Biological Sciences
Herpes Simplex Virus
Herpes simplex virus (HSV) is a common virus that causes cold sores and genital herpes. There are two types of HSV: HSV-1, which typically causes oral herpes, and HSV-2, which usually causes genital herpes. The virus is highly contagious and can be transmitted through direct contact with an infected person or their bodily fluids.
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11 Key excerpts on "Herpes Simplex Virus"
- Helga Rübsamen-Schaeff, Helmut Buschmann, Helga Rübsamen-Schaeff, Helmut Buschmann, Raimund Mannhold, Jörg Holenz(Authors)
- 2021(Publication Date)
- Wiley-VCH(Publisher)
5 Herpes Simplex VirusesAlexander BirkmannAiCuris Anti-Infective Cures AG, Wuppertal, Germany5.1 Introduction
Like all members of the family of the herpesviridae, Herpes Simplex Virus type 1 (HSV-1) and type 2 (HSV-2) are enveloped, double-stranded DNA viruses [1] . Their genome size is approximately 152 kb and comprises at least 74 open reading frames. The genome consists of two unique segments, the unique long (UL ) and the unique short (US ) regions, flanked by inverted repeat sequences. Together with the closely related varicella zoster virus (VZV), HSV-1 and -2 represent the human pathogenic members of the alphaherpesvirinae subfamily which share the prominent feature of latency in neurons [2] . HSV is transmitted via infectious viral particles derived from either active lesions, or (especially in the case of HSV-2) from asymptomatic shedding [3 , 4 ]. The primary infection typically occurs during childhood in the case of HSV-1, or later during adolescence in the case of HSV-2, since the latter virus is mainly transmitted sexually [5] . HSV normally enters the body via skin or mucosa and can lead to local lesions at the site of infection, which may or may not be accompanied by clinical signs of disease. Once it has entered the host, the virus spreads to the neurons of the peripheral nervous system, where it establishes a latent and life-long infection (a notable feature of all herpesviruses) [1] . Historically, HSV-1 was associated with infection “above the belt” (i.e. mouth and eye, where the virus persists in the trigeminal ganglion), whereas HSV-2 was attributed to infection “below the belt,” specifically genital herpes, by infecting the sacral ganglion [6] . However, nowadays, there is a significant overlap between the sites of HSV infection with an increasing proportion of genital herpes caused by HSV-1, which may be attributed to a decrease in childhood HSV-1 infections and an increase in the practice of oral sex [7 , 8 ]. Once neuronal latency has been established, HSV may be reactivated by an unknown molecular trigger and spread from the ganglion to the lower epidermal layers at or near the site of the initial infection where it replicates. The severity of such a recurrence can range from asymptomatic (only recognized by the ability to detect the virus on the skin) to painful ulcers, such as the typical orofacial cold sores or genital lesions. HSV outbreaks can substantially impact patients' quality of life; they can be painful and stigmatizing, leading to distress and even psychosocial problems [9 , 10 ]. Ocular HSV-1 infections can result in visual impairment [11] . Especially for genital herpes, it could be shown by quantitative polymerase chain reaction (PCR) analysis that these recurrences can occur frequently as asymptomatic episodes of viral shedding [3] . If occurring frequently, these shedding events can result in a high risk of transmission, even when no symptoms are present. At least 70% of HSV-2 transmissions take place during periods of asymptomatic shedding [12]
eBook - PDFVaccines
New Approaches to Immunological Problems
- Ronald W. Ellis(Author)
- 2014(Publication Date)
- Butterworth-Heinemann(Publisher)
Second, differences among strains of HSV were demonstrated by restriction endonuclease technology, which has become an important molecular epidemiologic tool (Buchman et al. 1978). Third, the utilization of type-specific antigens has advanced our understanding of clin-ical epidemiology of infection (Roizman et al. 1984; Johnson et al. 1989). Fourth, much work has been dedicated to the elucidation of the replication of HSV and the resultant gene products (Roizman and Sears 1990). A prin-cipal goal of these efforts is to define the biological properties of these gene products, a goal that is in the early stages of accomplishment. Fifth, the engineering of HSV and the expression of specific genes will provide tech-nology for new vaccines (Roizman and Jenkins 1985). Finally, the more recent but less-well-understood controversial observation of a latency-as-sociated transcript may lead to clues regarding the molecular pathogenesis of latency (Stevens et al. 1987). 10.2 INFECTIOUS AGENT OF HERPES SIMPLEX Herpes Simplex Viruses, types 1 and 2, are members of a family of large DNA viruses which contain centrally located, linear, double-stranded DNA. All of the herpesviruses consist of similar structural elements arranged in concentric layers (Roizman and Sears 1990; Nahmias and Norrild 1979; Roizman 1979). Other members of the human herpesvirus family include cytomegalovirus, varicella-zoster virus, Epstein-Barr virus, human herpes-virus no. 6, and the recently isolated human herpesvirus no. 7 (Frenkel et al. 1990). The structure and pathogenesis of these agents is delineated in the chapters reflecting the status of vaccine development against them. The DNA of HSV has a molecular weight of approximately 100 million and encodes about 80 polypeptides, few of which are understood biologi-cally. The viral genome consists of two components: a unique, long region called Uf, and a unique, short region called U s .
eBook - PDF- Dongyou Liu(Author)
- 2016(Publication Date)
- CRC Press(Publisher)
911 81.1 INTRODUCTION 81.1.1 C LASSIFICATION AND M ORPHOLOGY Herpes Simplex Virus (HSV) types 1 and 2, formally des-ignated human herpesvirus 1 and human herpesvirus 2 , respectively, are DNA viruses and members of the fam-ily Herpesviridae. Along with varicella-zoster virus (VZV; human herpesvirus 3) , human herpes virus 8 (the cause of Kaposi’s sarcoma) and more than 80 viruses, they constitute the subfamily Alphaherpesviridae, the genus Simplexvirus . The morphology of the HSV-1/2 as seen by electron microscopy (EM) is analogous for all members of the Herpesviridae . The pseudo-replica EM method exhibits a spherical virus particle 150–200 nm in diameter with four structural elements: (i) a central electron-dense core contain-ing the DNA wrapped as a toroid or spool and possibly in a liquid crystalline state; (ii) an icosahedral protein capsid sur-rounding the virus core, comprised of 162 capsomeres; (iii) a formless tegument surrounding the capsid; and (iv) a spiked trilaminar outer envelope (Figure 81.1). The core is composed of linear double-stranded DNA, the genome of which is 152 kb for HSV-1 and 155 kb for HSV-2. HSV-1 and HSV-2 share 83% nucleotide identity within their protein-coding regions. The genome is organized into a unique long (UL) and unique short (US) region. The viral capsid has a diameter of 100–110 nm and is a closed shell forming an icosadeltahedron with 162 capsomers arranged as 12 pentamers and 150 hexamers. Between the capsid and envelope appears the tegument that contains at least 12 proteins. The trilaminar virus envelope consists of a lipid bilayer with about 12 different viral glycoproteins embedded in it and is thought to be derived from patches of host cell nuclear membrane modified by the insertion of virus glyco-protein spikes. 81.1.2 E PIDEMIOLOGY HSV infection arises globally with no seasonal distribution and is endemic in all human populations examined. No ani-mal reservoirs are reported for the HSV-1/2 infection.
eBook - PDF- Edward Bittar(Author)
- 1998(Publication Date)
- Elsevier Science(Publisher)
Chapter 24 Herpesviruses J. BARKLIE CLEMENTS and S. MOIRA BROWN Introduction 394 Description and Classification of Herpesviruses 394 Herpesvirus Genomes 397 Herpesvirus Genes 399 DNA Replication 400 Clinical Manifestations 401 HSV 401 HCMV 402 VZV 402 EBV 402 HHV-6, -7, & -8 403 Latency 403 HSV 404 Establishment 404 Maintenance 404 Reactivation 405 HCMV 405 VZV 406 Principles of Medical Biology, Volume 9B Microbiology, pages 393-414. Copyright © 1997 by JAI Press Inc. All rights of reproduction in any form reserved. ISBN: 1-55938-814-5 393 394 J. BARKLIE CLEMENTS and S. MOIRA BROWN EBV 406 HHV-6 & -7 406 Pathogenesis 407 HSV 407 HCMV 408 VZV 408 EBV 408 HHV-6 & -7 409 Vaccines 409 HSV 409 HCMV 410 VZV 410 EBV 410 Antivirals 411 Vidarabine 411 Acyclovir 411 Gancyclovir 411 Idoxuridine 411 Summary and Conclusions 412 INTRODUCTION This chapter, which focuses on the human herpesviruses, begins by summarizing the molecular detail of these viruses, and our approach has been to concentrate on features which are common to the various viruses. This basic information is then related to clinical and biological studies of herpesvirus pathogenicity and latency. Finally, herpesvirus vaccines and antivirals are discussed. Recently, several reviews which deal with detailed aspects of the topics raised have been published, and these are cited as appropriate. DESCRIPTION AND CLASSIFICATION OF HERPESVIRUSES Herpesviruses are widely distributed in nature, infecting a variety of host species including fish, frogs, rodents, birds, marsupials and especially mammals, including man (Roizman, 1993). Herpesviruses differ widely in their pathogenic potential but share several important biological properties. Most notable is the ability, after primary infection, to establish latent infections throughout the lifetime of the host. Our current understanding of this close and continuing association between herpes-viruses and their hosts has been surveyed by Wagner and colleagues (1994).
eBook - PDFNeuroviral Infections
General Principles and DNA Viruses
- Sunit K. Singh, Daniel Ruzek, Sunit K. Singh, Daniel Ruzek(Authors)
- 2013(Publication Date)
- CRC Press(Publisher)
169 7 Herpes Simplex Virus and Human CNS Infections Marcela Kúdelová and Július Rajc ˇ áni 7.1 INTRODUCTION The exact origin of herpes in humans is unknown. Herpes Simplex Virus (HSV) causes fever blisters or cold sores around the lips or in the genital area. The dis-ease caused by the virus has been known for thousands of years. The characteristic CONTENTS 7.1 Introduction .................................................................................................. 169 7.2 Biological Properties .................................................................................... 171 7.2.1 HSV Virion Structure ....................................................................... 171 7.2.2 HSV Genome .................................................................................... 173 7.2.2.1 Structure of HSV Genome ................................................. 173 7.2.2.2 Classification and Functions of HSV Genes ...................... 174 7.2.3 Expression of HSV Genes ................................................................ 177 7.2.4 Replication Cycle of HSV ................................................................. 180 7.2.5 Latency ............................................................................................. 180 7.3 Clinical Presentation ..................................................................................... 182 7.3.1 General Considerations ..................................................................... 182 7.3.2 HSV Encephalitis .............................................................................. 183 7.3.3 Chronic Neural Disorders and Mental Diseases Associated with HSV-1 or HSV-2 ............................................................................... 186 7.4 Diagnosis of HSV Encephalitis .................................................................... 188 7.4.1 Neuroimaging ...................................................................................
eBook - PDF- Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Margaret A. Liu, Gary J. Nabel, James P. Nataro, Rino Rappuoli, Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Gary J. Nabel, James P. Nataro, Rino Rappuoli, Myrone M. Levine, Myron M. Levine, Gordon Dougan, Michael F. Good, Gary J. Nabel, James P. Nataro, Rino Rappuoli(Authors)
- 2016(Publication Date)
- CRC Press(Publisher)
61 Herpes Simplex Vaccines David M. Koelle University of Washington, Seattle, Washington, U.S.A. Lawrence R. Stanberry and Reuben S. Carpenter Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, New York, U.S.A. Richard J. Whitley Department of Pediatrics, Microbiology, Medicine, and Neurosurgery, University of Alabama at Birmingham, Birmingham, Alabama, U.S.A. INTRODUCTION Our knowledge of the pathogenesis, natural history, treatment and molecular biology of Herpes Simplex Virus (HSV) and its resultant infections has increased dramatically over the past decade. These advances, in part, paralleled the development of antiviral drugs that are selective and specific inhibitors of viral replication. The unequivocal establishment of the value of antiviral therapy has had a major impact on altering the severity of human disease and has major implications for long-range control of HSV infections. Recent clinical trials have demonstrated the possibility of decreasing HSV transmis-sion between sexual partners (1). However, some clinical dis-eases (e.g., herpes simplex encephalitis and neonatal HSV infections) are still associated with significant mortality and morbidity in spite of antiviral therapy. Even with the rapidly evolving knowledge of the molecular biology of HSV, the development of a successful vaccine—either subunit or live attenuated—has been difficult to achieve. The development of an HSV vaccine has attracted the interest of investigators for over 100 years, but the goal of producing a licensed vaccine that protects against HSV disease has not been realized. Only now is there one promising candi-date in registrational clinical trials. In large part, the unique properties of HSV—especially its ability to become latent and reactivate—and its human biology make the potential success of a vaccine more difficult to achieve than with many other viral pathogens.
eBook - PDFHuman Herpesvirus Infection
Biological Features, Transmission, Symptoms, Diagnosis and Treatment
- Ronaldo Luis Thomasini(Author)
- 2020(Publication Date)
- IntechOpen(Publisher)
To date a total of 8 human HVs are known, having the characteristic of establishing a life-long latent infection: a state from which the virus can be reactivated and result in recurring disease. The HV family is divided into three subfamilies (Alphaherpesvirinae, Human Herpesvirus Infection - Biological Features, Transmission, Symptoms, Diagnosis... 12 Betaherpesvirinae, and Gammaherpesvirinae); among these, only the α HV creates skin lesions in humans [2]. The Herpes Simplex Virus (HSV), creating the general clinical picture of herpetic disease, and the Varicella-Zoster Virus (VZV), which is the cause of chickenpox and Herpes Zoster (HZ), both belong to α HV. 2.1 Clinical aspects of α HV lesions The transmission of α HV occurs by close contact with a person who actively elim-inates the virus. The viral diffusion occurs from lesions; however, it can occur even if they are not visible. After the primary infection, the α HV remains quiescent in the nerve ganglia from which it can periodically reactivate, causing clinical manifesta-tions. The HSV commonly cause a relapsing mucocutaneous infection affecting the skin, mouth, lips, eyes and genitals. Serious common variants include encephalitis, meningitis, neonatal herpes, and infections disseminated in immunosuppressed patients. There are two types of HSV: Herpes Simplex Virus 1 (HSV-1) and Herpes Simplex Virus 2 (HSV-2) and both types can cause oral or genital infections. In most cases, the HSV-1 causes gingivostomatitis, cold sores, herpetic keratitis, and lesions in the upper body. The HSV-2 generally causes lesions to the genitals and to the skin of the lower half of the body. Approximately 70% of population in USA is seroposi-tive for HSV [3] but only the 20%, due to a decline in cellular immunity, presents the recurrent form that can occur with a variable frequency. The mucocutaneous manifestations occur in two forms: primary infection and recurrent infection.
eBook - PDF- Roland W Herzog, Sergei Zolotukhin(Authors)
- 2010(Publication Date)
- World Scientific(Publisher)
2 The host can keep the virus in check within the neurons of the PNS where it lies dormant or latent, sometimes for the lifetime of the host. Certain stimuli such as surgery, UV light, local trauma, fatigue, immune suppression, and fever lead to the virus exiting the latent or “quiescent” state and the re-establishment of the lytic life cycle in the PNS nerve cells, also known as “reactivation”. HSV is an enveloped, double-stranded DNA-containing virus that pos-sesses natural neurotropism as part of its life cycle within the human host. The virus particle (Fig. 5.1A) is composed of an icosahedral-shaped nucle-ocapsid containing the 152 kb linear dsDNA molecule encased in a lipid bilayer envelope that it acquires from the host cell when it buds from the cell as part of the egress process. The viral genome is composed of two segments, the unique long (U L ) and short (U S ) regions each of which are flanked by inverted repeats (Fig. 5.1A). Over 85 viral genes are present primarily within the unique long segment with several important regula-tory genes present in the repeat sequence, and thus are present within two copies in each viral genome. The viral genes can be categorized into two groups; those that are essential for virus replication in standard cells used to grow the virus in cell culture and those that are not essential to virus 70 Herpes Simplex Virus Vectors Fig. 5.1 Schematic diagram of HSV virion particle and viral genome. (A) EM photomicrograph of HSV virion particle with the four major virion components. The HSV linear dsDNA genome is contained within the icosahedral-shaped capsid that is surrounded by the tegument layer that in turn is enclosed within a lipid bilayer membrane containing the viral encoded glycoproteins. (B) The 152 kb linear dsDNA genome composed of the unique long ( U L ) and short ( U S ) segments, each flanked by inverted repeats.
eBook - PDFMucocutaneous Manifestations of Viral Diseases
An Illustrated Guide to Diagnosis and Management
- Stephen Tyring, Angela Yen Moore, Omar Lupi, Stephen Tyring, Angela Yen Moore, Omar Lupi(Authors)
- 2016(Publication Date)
- CRC Press(Publisher)
HSV type 1 was more frequently associated with non- genital infection, while HSV type 2 was associated with genital disease, although this distinction has changed over the past decade. This observation was seminal for many of the clinical, serologic, immunologic, and epidemiologic studies that have followed. Several other critical advances have aided our understanding of the natural history and pathogenesis of HSV infections. First, successful antiviral therapy was established for HSE [23] and, subsequently, for virtually all HSV infections [24–30], as recently reviewed [24]. Second, differences between strains of HSV were demonstrated by restriction endonuclease analyses of viral DNA, allowing for molecular epidemiologic studies [31]. Third, the use of type-specific antigens for serologic studies has advanced our understanding of the epidemiology of infection [32]. Fourth, the elucidation of the molecular events of viral replication and the resultant gene products aids in the development of vaccines and antiviral drugs. Fifth, the engineering of HSV and the expression of specific genes will provide technology for new vaccines and gene therapy [10]. Finally, the recent advances in our knowledge of the molecular basis of latency and the definition of a gene responsible for neurovirulence are leading to clues regarding Introduction Our knowledge of human Herpes Simplex Virus (HSV) infections has increased dramatically since the initial historical descriptions of the clinical manifestations and the histopathology of HSV lesions. Advances in our understanding of the natural history and pathogenesis of HSV infections have been paralleled by the development of both sensitive and specific serologic tests, which distinguish HSV-1 from HSV-2 infections and antiviral drugs that are selective inhibitors of viral replication. Type-specific serologic markers of infection have allowed for a detailed evaluation of the epidemiology of both HSV-1 and HSV-2 infections.
eBook - PDF- Jozsef Ongradi(Author)
- 2016(Publication Date)
- IntechOpen(Publisher)
[21] Kaye, S. and A. Choudhary. Herpes simplex keratitis. Prog Retin Eye Res. 2006; 25: p. 355–380. DOI:10.1016/j.preteyeres.2006.05.001. Herpesviridae 128 [22] Lafferty, W.E., et al. Recurrences after oral and genital Herpes Simplex Virus infection. Influence of site of infection and viral type. N Engl J Med. 1987; 316: p. 1444–1449. DOI: 10.1056/NEJM198706043162304. [23] Kaneko, H., et al. Evaluation of mixed infection cases with both Herpes Simplex Virus types 1 and 2. J Med Virol. 2008; 80: p. 883–887. DOI:10.1002/jmv.21154. [24] Obara, Y., et al. Distribution of Herpes Simplex Virus types 1 and 2 genomes in human spinal ganglia studied by PCR and in situ hybridization. J Med Virol. 1997; 52: p. 136– 142. [25] Solomon, L., et al. Epidemiology of recurrent genital Herpes Simplex Virus types 1 and 2. Sex Transm Infect. 2003; 79: p. 456–459. [26] Janier, M., et al. Virological, serological and epidemiological study of 255 consecutive cases of genital herpes in a sexually transmitted disease clinic of Paris (France): a prospective study. Int J STD AIDS. 2006; 17: p. 44–49. DOI: 10.1258/095646206775220531. [27] Benedetti, J., L. Corey, and R. Ashley. Recurrence rates in genital herpes after sympto‐ matic first-episode infection. Ann Intern Med. 1994; 121: p. 847–854. [28] Krummenacher, C., et al. Comparative usage of herpesvirus entry mediator A and nectin-1 by laboratory strains and clinical isolates of Herpes Simplex Virus. Virology. 2004; 322: p. 286–299. DOI:10.1016/j.virol.2004.02.005. [29] Grinde, B. Herpesviruses: latency and reactivation—viral strategies and host response. J Oral Microbiol. 2013; 5:22766. DOI:10.3402/jom.v5i0.22766. [30] Mogensen, T.H. Pathogen recognition and inflammatory signaling in innate immune defenses. Clin Microbiol Rev. 2009; 22: p. 240–273. DOI: 10.1128/CMR.00046-08. [31] Tang, D., et al. PAMPs and DAMPs: signal 0s that spur autophagy and immunity. Immunol Rev. 2012; 249: p. 158–175. DOI:10.1111/j.1600-065X.2012.01146.x.
- Pratibha Singhi, Diane E Griffin, Charles R Newton(Authors)
- 2014(Publication Date)
- Mac Keith Press(Publisher)
8 Herpes Simplex Virus INFECTIONS Richard J Whitley Herpes Simplex Virus (HSV) infections of the central nervous system (CNS) are among the most devastating infections acquired by humans, in spite of efficacious antiviral therapy. Two distinct types of HSV infection of the CNS are recognized: (1) neonatal HSV enceph-alitis that occurs during the first month of life and is usually caused by HSV-2; and (2) herpes simplex encephalitis (HSE) that is recognized as the most common cause of sporadic fatal encephalitis and is almost uniformly caused by HSV-1. Intranuclear inclusion bodies consistent with HSV infection were demonstrated first in the brain of a neonate with en-cephalitis from which virus was isolated (Smith et al. 1941). The first adult patient with HSE providing similar proof of viral disease was described in 1944 (Zarafonetis et al. 1944). The most striking pathological findings in this patient’s brain were in the left temporal lobe, in which perivascular cuffs of lymphocytes and numerous small haemorrhages were found. This temporal lobe localization subsequently has been determined to be characteristic of HSE in individuals older than 3 months. Pathology The histopathological findings of HSV infection of the CNS following either neonatal encephalitis or HSE are similar. These findings include ballooning of infected cells and the appearance of chromatin within the nuclei followed by degeneration of the cellular nuclei. Cells lose intact plasma membranes and form multinucleated giant cells. As host defenses are mounted, an influx of mononuclear cells can be detected in infected tissue. Macroscopically, HSE results in acute inflammation, congestion and/or haemorrhage, most prominently in the temporal lobes and usually asymmetrically in adults and more diffusely in newborn infants.
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