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About 10,000 papers for “Viral replication”
Aslanimehr, Masoumeh · HRB National Drugs Library (Health Research Board) · 2022
The Joint Committee wishes to acknowledge the considerable work done by the sub-Committee, and each of its individual members, on what is an
Cited by 0Open access
Germán Rosas-Acosta · InTech eBooks · 2013
This book provides a collection of in-depth reviews broadly related to the mechanisms of viral replication as applied to various viruses of critical relevance for human or animal disease. Specifically, this book contains six different chapters: 1) Influenza A Virus Multiplication and the Cellular SUMOylation System; 2) West Nile Virus: Basic Principles, Replication Mechanism, Immune Response and Important Genetic Determinants of Virulence; 3) Hepatitis B Virus Genetic Diversity: Disease Pathogenesis; 4) An Overview of the Immune Evasion Strategies Adopted by Different Viruses With Special Reference to Classical Swine Fever Virus; 5) Viral Replication Strategies: Manipulation of ER Stress Response Pathways and Promotion of IRES-Dependent Translation; 6) Antiviral Replication Agents. This book is aimed at students, scholars, professors, and investigators who are peripherally related to, or somehow intrigued by, the different areas of virology covered in this book, as well as at those individuals with greater expertise and knowledge in the topics herein presented who may want up-to-date in depth reviews related to such topics.
Cited by 5
Kenneth Soderstrom · xPharm: The Comprehensive Pharmacology Reference · 2007
Cited by 1
Frederick A. Murphy, E. Paul J. Gibbs, Marian C. Horzinek et al. · Elsevier eBooks · 1999
Cited by 1
Karen Z. Lancaster (252215), Julie K. Pfeiffer (252217) · Figshare · 2015
<p>Mice were intramuscularly inoculated with 2×10<sup>7</sup> PFU of light-sensitive/neutral red poliovirus in the dark, tissues were harvested at 2, 6, 30 and 72 hpi in the dark, and virus was extracted in the dark. Half of the virus sample for each tissue was exposed to light (inactivating non-replicated viruses, to quantify replicated viruses), and half was maintained in the dark (to quantify all viruses). Virus in light-exposed and non-exposed samples was quantified by plaque assay. Total titer represents titer from non-light-exposed sample and is expressed as PFU/tissue (grey lines). Therefore, the grey lines represent titer from inoculum virus plus replicated virus. The percent of replicated viruses was obtained by dividing the light-exposed titer by the non-light-exposed titer for each individual sample (black bars). Mean with SEM from 3–7 mice is shown.</p>
Cited by 0Open access
J. Charles Whitbeck (7460348), Anu Thomas (220043), Kathryn Kadash-Edmondson (9656384) et al. · Figshare · 2020
<p>Vero or BHK DC-SIGN cells were seeded in 6-well tissue culture plates and grown for 1 d. Medium was replaced with ZIKV RVPs (1 mL/well) or live DENV2 virus in BHK Infection Medium. After 1 h at 37°C, 1 mL of medium was added and cells were grown for 4 d (37°C, 5% CO<sub>2</sub>). Cell monolayers were fixed, blocked, and stained for flavivirus E protein using MAb 4G2 (2 μg/mL) and goat anti-mouse Alexa Fluor 488. Fluorescence (<b>Green</b>) and phase-contrast microscopy (<b>Phase</b>) results are shown.</p> <p>(TIF)</p>
Cited by 0Open access
Ren Sun, Qingmei Jia, Ting-ting Wu et al. · 2003
Cited by 0
Topics in International Health Acute Respiratory Infection CD-ROM, The Wellcome Trust · Acervo Digital da Universidade Estadual Paulista (Universidade Estadual Paulista) · 2011
Cited by 0
Nigel D. Stow, Ronald T. Hay · 1993
Abstract During the last decade considerable interest has focused upon the mechanisms by which the genomes of DNA animal viruses are replicated. These studies provide information relevant not only to our understanding of viral growth and potential strategies for intervention, but also to processes occurring during the replication of eukaryotic chromosomes. The genomes of DNA viruses provide attractive models for the study of cellular DNA synthesis because they are relatively simple, readily manipulated, accumulate to high levels during lytic infection, and, in some cases, can be faithfully replicated in cell-free systems. Some viruses (for example Epstein-Barr virus and bovine papilloma virus (BPV)) additionally establish latent infections in dividing cells during which genome replication is likely to be regulated by mechanisms similar to those operating upon the host chromosomes.
Cited by 0
Joan L. Kenney (327529), A. Paige Adams (122448), Rodion Gorchakov (211881) et al. · Figshare · 2015
<p>Comparison of two parental viruses IAB TrD and IE 68U201 and four chimeric viruses, IAB/IE/IAB, IE/IAB/IE, IAB/IE, and IE/IAB, at a multiplicity of infection (MOI) of 5 on Vero (A) and C6/36 (B) cells. Error bars represent the standard deviation of the means.</p>
Cited by 0Open access
Gregory A. Sowd (299740), Nancy Yan Li (399056), Ellen Fanning (21886) · Figshare · 2015
<p>(A) Experimental scheme for treatment of cells with inhibitor during phases of a 48 h SV40 infection. Early: inhibitor present from −0.5 to 20 hpi. Late: inhibitor present from 20 to 48 hpi. DMSO and Full: solvent or inhibitor, respectively, present from −0.5 to 48 hpi. (B) Western blot of cells treated with Ku-55933 as described in (A). (C) Immunofluorescence of cells treated with Ku-55933 as described in (A) and fixed at 48 hpi. Scale bars, 10 µm. (D) Tag staining patterns, as in (C), were quantified. Graph shows the average of 3 independent experiments.</p>
Cited by 0Open access
David L. Woodland · Viral Immunology · 2010
Cited by 0
Imran Shahid, Abdullah Rzgallah Alzahrani · Directory of Open access Books (OAPEN Foundation) · 2025
Viral replication and production are always phenomenal in a virus's life cycle (either lysogenic or lytic) to produce mutated viral genomes, viral variants, and infectious viral particles. The viral infectivity of a host cell and the progression of an acute viral infection to a chronic form also rely on the pace and fidelity of viral polymerase enzymes. The intricate interplay between the viral genome and the host proteome, virus kinetics/dynamics, and the regulation of viral replication by host cellular networks and cell signaling also predicts the adaptability, evolution, and pathogenesis of highly infectious viruses. The latest advancements in biotechnology and genetic engineering have revolutionized diagnostic and treatment strategies for various viral infections, including hepatitis B and C, influenza, and COVID-19. Similarly, the design and development of various innovative artificial intelligence (AI) tools and machine learning (ML) algorithms have paved the way for elucidating viral replication, transcription, and host invasion mechanisms in great detail. This book provides an overview of the current insights into viral replication mechanisms and viral progeny processes, focusing on dengue virus (DENV), hepatitis B virus (HBV), hepatitis C virus (HCV), morbillivirus, and SARS-CoV-2. The book also briefly sheds light on the replication and biogenesis of infectious viral particles, as well as the regulation by host cell enzymes, growth factors, proteins, receptors, and cell signaling. Viral Replication and Production also concisely explicit the uses of novel gene-level approaches to treat the next generation of viral infections, and also demonstrates how AI, computational virology, ML, and mathematical modeling of viral replication, and virion dynamics could be helpful in the future prediction of an epidemic or pandemic of emerging and re-emerging viral pathogens and to evaluate their impacts on communities and healthcare systems. This book will serve as a valuable resource for further exploring viral replication mechanisms and the processes of virion biogenesis.
Cited by 0Open access
Imran Shahid, Abdullah Rzgallah Alzahrani · IntechOpen eBooks · 2025
Viral replication and production are always phenomenal in a virus's life cycle (either lysogenic or lytic) to produce mutated viral genomes, viral variants, and infectious viral particles. The viral infectivity of a host cell and the progression of an acute viral infection to a chronic form also rely on the pace and fidelity of viral polymerase enzymes. The intricate interplay between the viral genome and the host proteome, virus kinetics/dynamics, and the regulation of viral replication by host cellular networks and cell signaling also predicts the adaptability, evolution, and pathogenesis of highly infectious viruses. The latest advancements in biotechnology and genetic engineering have revolutionized diagnostic and treatment strategies for various viral infections, including hepatitis B and C, influenza, and COVID-19. Similarly, the design and development of various innovative artificial intelligence (AI) tools and machine learning (ML) algorithms have paved the way for elucidating viral replication, transcription, and host invasion mechanisms in great detail. This book provides an overview of the current insights into viral replication mechanisms and viral progeny processes, focusing on dengue virus (DENV), hepatitis B virus (HBV), hepatitis C virus (HCV), morbillivirus, and SARS-CoV-2. The book also briefly sheds light on the replication and biogenesis of infectious viral particles, as well as the regulation by host cell enzymes, growth factors, proteins, receptors, and cell signaling. <i>Viral Replication and Production</i> also concisely explicit the uses of novel gene-level approaches to treat the next generation of viral infections, and also demonstrates how AI, computational virology, ML, and mathematical modeling of viral replication, and virion dynamics could be helpful in the future prediction of an epidemic or pandemic of emerging and re-emerging viral pathogens and to evaluate their impacts on communities and healthcare systems. This book will serve as a valuable resource for further exploring viral replication mechanisms and the processes of virion biogenesis.
Cited by 0
Farshad Guirakhoo · The biomedical & life sciences collection. · 2015
Cited by 0
Mark Marsh, Annegret Pelchen–Matthews · Traffic · 2000
Although initially recognised as essential for the entry of certain viruses, endocytosis is now known to also play important roles in the replication of, and adaptation to, the host cell of a number of viruses. Here we consider several aspects of this association and recent results that have emerged to support this view.
Cited by 90Open access
Christopher A. Lundquist, Jing Zhou, Christopher Aiken et al. · 2003
Cited by 0
Moritz Klawitter · Figshare · 2022
Viral replication in human PBMCs after viral infection.
Cited by 0Open access
Agol Vi · PubMed · 1972
Cited by 1
Sigrid S. Thach, Robert E. Thach · Journal of Molecular Biology · 1973
Cited by 28