Capsid Coding Sequence Is Required for Efficient Replication of Human
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The Positive Rhinovirus/Enterovirus Detection and SARS-Cov-2 Persistence Beyond the Acute Infection Phase: an Intra-Household Surveillance Study
viruses Communication The Positive Rhinovirus/Enterovirus Detection and SARS-CoV-2 Persistence beyond the Acute Infection Phase: An Intra-Household Surveillance Study Pedro Brotons 1,2,3, Iolanda Jordan 1,3,4, Quique Bassat 3,5,6,7,8 , Desiree Henares 1,3, Mariona Fernandez de Sevilla 1,3,5, Sara Ajanovic 7, Alba Redin 1,2, Vicky Fumado 1,5, Barbara Baro 7 , Joana Claverol 9, Rosauro Varo 7 , Daniel Cuadras 9 , Jochen Hecht 10, Irene Barrabeig 3,11, Juan Jose Garcia-Garcia 1,3,5, Cristian Launes 1,3,5,† and Carmen Muñoz-Almagro 1,2,3,12,*,† 1 Pediatric Infectious Diseases Research Group, Institut de Recerca Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain; [email protected] (P.B.); [email protected] (I.J.); [email protected] (D.H.); [email protected] (M.F.d.S.); [email protected] (A.R.); [email protected] (V.F.); [email protected] (J.J.G.-G.); [email protected] (C.L.) 2 Department of Medicine, School of Medicine, Universitat Internacional de Catalunya, Sant Cugat, 08195 Barcelona, Spain 3 Consorcio de Investigacion Biomédica en Red Epidemiologia y Salud Pública (CIBERESP), 28029 Madrid, Spain; [email protected] (Q.B.); [email protected] (I.B.) 4 Pediatric Intensive Care Unit, Hospital Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain 5 Pediatrics Department, Hospital Sant Joan de Déu, Esplugues de Llobregat, 08950 Barcelona, Spain 6 Centro de Investigação em Saúde de Manhiça (CISM), Manhiça 1929, Mozambique Citation: Brotons, P.; Jordan, I.; 7 ISGlobal, Hospital Clínic-Universitat de Barcelona, 08036 Barcelona, Spain; [email protected] (S.A.); Bassat, Q.; Henares, D.; Fernandez de [email protected] (B.B.); [email protected] (R.V.) Sevilla, M.; Ajanovic, S.; Redin, A.; 8 Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010 Barcelona, Spain Fumado, V.; Baro, B.; Claverol, J.; et al. -
Global Distribution of Novel Rhinovirus Genotype
DISPATCHES in resource-poor regions (1). Streptococcus pneumoniae Global Distribution and Haemophilus infl uenzae are important bacterial causes of ARI, although their impact is expected to decline with of Novel Rhinovirus increasing vaccine coverage. Collectively, however, virus- es dominate as causative agents in ARI. Viruses frequently Genotype implicated in ARI include infl uenza virus, respiratory syn- Thomas Briese,* Neil Renwick,* Marietjie Venter,† cytial virus, metapneumovirus, parainfl uenza virus, human Richard G. Jarman,‡ Dhrubaa Ghosh,§ enterovirus (HEV), and human rhinovirus (HRV). Sophie Köndgen,¶ Sanjaya K. Shrestha,# HRVs are grouped taxonomically into Human rhinovi- A. Mette Hoegh,** Inmaculada Casas,†† Edgard rus A (HRV-A) and Human rhinovirus B (HRV-B), 2 spe- Valerie Adjogoua,‡‡ cies within the family Picornaviridae (International Com- Chantal Akoua-Koffi ,‡‡ Khin Saw Myint,‡ David T. mittee on Taxonomy of Viruses database [ICTVdb]; http:// Williams,§§ Glenys Chidlow,¶¶ phene.cpmc.columbia.edu). These nonenveloped, positive- Ria van den Berg,† Cristina Calvo,## sense, single-stranded RNA viruses have been classifi ed se- Orienka Koch,† Gustavo Palacios,* rologically and on the basis of antiviral susceptibility pro- Vishal Kapoor,* Joseph Villari,* fi le, nucleotide sequence relatedness, and receptor usage (2). Samuel R. Dominguez,*** Kathryn V. Holmes,*** Phylogenetic analyses of viral protein VP4/VP2 and VP1 Gerry Harnett,¶¶ David Smith,¶¶ coding regions indicate the presence of 74 serotypes in ge- John S. Mackenzie,§§ Heinz Ellerbrok,¶ netic group A and 25 serotypes in genetic group B (2). Brunhilde Schweiger,¶ Kristian Schønning,** Isolated in the 1950s from persons with upper respi- Mandeep S. Chadha,§ Fabian H. Leendertz,¶ A.C. ratory tract symptoms (2,3), HRVs have become known Mishra,§ Robert V. -
Atomic Structure of a Rhinovirus C, a Virus Species Linked to Severe
Atomic structure of a rhinovirus C, a virus species SEE COMMENTARY linked to severe childhood asthma Yue Liua, Marchel G. Hillb, Thomas Klosea, Zhenguo Chena, Kelly Wattersb, Yury A. Bochkovc, Wen Jianga, Ann C. Palmenbergb,1, and Michael G. Rossmanna,1 aDepartment of Biological Sciences, Purdue University, West Lafayette, IN 47907; bInstitute for Molecular Virology, University of Wisconsin, Madison, WI 53706; and cDepartment of Pediatrics, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53706 Edited by Peter Palese, Icahn School of Medicine at Mount Sinai, New York, NY, and approved June 7, 2016 (received for review April 25, 2016) Isolates of rhinovirus C (RV-C), a recently identified Enterovirus Picornavirus capsids are assembled from 60 copies of biolog- (EV) species, are the causative agents of severe respiratory infec- ical protomers, each composed of four proteins: VP1, VP2, VP3, tions among children and are linked to childhood asthma exacer- and VP4 (2). The three large surface polypeptides, VP1, VP2, bations. The RV-C have been refractory to structure determination and VP3, are folded into eight-stranded antiparallel “jelly rolls.” because they are difficult to propagate in vitro. Here, we report During the assembly process, autocatalytic cleavage of precursor the cryo-EM atomic structures of the full virion and native empty VP0 into VP2 and VP4 in the presence of viral RNA results in particle (NEP) of RV-C15a. The virus has 60 “fingers” on the virus the formation of full infectious virions (20). The arrangement of outer surface that probably function as dominant immunogens. jelly rolls in the virions exhibits pseudo T = 3 icosahedral sym- Because the NEPs also display these fingers, they may have utility metry with an outer diameter of ∼300 Å (2, 3). -
Herpes Simplex Virus Type 1 Oril Is Not Required for Virus Infection In
JOURNAL OF VIROLOGY, Nov. 1987, p. 3528-3535 Vol. 61, No. 11 0022-538X/87/113528-08$02.00/0 Copyright C 1987, American Society for Microbiology Herpes Simplex Virus Type 1 oriL Is Not Required for Virus Replication or for the Establishment and Reactivation of Latent Infection in Mice MARYELLEN POLVINO-BODNAR, PAULO K. ORBERG, AND PRISCILLA A. SCHAFFER* Laboratory of Tumor Virus Genetics, Dana-Farber Cancer Institute, and Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115 Received 11 May 1987/Accepted 31 July 1987 During the course of experiments designed to isolate deletion mutants of herpes simplex virus type 1 in the gene encoding the major DNA-binding protein, ICP8, a mutant, d61, that grew efficiently in ICP8-expressing Vero cells but not in normal Vero cells was isolated (P. K. Orberg and P. A. Schaffer, J. Virol. 61:1136-1146, 1987). d61 was derived by cotransfection of ICP8-expressing Vero cells with infectious wild-type viral DNA and a plasmid, pDX, that contains an engineered 780-base-pair (bp) deletion in the ICP8 gene, as well as a spontaneous -55-bp deletion in OriL. Gel electrophoresis and Southern blot analysis indicated that d61 DNA carried both deletions present in pDX. The ability of d61 to replicate despite the deletion in OriL suggested that a functional OriL is not essential for virus replication in vitro. Because d61 harbored two mutations, a second mutant, ts+7, with a deletion in oriL-associated sequences and an intact ICP8 gene was constructed. Both d61 and ts+7 replicated efficiently in their respective permissive host cells, although their yields were slightly lower than those of control viruses with intact oriL sequences. -
Foamy Virus Assembly with Emphasis on Pol Encapsidation
Viruses 2013, 5, 886-900; doi:10.3390/v5030886 OPEN ACCESS viruses ISSN 1999-4915 www.mdpi.com/journal/viruses Review Foamy Virus Assembly with Emphasis on Pol Encapsidation Eun-Gyung Lee 1, Carolyn R. Stenbak 2 and Maxine L. Linial 1,* 1 Fred Hutchinson Cancer Research Center, Basic Sciences Division; 1100 Fairview Avenue North, Seattle, WA 98109, USA; E-Mails: [email protected] (EGL); [email protected] (MLL) 2 Seattle University, Biology Department; 901 12th Avenue, Seattle, WA 98122, USA; E-Mail: [email protected] * Authors to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +1-206- 667-4442; Fax: +1-206-667-5939 Received: 31 January 2013; in revised form: 11 March 2013 / Accepted: 14 March 2013 / Published: 20 March 2013 Abstract: Foamy viruses (FVs) differ from all other genera of retroviruses (orthoretroviruses) in many aspects of viral replication. In this review, we discuss FV assembly, with special emphasis on Pol incorporation. FV assembly takes place intracellularly, near the pericentriolar region, at a site similar to that used by betaretroviruses. The regions of Gag, Pol and genomic RNA required for viral assembly are described. In contrast to orthoretroviral Pol, which is synthesized as a Gag-Pol fusion protein and packaged through Gag-Gag interactions, FV Pol is synthesized from a spliced mRNA lacking all Gag sequences. Thus, encapsidation of FV Pol requires a different mechanism. We detail how WT Pol lacking Gag sequences is incorporated into virus particles. In addition, a mutant in which Pol is expressed as an orthoretroviral-like Gag-Pol fusion protein is discussed. -
Topological Analysis of the Gp41 MPER on Lipid Bilayers Relevant to the Metastable HIV-1 Envelope Prefusion State
Topological analysis of the gp41 MPER on lipid bilayers relevant to the metastable HIV-1 envelope prefusion state Yi Wanga,b, Pavanjeet Kaurc,d, Zhen-Yu J. Sune,1, Mostafa A. Elbahnasawya,b,2, Zahra Hayatic,d, Zhi-Song Qiaoa,b,3, Nhat N. Buic, Camila Chilea,b,4, Mahmoud L. Nasre,5, Gerhard Wagnere, Jia-Huai Wanga,f, Likai Songc, Ellis L. Reinherza,b,6, and Mikyung Kima,g,6 aLaboratory of Immunobiology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115; bDepartment of Medicine, Harvard Medical School, Boston, MA 02115; cNational High Magnetic Field Laboratory, Florida State University, Tallahassee, FL 32306; dDepartment of Physics, Florida State University, Tallahassee, FL 32306; eDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115; fDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215; and gDepartment of Dermatology, Harvard Medical School, Boston, MA 02215 Edited by Peter Palese, Icahn School of Medicine at Mount Sinai, New York, NY, and approved September 23, 2019 (received for review July 18, 2019) The membrane proximal external region (MPER) of HIV-1 envelope immunologically vulnerable epitopes targeted by several of the most glycoprotein (gp) 41 is an attractive vaccine target for elicitation of broadly neutralizing antibodies (bNAbs) developed during the broadly neutralizing antibodies (bNAbs) by vaccination. However, course of natural HIV-1 infection (10–13). Insertion, deletion, current details regarding the quaternary structural organization of and mutations of residues in the MPER defined the functional the MPER within the native prefusion trimer [(gp120/41)3] are elu- importance of the MPER in Env incorporation, viral fusion, and sive and even contradictory, hindering rational MPER immunogen infectivity (14–16). -
(Infected Cell Protein 8) of Herpes Simplex Virus L*
THEJOURNAL OF BIOLOGICAL CHEMISTRY Vol. 262, No. 9, Issue of March 25, pp. 4260-4266, 1987 0 1987 by The American Society of Biological Chemists, Inc Printed in U.S. A. Interaction between theDNA Polymerase and Single-stranded DNA- binding Protein (Infected Cell Protein 8) of Herpes Simplex Virus l* (Received for publication, September 22, 1986) Michael E. O’DonnellS, Per EliasQ,Barbara E. Funnellll, and I. R. Lehman From the Department of Biochemistry, Stanford University School of Medicine, Stanford, California 94305 The herpes virus-encoded DNA replication protein, ICP8 completely inhibits replication of singly primed ssDNA infected cell protein 8 (ICPS), binds specifically to templates by the herpespolymerase. On the other hand, ICP8 single-stranded DNA with a stoichiometry of one ICPS strongly stimulates replication of duplex DNA. It does so, molecule/l2 nucleotides. In the absence of single- however, onlyin the presence of anuclear extract from stranded DNA, it assembles into long filamentous herpes-infected cells. structures. Binding of ICPS inhibits DNA synthesis by the herpes-induced DNA polymerase on singly primed EXPERIMENTALPROCEDURES single-stranded DNA circles. In contrast, ICPS greatly Materials-DNase I and venom phosphodiesterase were obtained stimulates replication of circular duplex DNA by the from Worthington. The syntheticoligodeoxynucleotide (44-mer) was polymerase. Stimulation occurs only in the presence of synthesized by the solid-phase coupling of protected phosphoramidate a nuclear extract from herpes-infected cells. Appear- nucleoside derivatives (11).3H-Labeled #X ssDNA was a gift from ance of the stimulatory activity in nuclear extracts Dr. R. Bryant (this department). pMOB45 (10.5 kilobases) linear coincides closely with the time of appearance of her- duplex plasmid DNA was a gift from Dr. -
Understanding Human Astrovirus from Pathogenesis to Treatment
University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 6-2020 Understanding Human Astrovirus from Pathogenesis to Treatment Virginia Hargest University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Diseases Commons, Medical Sciences Commons, and the Viruses Commons Recommended Citation Hargest, Virginia (0000-0003-3883-1232), "Understanding Human Astrovirus from Pathogenesis to Treatment" (2020). Theses and Dissertations (ETD). Paper 523. http://dx.doi.org/10.21007/ etd.cghs.2020.0507. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Understanding Human Astrovirus from Pathogenesis to Treatment Abstract While human astroviruses (HAstV) were discovered nearly 45 years ago, these small positive-sense RNA viruses remain critically understudied. These studies provide fundamental new research on astrovirus pathogenesis and disruption of the gut epithelium by induction of epithelial-mesenchymal transition (EMT) following astrovirus infection. Here we characterize HAstV-induced EMT as an upregulation of SNAI1 and VIM with a down regulation of CDH1 and OCLN, loss of cell-cell junctions most notably at 18 hours post-infection (hpi), and loss of cellular polarity by 24 hpi. While active transforming growth factor- (TGF-) increases during HAstV infection, inhibition of TGF- signaling does not hinder EMT induction. However, HAstV-induced EMT does require active viral replication. -
Two Interferon-Independent Double-Stranded RNA-Induced Host
Two interferon-independent double-stranded RNA- induced host defense strategies suppress the common cold virus at warm temperature Ellen F. Foxmana,b, James A. Storera,1, Kiran Vanajac, Andre Levchenkoc, and Akiko Iwasakia,d,2 aDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; bDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520; cDepartment of Biomedical Engineering, Systems Biology Institute, Yale University, Yale University School of Medicine, New Haven, CT 06520; and dHoward Hughes Medical Institute, New Haven, CT 06520 Edited by Jonathan C. Kagan, Children’s Hospital Boston, Boston, MA, and accepted by Editorial Board Member Tadatsugu Taniguchi June 6, 2016 (received for review February 4, 2016) Most strains of rhinovirus (RV), the common cold virus, replicate receptor, IFN-αβR (4). However, some restriction of viral rep- better at cool temperatures found in the nasal cavity (33–35 °C) than lication at 37 °C persisted even in the genetic absence of mole- at lung temperature (37 °C). Recent studies found that although cules required for the type 1 IFN response, including the RLR 37 °C temperature suppressed RV growth largely by engaging signaling adaptor, mitochondrial antiviral signaling protein (MAVS), the type 1 IFN response in infected epithelial cells, a significant and IFN-αβR. These observations promptedustoexplorewhether temperature dependence to viral replication remained in cells de- other additional host defense mechanisms also participate in the void of IFN induction or signaling. To gain insight into IFN-independent temperature-dependent restriction of RV replication. mechanisms limiting RV replication at 37 °C, we studied RV infec- In this study, we examined IFN-independent mechanisms in- tion in human bronchial epithelial cells and H1-HeLa cells. -
Astrovirus MLB2, a New Gastroenteric Virus Associated with Meningitis and Disseminated Infection Samuel Cordey,1 Diem-Lan Vu,1 Manuel Schibler, Arnaud G
RESEARCH Astrovirus MLB2, a New Gastroenteric Virus Associated with Meningitis and Disseminated Infection Samuel Cordey,1 Diem-Lan Vu,1 Manuel Schibler, Arnaud G. L’Huillier, Francisco Brito, Mylène Docquier, Klara M. Posfay-Barbe, Thomas J. Petty, Lara Turin, Evgeny M. Zdobnov, Laurent Kaiser Next-generation sequencing has identified novel astrovi- observed in community healthcare centers (2,3). Symp- ruses for which a pathogenic role is not clearly defined. toms are generally mild, with patient hospitalization We identified astrovirus MLB2 infection in an immunocom- usually not required; asymptomatic carriage has been petent case-patient and an immunocompromised patient described in 2% of children (4). who experienced diverse clinical manifestations, notably, Screening of fecal samples from persons with diarrhea meningitis and disseminated infection. The initial case-pa- and control samples in different parts of the world by un- tient was identified by next-generation sequencing, which revealed astrovirus MLB2 RNA in cerebrospinal fluid, biased next-generation sequencing (NGS) or reverse tran- plasma, urine, and anal swab specimens. We then used scription PCR (RT-PCR) has revealed the sporadic pres- specific real-time reverse transcription PCR to screen 943 ence of members of the Astroviridae family, previously fecal and 424 cerebrospinal fluid samples from hospital- unrecognized in humans, that are phylogenetically substan- ized patients and identified a second case of meningitis, tially distant from classic HAstVs (3,5–9). These viruses with positive results for the agent in the patient’s feces have been named HAstV-VA/HMO and HAstV-MLB, for and plasma. This screening revealed 5 additional positive Virginia, human-mink-ovine, and Melbourne, respectively, fecal samples: 1 from an infant with acute diarrhea and according to the place where they were first identified and 4 from children who had received transplants. -
Cold and Flu Fact Sheet
Cold and Flu Fact Sheet The common cold, including chest colds, head colds, and the seasonal flu are caused by viruses that can put a damper on your holiday spirit. While Cold and Flu season can start as early as October and can last as late as May, activity peaks during Christmas time and will want to make you say Bah-Humbug! General Information Virology Clinical manifestations Cold - The common cold is a viral infection of the upper Cold - Symptoms of a common cold usually appear about respiratory tract. The most commonly implicated virus is a one to three days after exposure to a cold-causing virus. rhinovirus. Other commonly implicated viruses include Signs and symptoms typically include a runny/stuffy nose, human coronavirus, influenza viruses, and adenovirus. itchy/sore throat, cough, congestion, slight body aches and Frequently, more than one virus is present. The difficultly mild headache, sneezing, water eyes, and mild fatigue. with pathogens associated with the common cold is that some viruses are enveloped, meaning they are easy to kill Flu - Symptoms of seasonal influenza are very similar to (such as influenza) while others are non-enveloped, those of the common cold, except the flu can be meaning they are harder to kill (such as rhinovirus). This distinguished by a high fever and more severe symptoms emphasizes the importance of choosing disinfectant of the common cold. products with the ability to kill both enveloped and non- enveloped viruses. Pandemics and Outbreaks A pandemic is a global disease outbreak. It is determined Flu - Influenza (commonly known as the flu) are influenza by how the disease spreads, not by how many deaths it viruses which are enveloped, RNA viruses that make up causes. -
Enzyme Activities in Four Different Forms of Human Immunodeficiency
Proc. Nati. Acad. Sci. USA Vol. 88, pp. 45%-4600, June 1991 Biochemistry Enzyme activities in four different forms of human immunodeficiency virus 1 poi gene products (reverse transcriptase/RNase H/crossover linker mutagenesis/baculoirus expression system) YU-WEN HU AND C. YONG KANG Department of Microbiology and Immunology, University of Ottawa, Faculty of Medicine, Ottawa, ON, Canada K1H 8M5 Communicated by Max D. Summers, February 19, 1991 (received for review December 3, 1990) ABSTRACT Five cassettes of the pol gene of human im- activity (10, 11) but no RNase H activity (3, 7, 12, 13). The munodeficiency virus 1 were constructed and inserted under reverse transcriptase isolated from purified HIV-1 has a the control of the polyhedrin gene promoter of Autographa molecular mass of 95 (14) to 110 (15) kDa, as determined by calfornica nuclear polyhedrosis virus by homologous recom- gel filtration and glycerol gradient centrifugation, respec- bination. The first cassette polF contains the full-length pol tively. However, the 98-kDa nonprocessed polyprotein ex- open reading frame; the second cassette pollOO starts with the pressed in Escherichia coli displayed little or no reverse first AUG codon of the pol gene and deletes 103 amino acids transcriptase activity (16). The p66/pSi heterodimer ex- from the amino terminus of the pol gene product; the third pressed in E. coli has an apparent molecular mass of 120-130 cassette po197 deletes the entire protease coding sequence; the kDa and was active (5, 6). In addition, there is a 165-kDa fourth cassette po166 deletes both the protease and endonucle- putative gag-pol precursor polyprotein that also possesses ase/integrase coding sequences; and the fifth cassette polSl reverse transcriptase activity (10).