Herpesviruses are divided into three groups: The α herpesviruses, herpes simplex virus types 1 and 2, and varicella-zoster virus, have a short replicative cycle, induce cytopathology in monolayer cell cultures, and have a broad host range; β herpesviruses, cytomegalovirus, and huma Herpes virus replication i) Binding to the cell surface: As with many other viruses, cell tropism is determined by the availability of the correct receptor on the surface of the cell to be infected
Herpes simplex virus (HSV) replicated in mitogen-stimulated human T cells. Virus replication was obtained in highly enriched mitogen-stimulated T cells of the OKT 3+, OKT 4+, or OKT 8+ subtype, in stimulated B cells, and in macrophages precultured for 7 days The virion host shutoff protein (VHS or UL41) is very important to viral replication. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene expression of viral proteins. The viral genome immediately travels to the nucleus, but the VHS protein remains in the cytoplasm Steps in Viral Replication: Assembly and Release (Sixth and Seventh Steps) Process involves bringing together newly formed genomic nucleic acid and structural proteins to form the nucleocapsid of the virus Nonenveloped viruses exhibit full maturation in the cytoplasm or nucleus with disintegration of cel Here we showed that honokiol had no effect on herpes simplex virus-1 (HSV-1) entry, but inhibited HSV-1 viral DNA replication, gene expression and the production of new progeny viruses. The combination of honokiol and clinical drug acyclovir augmented inhibition of HSV-1 infection Human peripheral blood leukocytes, lymphocyte subpopulations, and hemic cell lines were examined for their ability to supprot HSV and CMV replication. Mitogen-stimulated mononuclear leukocytes, B lymphocytes, and T lymphcytes supported the replication of HSV to high titers over 3 to 5 days of infection
The replication of type 2 herpes simplex virus in human endocervical tissue in organ culture was investigated. The temporal profile of virus replication was related to the initial virus inoculum; high input inocula induced a rapid increase in virus titre while lower multiplicities induced a more slow-rising increase in virus titre The virus enters the body through inhalation and affects cattle worldwide. interferon: Any of a group of glycoproteins, produced by the immune system, that prevent viral replication in infected cells. The study of animal viruses is important from a veterinary viewpoint. Many animal viruses are also important from a human medical perspective Replication of herpes simplex virus DNA: localization of replication recognition signals within defective virus genomes Like many other viruses, herpesviruses confine their gene expression and replication to distinct intranuclear sites known as replication compartments (RCs). In this short review, we discuss the formation of these structures, their ability to attract viral and cellular proteins, and the impact of interactions between distinct individual RCs
Although there is no firm proof for the existence of thetareplication intermediates that initiate at one or more of the HSV-1 origins in vivo, genome circularization is a prerequisite for viral replication, and replication requires either ori S or ori L and the action of a viral protein that possesses all the properties of an initiator protein (UL9 protein) Replication of Herpes Simplex Virus. SOURCE: Perry, et al., Microbial Life, First Edition, published by Sinauer Associates. Microbial Life is available from Oxford University Press Resveratrol, a phytoalexin, was found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner. The observed reduction in virus yield was not caused by the direct inactivation of HSV by resveratrol nor inhibition of virus attachment to the cell replication of herpes virus. STUDY. Flashcards. Learn. Write. Spell. Test. PLAY. Match. Gravity. Created by. brittanyhickey. Terms in this set (45) what are the nomenclatures for herpes virus. HSV, EBV, HHV1-8. what enzymes does herpes virus encode. thymidine kinase or DNA polymerase. describe the structure of herpes Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. Through the generation of abundant copies of its genome and packaging these copies, the virus continues infecting new hosts. Replication between viruses is greatly varied and depends on the type of genes.
Herpes simplex virus type 1 DNA replication isspecifically required for high-frequency homologous recombinationbetween repeated sequences. J. Virol. 69 : 3084-3089 transcription or replication of the viral RNA genome. So, RNA viruses should carry or code for their own RdRp for productive replication. Eukaryotic cells are not equipped to translate polycistronic mRNA into several individual proteins. RNA viruses mostly replicate in cytoplasm and have no access to the RNA splicing enzymes present in the nucleus Human Herpes Virus - 6 • HHV-6 detected in patients with lymphoproliferative diseases. • Genetically distinct but morphologically similar to other herpes virus. • Replicates in lymphoid tissue preferentially in T lymphocytes. • Cytopathic for T lymphocytes in cell culture
Herpes simplex virus type 1 (HSV-1) is the prototype and best-studied virus of the α-herpesvirus group. HSV-1 undergoes a rapid productive replication cycle in host epithelial cells in vivo and in susceptible cultured cells in vitro.However, HSV-1 is also neurotropic and establishes life-long latent infections in the sensory neurons of the host, where the genome is in a nonreplicating. Steps of Virus Replication Cycle 1 Attachment to target cell. 2 Penetration (entry) from cell membrane. 3 Uncoating. 4 Expression (transcription and translation) of viral proteins. 5 Replication of the viral nucleic acid. 6 Virus assembly. 7 Maturation. 8 Release from infected cell The herpes simplex virus (HSV) ICP34.5 null mutant 1716 replicates selectively in actively dividing cells and has been proposed as a potential treatment for cancer, particularly brain tumours. We. T1 - Herpes virus replication. AU - Boehmer, Paul E. AU - Nimonkar, Amitabh V. PY - 2003/1/1. Y1 - 2003/1/1. N2 - Herpesviruses are large double stranded DNA animal viruses with the distinguishing ability to establish latent, life-long infections other hand, herpes simplex virus (HSV) is latent in postmitotic neurons, and there is no evidence for any viral DNA replication during latency. In this review, I focus on lytic DNA replication, with an emphasis on studies of HSV DNA replication, the herpesvirus system about which most is known. DNA Replication in Eukaryotic Cell
The herpes simplex virus 1 (HSV-1) genome encodes seven polypeptides that are required for its replication. These include a heterodimeric DNA polymerase, a single-strand-DNA-binding protein, a. Infection and replication of herpes simplex virus type 1 in an organotypic epithelial culture system Virology , 230 ( 2 ) ( 1997 ) , pp. 236 - 243 Article Download PDF View Record in Scopus Google Schola The present invention provides a method of inhibiting the formation of infectious herpes virus particles, particularly infectious herpes simplex virus (HSV) particles, in a host cell. The method involves administering an effective amount of indole-3-carbinol to a herpes virus infected host cell. The present invention also provides a method of treating a herpes virus infection, particularly an.
Herpes virus replication. i) Binding to the cell surface: As with many other viruses, cell tropism is determined by the availability of the correct receptor on the surface of the cell to be infected. The virus fuses with the cell membrane at ambient pH and so there is the possibility of syncytia formation between infected cells and therefore. Human Herpesviruses - August 200 Viral Replication Scott M. Hammer, M.D. Viral Replication: Basic Concepts • Viruses are obligate intracellular parasites • Viruses carry their genome (RNA or DNA) and sometimes functional proteins required for early steps in replication cycle • Viruses depend on host cell machinery to complete replication cycle and must commandee
In case of enveloped viruses, the envelope is derived from the nuclear membrane (herpes virus) and from plasma membrane when the assembly occurs in the cytoplasm of host cell (orthomyxoviruses and paramyxoviruses). 6. Release. Enveloped viruses are released by a process of budding from the cell membrane over a period of time REPLICATION OF VIRUS ⇒ Genetic information for viral replication is contained in the viral nucleic acid but lacking the biosynthetic enzymes. ⇒ The virus depends on the synthetic machinery of the host cell for replication. ⇒ The viral multiplication cycle can be divided into six sequential phases as:-Adsorption or Attachment; Penetration. Figure 17 Possible genomic structures of herpes viruses: Late phase. DNA replication. Herpesviruses code for several proteins, in addition to the DNA polymerase, that are needed for DNA replication. The precise mechanism of DNA replication is not known. DNA replication is accompanied by a lot of recombination Infection: Herpes virus: 8 types. The herpes family of viruses includes 8 different viruses that affect human beings. The viruses are known by numbers as human herpes virus 1 through 8 (HHV1 - HHV8). Human herpes virus 1 Human herpes virus 1 (HHV1) is also known as herpes simplex virus 1 (HSV1). It is typically the cause of cold sores around the mouth The results are discussed in terms of their significance to possible models of herpes simplex virus DNA replication. Appearance of terminal fragments during a cold thymidine chase. Infected Vero.
The Herpesviridae comprise a large class of animal viruses of considerable public health importance. Of the Herpesviridae, replication of herpes simplex virus type-1 (HSV-1) has been the most extensively studied.The linear 152-kbp HSV-1 genome contains three origins of DNA replication and approximately 75 open-reading frames. Of these frames, seven encode proteins that are required for origin. Replication of herpes simplex virus takes place in the cell nucleus and is carried out by a replisome composed of six viral proteins:theUL30-UL42DNApolymerase,theUL5-UL8-UL52 helicase-primase, and the UL29 single-stranded DNA-binding protein ICP8. The replisome is loaded on origins of replication bytheUL9initiatororigin-bindingprotein. Herpes is a family of DNA viruses called Herpesviridae. The herpes family of viruses consists of three families of viruses; Alphaherpesviridae, Betaherpesviridae, and Gammaherpesviridae. Among these families are many commonly known viruses that are causative agents of many diseases, such as HSV-1 and HSV-2 for cold sores and genital warts.
Herpes simplex virus. 1. INTRODUCTION EPIDEMIOLOGY AND TRANSMISSION STRUCTURE REPLICATION PATHOGENESIS AND CLINICAL SIGNIFICANCE LABORATORY DIAGNOSIS TREATMENT AND PREVENTION. 2. Herpes (Greek: creep or crawl) Herpes simplex viruses belong to the ubiquitous Herpesviridae family Human herpes simplex virus (HSV) causes contagious infection with a. The overall sequence homology between herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) is about 50%, with homologous sequences distributed over the entire genome (Corey, 2005). The cellular replication cycle of HSV takes 4-12 hours, and HSV replication usually results in cell death portion of a genome appropraite for packing into herpes virus. how virus captures membranes 1.) ripping a piece off of nuclear membrane - makes the virus immunogically invisible - evades the immune system in this way 2.) budding of the viral particle - buds from the golgi membrane 3 predict that microorganisms also replicate under tight regulations to accomplish the required DNA replication fidelity for selection and fitness. This notion also applies to herpes simplex virus type 1 (HSV-1), which replicates DNA with a genomic mutation rate similar to those of other DNA-based microbes examined (Drake an d Hwang, 2005)
Resveratrol, a phytoalexin, was found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner. The observed reduction in virus yield was not caused by the direct inactivation of HSV by resveratrol nor inhibition of virus attachment to the cell. The chemical did, however, target an early. The herpes simplex virus (HSV) ICP34.5 null mutant 1716 replicates selectively in actively dividing cells and has been proposed as a potential treatment for cancer, particularly brain tumours. We. In preliminary studies we found that the oxidized cobra neurotoxin inhibited the replication of herpes simplex virus type 1 (HSV-1) both in vivo and in vitro (Yourist et al., 1979)..
Adeno-associated virus (AAV) genome replication only occurs in the presence of a co-infecting helper virus such as adenovirus type 5 (AdV5) or herpes simplex virus type 1 (HSV-1). AdV5-supported replication of the AAV genome has been described to occur in a strand-displacement rolling hairpin replication (RHR) mechanism initiated at the AAV 3' inverted terminal repeat (ITR) end The negative control compound, WHI-P258, did not show any effect on virus titer compared to controls. Furthermore, we observed that virus replication in U937 and THP-1, which did not show SOCS3 induction by HSV-1 infection, did not interfere by the addition of WHI-P131 (data not shown). Download : Download full-size image; Fig. 5 Herpes simplex virus Research Normally this circularization does not happen, but DeLuca postulates a model where the decision point whether virus infection proceeds on to replication or latency is a result of whether the viral DNA is driven to form a circle. If it does, viral DNA replication cannot proceed and latency follows naturally Krisky, D., Marconi, P., Oligino, T. et al. Development of herpes simplex virus replication-defective multigene vectors for combination gene therapy applications. Gene Ther 5, 1517-1530 (1998.
【Abstract】Tubeimoside (TBMS) 1 is a unique pentacyclic triterpenoid saponin composed of bayogenin and four sugars: glucose, rhamnose, xylose and arabinose.Previous studies have shown that TBMS1 has activity against the human immunodeficiency virus. We investigated the inhibitory effects of TBMS1 on the proliferation and genomic replication of herpes simplex virus type 1 (HSV-1) and 2 (HSV-2) virus [vi´rus] any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as filtrable because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living. assay of Herpes Virus type-1 (HSV-1) replication in VERO cells, in the presence or absence of the spice. 10,000 TCID 50 /mL of the HSV-1 was kept for 3 h at 4o C, with 300 ppm of rosemary extract, and 100 ppm of butyl hydroxyl toluene (BHT). Then, these viruses were inoculated in VERO cells incubated at 37o C in CO 2-5 %, for seven days Figure 1. Organization of the HSV-1 replication fork. (A) Herpes simplex virus (HSV) replication fork.Two heterotrimeric complexes of the helicase-primase (H/P) (dark gray spheres with white centers) are shown at the replication fork Some of these viruses require host cell polymerases to replicate their genome, while others, such as adenoviruses or herpes viruses, encode their own replication factors. However, in either cases, replication of the viral genome is highly dependent on a cellular state permissive to DNA replication and, thus, on the cell cycle
Regulation of herpes simplex virus 1 replication using tumour-associated promoters. Ann. Surg. 236, 502-12 (2002). PubMed PubMed Central Article Google Scholar 18. Kasuya, H. et al. Selectivity. G207 is a conditionally replicating derivative of herpes simplex virus (HSV) type-1 strain F engineered with deletions of both γ134.5 loci and a lacZ insertion disabling the UL39 gene. We have.
Occasionally, however, the virus may reactivate and cause milder cold sore symptoms.. In total, there are eight herpes viruses that can affect humans. Some versions of the virus can cause. Author Summary HSV-1 is a ubiquitous human pathogen that causes persistent infections for the lifetime of the infected host. Of major interest are the mechanisms underlying how the virus utilizes cellular resources to rapidly replicate with high fidelity. We show that DNA repair and late transcription are coupled to genome replication by identifying the viral and cellular factors that.
Herpes simplex virus Research Animations of steps of HSV Infection and Replication HSV DNA Replication. HSV initiates rounds of DNA replication at one or all of the three origins of replication (Ori 1, Ori 2, and Ori 3). The initial step of HSV DNA replication is denaturation of the DNA at the replication origin with origin binding protein (UL9) Herpes simplex virus types 1 and 2 (HSV-1, -2) infect and also establish latency in neurons. In the present study, the authors investigated the influence of neuronal activity on the replication of HSV-1. The results showed that the sodium channel blocker tetrodotoxin (TTX) and the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) could significantly increase viral replication in. Herpes family viruses are the leading cause of viral diseases in humans. There are at least 25 identified viruses in the family of Herpesviridae. They are very contagious and once infected remain in the human host for life. After infection, it retreats along nerve fibres to nerve cells near the brain or spinal cord, where it remains dormant
Herpes is one of the most common sexually transmitted diseases (STDs), prompting many to wonder how to get rid of herpes naturally. The herpes virus can live dormant inside a person's immune system for a lifetime, periodically causing blisters that burst and turn into open cold sores or ulcers before healing. When left alone, herpes cold sores usually last about 10-14 days and are. Replication of herpes simplex virus in WI-38 cells was inhibited by phosphonoacetic acid, as measured by decreased virus cytopathogenic effect and incorporation of radiolabeled thymidine in virus-infected cells. The drug appeared to have no effect on adsorption, penetration, or release of the virus nor on the synthesis of ribonucleic acid or protein. It appeared to inhibit virus. Genistein, an inhibitor of protein-tyrosine kinase, inhibited the replication of herpes simplex virus type 1 (HSV-1) at genistein concentrations of more than 25 µM, whereas the related compounds, which do not inhibit protein-tyrosine kinases, did not affect the replication of HSV-1. In the presence of genistein, the phosphorylation of tyrosine residues in specific viral polypeptides was.
Herpes simplex virus Research HSV Replication Upon infecting a cell, HSV is immediately faced with an important decision, whether to proceed to productive infection or whether to establish a latent infection.As outlined in the figure below, the most recent models posit that when viral DNA migrates to nuclear pods it is either circularized by cellular DNA repair enzymes acting on the a. 2. The members of this family are also known as herpesviruses . Name is derived from the Greek word herpein (to creep or crawl). Latent, reactivation , recurring and lytic infections are typical of this group of viruses. Herpesviridae , a large family of DNA viruses that cause diseases in animals and humans Honokiol is a pleiotropic natural compound isolated from Magnolia and has multiple biological and clinically relevant effects, including anticancer and antimicrobial function. However, the antiviral activity of honokiol has not yet been well studied. Here we showed that honokiol had no effect on herpes simplex virus-1 (HSV-1) entry, but inhibited HSV-1 viral DNA replication, gene expression.
Virus replication and induction of interferon in human epidermal keratinocytes following infection with herpes simplex virus. J Invest Dermatol 1984; 82:94. Campadelli-Fiume G, Cocchi F, Menotti L, Lopez M Virus replication of host cell can have three possible outcomes. i. Productive infection: It occurs in permissive cell which results in viral replication within it producing progeny viruses that can infect other compatible host cells. The complete infectious virus produced in such infection is called virions. ii
Herpes simplex viruses type 1 and type 2 (HSV-1 and HSV-2) produce lifelong infections and are highly prevalent in the human population. Both viruses elicit numerous clinical manifestations and produce mild-to-severe diseases that affect the skin, eyes, and brain, among others. Despite the existence of numerous antivirals against HSV, such as acyclovir and acyclovir-related analogs, virus. recombination to replicate their genomes and both viruses encode specialized gene products which are required for recombination- dependent replication. In this review, we examine the linkage between replication and recombination in the eukaryotic pathogen, Herpes Simplex Virus Type 1 (HSV-1). The evidence tha Lithium chloride inhibited the replication of type 1 and type 2Herpes simplex virus at concentrations which permitted host cell replication. Virus polypeptide and antigen synthesis were unaffected while viral DNA synthesis was inhibited. The replication of two other DNA viruses, pseudorabies and vaccinia virus, was inhibited but there was no inhibition of two RNA viruses, namely, EMC and. Abstract. The effects of DNA-damaging agents on the replication of herpes simplex virus type 1 (HSV-1) were assessed in vitro. Monolayers of human lung fibroblast cell lines were exposed to DNA-damaging agents (methyl methanesulfonate (MMS), methyl methanethiosulfonate (MMTS), ultraviolet light (UV), or gamma radiation (GR)) at specific intervals, before or after inoculation with low levels of.
Inhibition of Herpes Simplex Virus Replication by Tobacco Extracts1 Jan-Michael Hirsch, Bo Svennerholm, and Anders Vahlne2 Departments of Oral Surgery, Faculty of Odontology [J-M. H.], and of Virology, Institute of Medical Microbiology [B. S., A. V.], University of Göteborg,Göteborg.Sweden ABSTRAC Replication of herpes simplex virus in T lymphocytes. Replication of viruses have been examined in a number of cell systems and the duration of successive steps in the replication cycle depends upon the types of cells, the virus strain, and the multiplicity of infection. Citations & impact . Impact metrics. 1 Article citation. Jump to Citation Effects of time of addition of monogalactosyl diacylglyceride (MGDG) on herpes simplex virus (HSV)-2 replication. MGDG at a concentration of 25 μg/ml (closed bar) or 50 μg/ml (open bar) was added to the medium 3 h prior to virus infection (A), during infection for 1 h (B), during infection for 1 h and throughout the incubation thereafter (C),.
A subset of herpes simplex Weger, S. (2012). Roles of E4orf6 and VA I RNA in adenovirus- virus replication genes provides helper functions for productive mediated stimulation of human parvovirus B19 DNA replication and adeno-associated virus replication. J Virol 65, 2476-2483. structural gene expression. J Virol 86, 5099-5109 Viral DNA replication takes places in the host cell nucleus, by means of the rolling circle mechanism characteristic of herpesviruses. Virions are packaged and assembled within the host nucleus. Virus particles bud out of the nucleus into the cytoplasm, where acquire tegument proteins encoded by viral genes U31 and U54 The genome of Herpes simplex virus I (HSV-1) is 152 kb of linear double-stranded DNA, containing three origins of replication and over 90 unique ORFs (1 ⇓ -3). Genome replication and transcription occur in the host cell nucleus When resveratrol was tested at a concentration of 6.25% and 12.5% administered five times a day, 6.25% limited virus replication only on day 1 and delayed development of extravaginal disease by 1 day. However, 12.5% resveratrol inhibited HSV-2 replication beginning on day 1 and abolished extravaginal disease Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students. Sex Transm Dis . 2003 Oct. 30 (10):797-800. [Medline]
Herpes virus remains dormant in human cells and could reactivate under immunosuppressed conditions, such as prolonged critical illnesses. The phenomenon of viral replication during intensive care is well known, even in patients without a history of immunosuppression, but it usually does not have a clinical impact. Systemic reactivation leads to viral DNA in blood Herpes Virus 7. First isolated from peripheral blood lymphocytes in a healthy patient, HV - 7 typically occurs in later childhood. The virus takes up residence in the salivary glands and is also found in the saliva. Although HV - 7 is a distinct virus from HV - 6, they share about 50 percent of the same DNA
By viewing virus development in real time, the experiments reported here reveal novel processes—rapid directional translocations—that are likely to be important elements of virus replication. Herpes simplex virus type 1 (HSV-1) was labeled by the fusion of the green fluorescent protein to a structural protein of its tegument (VP11/12), the product of gene UL46. Infection of cultured cells. Adeno-associated virus (AAV)-based gene therapy vectors have shown increasing promise over recent years, and the development of herpes simplex virus (HSV)-based packaging systems for recombinant AAV vectors has increased interest in the molecular interactions of AAV with its helper virus (6,12,38) Roizman B. and Sears A. E. (1993) Herpes simplex viruses and their replication, in The Human Herpesviruses (Roizman B., Whitley R. J., and Lopez C., eds.), Raven, New York, pp. 11-68. Google Scholar. 60. Honess R. and Roizman B. (1974) Regulation of herpes simplex virus macromolecular synthesis. I. Cascade regulation of the synthesis of three. Title: Distinct effects of knocking down MEK1 and MEK2 on replication of herpes simplex virus type 2. Abstract: During infection, viruses hijack various host cell components and programs for their amplification, among which is the canonical ERK signaling pathway, mainly consisting of three tiered serine/threonine kinases, Raf, MEK and ERK Introduction. Oncolytic viruses (OVs) 1,2 such as oncolytic herpes simplex virus (oHSV) are an emerging treatment strategy for glioblastoma (GBM). 3-10 GBM is the most common primary malignant brain tumor that is almost always lethal and has no effective treatments. 11,12 OVs selectively replicate in and kill cancer cells and induce immunogenic cell death while stimulating anti-tumor.
Like all herpesviruses, herpes simplex virus 1 (HSV1) is able to produce lytic or latent infections depending on the host cell type. Lytic infections occur in a broad range of cells while latency is highly specific for neurons. Although latency suggests itself as an attractive target for novel anti-HSV1 therapies, progress in their development has been slowed due in part to a lack of agreement. Genome replication affects transcription factor binding mediating the cascade of herpes simplex virus transcription Sarah E. Dremela and Neal A. DeLucaa,1 aDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219 Edited by Bernard Roizman, The University of Chicago, Chicago, IL, and approved January 9, 2019 (received for review. T1 - Glycoprotein 110, the Epstein-Barr virus homolog of herpes simplex virus glycoprotein B, is essential for Epstein-Barr virus replication in vivo. AU - Herrold, Ruth E. AU - Marchini, Andrew. AU - Fruehling, Sara. AU - Longnecker, Richard. PY - 1996. Y1 - 199 View 0 peer reviews of A review study on the effect of Iranian herbal medicines against in vitro replication of herpes simplex virus on Publons Download Web of Science™ My Research Assistant : Bring the power of the Web of Science to your mobile device, wherever inspiration strikes
