFN-a and STING-NF-kB How different pathogen-sensing for IFN-b expression in iMos mechanisms contribute to the expression of IFN-I in vivo is unclear. Sigal and colleagues report that in lymph nodes of ectromelia-virus-infected mice, CD11c+ cells use TLR9-MyD88-IRF7 to recruit inflammatory monocytes (iMos). In turn, infected iMos express IFN-a and IFN-b through STING-IRF7 and STING-NF-kB, respectively. Xu et al., 2015, Immunity 43, 1148–1159 December 15, 2015 ª2015 Elsevier Inc. http://dx.doi.org/10.1016/j.immuni.2015.11.015 Immunity Article Sequential Activation of Two Pathogen-Sensing Pathways Required for Type I Interferon Expression and Resistance to an Acute DNA Virus Infection Ren-Huan Xu,1,5 Eric B. Wong,1,6 Daniel Rubio,1,7 Felicia Roscoe,1 Xueying Ma,1 Savita Nair,1 Sanda Remakus,1 Reto Schwendener,2 Shinu John,3 Mark Shlomchik,4 and Luis J. Sigal1,6,* 1Immune Cell Development and Host Defense Program, The Research Institute at Fox Chase Cancer Center, 333 Cottman Avenue,
    [Show full text]
  • New Insights Into the Evolutionary and Genomic Landscape of Molluscum Contagiosum Virus (MCV) Based on Nine MCV1 and Six MCV2 Complete Genome Sequences
    viruses Article New Insights into the Evolutionary and Genomic Landscape of Molluscum Contagiosum Virus (MCV) based on Nine MCV1 and Six MCV2 Complete Genome Sequences Tomaž M. Zorec 1 , Denis Kutnjak 2 , Lea Hošnjak 1 , Blanka Kušar 1, Katarina Trˇcko 3, Boštjan J. Kocjan 1 , Yu Li 4, Miljenko Križmari´c 5, Jovan Miljkovi´c 5, Maja Ravnikar 2 and Mario Poljak 1,* 1 Institute of Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, Zaloška 4, SI-1000 Ljubljana, Slovenia; [email protected] (T.M.Z.); [email protected] (L.H.); [email protected] (B.K.); [email protected] (B.J.K.) 2 Department of Biotechnology and Systems Biology, National Institute of Biology, Veˇcna pot 111, SI-1000 Ljubljana, Slovenia; [email protected] (D.K.); [email protected] (M.R.) 3 Department of Dermatovenereology, University Medical Centre Maribor, Ljubljanska ulica 5, SI-2000 Maribor, Slovenia; [email protected] 4 Poxvirus and Rabies Branch, Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Atlanta, GA 30333, USA; [email protected] 5 Faculty of Medicine, University of Maribor, Taborska Ulica 6b, SI-2000 Maribor, Slovenia; [email protected] (M.K.); [email protected] (J.M.) * Correspondence: [email protected]; Tel.: +386-1-543-7415 Received: 9 October 2018; Accepted: 25 October 2018; Published: 26 October 2018 Abstract: Molluscum contagiosum virus (MCV) is the sole member of the Molluscipoxvirus genus and the causative agent of molluscum contagiosum (MC), a common skin disease.
    [Show full text]