3 edition of An analysis of viral transactivators in HSV-1 latency found in the catalog.
An analysis of viral transactivators in HSV-1 latency
Written in English
|Statement||by Randall Lindsay Fawl.|
|LC Classifications||Microfilm 94/2326 (Q)|
|The Physical Object|
|Pagination||x, 110 leaves|
|Number of Pages||110|
|LC Control Number||94629115|
Exploring how herpes simplex virus changes when passed between family members Date: Octo Source: Penn State Summary: A new study offers a rare glimpse into the genetics of a herpes.
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Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are closely related ancient human pathogens responsible for a number of diseases of minor, moderate and severe pathology including oral and genital ulceration, virally induced blindness, viral encephalitis and disseminated infection of neonates.
For efficient infection, the corneas of anesthetized Balb/c mice are first scarified prior to addition of HSV-1 viral inoculum to the surface of the eye.
From the site of infection, HSV-1 infects sensory neurons at axonal terminals and establishes latency in the neurons of the trigeminal and other sensory by: 2.
During herpes simplex virus (HSV) latency, most viral genes are silenced, with the exception of one region of the genome encoding the latency-associated transcript (LAT). This long noncoding RNA was originally described as having a role in enhancing HSV-1 by: 9.
For HSV-2, inoculation into the guinea pig vagina results in latency in which virus is periodically shed to form lesions that can be scored. Therefore, the rabbit and guinea pig provide reasonable models for HSV-1 and HSV-2, respectively, in humans but they are more difficult and expensive to use than the by: The latency associated transcript (LAT) encoded by Herpes simplex virus 1 (HSV-1) and the latency related gene (LR) of bovine herpes virus 1 (BHV-1) are abundantly expressed during latency.
Both are transcribed antisense relative to a viral transactivator, ICP0 and bovine ICP0 by: 1. During herpes simplex virus type 1 (HSV-1) neuronal latency, the only viral RNA detected is from the latency-associated transcript (LAT) gene. We have made a LAT deletion mutant of McKrae, an HSV-1 strain with a very high in vivo spontaneous reactivation by: Here, we utilized an adeno-associated virus (AAV) vector to deliver a LAT-targeting hammerhead ribozyme to HSVinfected neurons of rabbits after the establishment of HSV-1 latency.
Blinding ocular herpetic disease in humans is due to herpes simplex virus type 1 (HSV-1) reactivations from latency, rather than to primary acute infection.
The cellular and molecular immune mechanisms that control the HSV-1 latency-reactivation cycle remain to be fully elucidated.
The aim of this study was to determine if reactivation of the HSV-1 latency Cited by: during the establishment and maintenance of latency Tiffany Ann Russell The viral transactivators: expression and function of the immediate early genes 36 The HSV-1 genome and the impact of viral DNA replication during the acuteAuthor: Tiffany Ann Russell.
the virus during latency, speciﬁcally to aid the virus in perpetuating its latent state. Figure 1 Map of HSV-1 virus constructs involving genetic alterations within the LAT region. (A) Diagram of the genomic structure of HSV (B) Expanded view of the LAT region of the genome.
(C) Virus mutants containing deleted sequences are denoted with. In this study we assess the role of the HSV-1 latency-associated transcript in the control of viral genome silencing and reactivation in mouse nervous tissue and individual neurons. We show that the latency-associated transcript decreases the expression of reporter genes engineered into the HSV-1 genome.
The HSV-1 Latency-Associated Transcript Functions to Repress Latent Phase Lytic Gene Expression and Suppress Virus Reactivation from Latently Infected Available via license: CC BY Repression of the HSV-1 latency-associated transcript (LAT) promoter by the early growth response (EGR) proteins: Involvement of a binding site immediately downstream of the TATA box July The latency associated transcripts (LAT) of herpes simplex virus type 1 (HSV-1) are encoded by diploid genes that are expressed during latent infections.
Two LAT variant viruses, andwere compared with the parental strain 17 +.Cited by: 5. Previous infection with human herpes simplex virus type-1 (HSV-1) or Sindbis virus (an RNA virus incapable of latent infection) triggered neither protection from bacterial infection nor chronic.
However, the mechanisms that allow establishment and maintenance of the latent state remain poorly understood. Herpes simplex virus 1 (HSV-1) establishes latency in neurons of sensory ganglia, where the only abundant viral gene product is a non-coding RNA, the latency associated transcript (LAT).
Homogenates of TGs that were obtained ≥14 d after HSV-1 corneal infection were devoid of replicating virus, demonstrating that HSV-1 latency was uniformly established by that time. As CD8 + T cells were at maximal density in the TGs by 14 d after infection, we expected that cultures of these TGs would be less dependent on exogenous CD8 + T cells for protection from HSV-1 by: Herpes Simplex Virus: Methods and Protocols provides a wide collection of protocols employed in various levels of herpes virus research, including basic protocols on growing viruses in cell culture and cloning, manipulating and preparing viral DNA.
Other chapters describe approaches to design and apply HSV-1 vectors for vaccination, cancer and gene therapy or to study.
Main Text. After initial infection, the HSV-1 genome remains dormant in neurons for the lifetime of the host in a state known as latency. From this dormant state, the viral genome can become periodically reactivated in response to stress and other Cited by: 3.
Towards an understanding of the molecular basis of herpes simplex virus latency In this review, attention will focus on the alpha neurotropic herpes simplex viruses; herpes simplex virus type 1 (HSV-1) that is acquired early in life and results in oral infections, and herpes simplex virus type 2 (HSV-2) that is acquired sexually and results Cited by: HSV-1 and HSV-2 have been shown to encode 16 and 18 miRNAs, respectively, and there is a concentration of miRNAs within or adjacent to the LAT locus.
In the case of HSV-1, six miRNAs (miR-H2, H3, H4, H5, H7 and H8) are encoded within the Cited by: Latent herpes simplex virus 1 (HSV-1) genome remains as an episome in the nucleus of the infected neurons. Accordingly, depending on the location of the viral genomes in the nucleus, they could be targeted by different types of epigenetic regulations important for the establishment and stability of latency, and ultimately for the capacity of Author: Camille Cohen, Armelle Corpet, Mohamed Ali Maroui, Franceline Juillard, Patrick Lomonte.
For the best-studied αHVs, including herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), pseudorabies virus and bovine herpesvirus 1 (BHV-1), viral latency has been shown to be accompanied by the Cited by: Herpes simplex virus type 1 (HSV-1) establishes latency in human sensory ganglia, during which time the viral genome is transcriptionally silent with the exception of the latency-associated.
Introduction. Patterns of regulated gene expression and function during productive and latent infection have been extensively studied and described for Herpes simplex virus type 1 (HSV-1) (Roizman and Knipe,Wagner et al., and references therein).Therefore, it serves as an important model for these processes in all herpes viruses, specially the alpha (neurotropic) Cited by: Several herpes simplex virus 1 microRNAs are encoded within or near the latency associated transcript (LAT) locus, and are expressed abundantly during of these microRNAs can repress the expression of important viral proteins and are hypothesized to play important roles in establishing and/or maintaining latent by: The HSV-1 miR-LAT lies within one of the latency associated transcripts (LATs), the only viral RNAs known to be expressed in latency.
EBV and KSHV miRNAs also are expressed during latent infection. Because they are nonimmunogenic, miRNAs should be optimal agents for suppression of anti-viral responses and to modify behaviors of latently Cited by: This introductory chapter gives a brief overview of HSV-1 biology and life cycle, covering basic aspects of virus structure, the prevalence of and diseases caused by the virus, replication in cultured cells, viral latency, antiviral defenses, and the mechanisms that the virus uses to counteract these : Christopher E Denes, Roger D Everett, Russell J Diefenbach, Russell J Diefenbach.
The latency-associated transcript (LAT) of herpes simplex virus-1 (HSV-1) is the only viral gene expressed during latent infection in neurons 3. LAT inhibits apoptosis and maintains latency by. The rank is again based on the P value PV SH computed according to the local first order MM or the global third order MM.
ICP0 in HSV-1, BZLF1 and BRLF1 in EBV, and Zta and Rta in KSHV are among the virus-specific targets most likely to be targeted by virus-coded miRNAs (top –2% of virus-specific targets).
The BZLF1/BRLF1 3′ UTR of EBV. Bovine herpes virus 1 (BHV-1) is an important pathogen of cattle because it induces a variety of clinical disorders (conjunctivitus, tracheitis, and genital infections).
Furthermore, BHV-1 is an initiator of bovine respiratory disease complex (BRDC). The ability of BHV-1 to induce immune-suppression enables secondary bacterial infections to cause pneumonia. Latency analysis of three herpes simplex virus type 1 (HSV-I) strain 17 syn+ deletion variants (, and ) showed that they established, maintained and reactivated from latency.
The kinetics of reactivation of and were similar to the parent HSV-1, 17 syn+, in which reactivation occurred days post-explantation, but Herpes simplex virus type 1 (HSV-1) is widespread double-stranded DNA (dsDNA) virus that establishes life-long latency and causes diverse severe symptoms.
The mechanisms of HSV-1 infection and HSV-1’s interactions with various host cells have been studied and reviewed extensively. Type I interferons were secreted by host cells upon HSV infection and play a vital role in controlling virus Author: Weiwei Wan, Liangjie Wang, Xi Chen, Shenglin Zhu, Weijuan Shang, Gengfu Xiao, Lei-Ke Zhang.
HHV Latency Associated Transcript (HHV LAT) is a length of RNA which accumulates in cells hosting long-term, or latent, Human Herpes Virus (HHV) infections. The LAT RNA is produced by genetic transcription from a certain region of the viral DNA. LAT regulates the viral genome and interferes with.
Review The latency associated transcripts (LAT) of herpes simplex virus: still no end in sight Timothy M Block1 and James M Hill2 1Kimmel Cancer Institute, Jefferson Medical College, Philadelphia, Pennsylvania ;2LSU Eye Center and Departments of Ophthalmology, Microbiology & Immunology, and Pharmacology, Louisiana State University Medical.
Herpes simplex virus 1 and 2 (HSV-1 and HSV-2), also known by their taxonomical names Human alphaherpesvirus 1 and Human alphaherpesvirus 2, are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of : incertae sedis.
Viruses are strictly dependent on cells to propagate and many incorporate host proteins in their viral particles, but the significance of this incorporation is poorly understood. Recently, we performed the first comprehensive characterization of the mature herpes simplex virus type 1 (HSV-1) in which up to 49 distinct cellular proteins were identified by mass by: Bovine respiratory disease complex (BRDC) causes more than 50 percent of all morbidities and mortalities in cattle, costing producers over one billion dollars annually.
Stress during shipping (excitement, exhaustion, change of feed, over-crowding and weaning) are risk factors for BRDC.
Primary viral infection and/or stress induced immune suppression can result in life-threatening. Herpes simplex is a viral infection caused by the herpes simplex virus. Infections are categorized based on the part of the body infected.
Oral herpes involves the face or mouth. It may result in small blisters in groups often called cold sores or fever blisters or may just cause a sore throat. Genital herpes, often simply known as herpes, may have minimal symptoms or form blisters Specialty: Infectious disease.
Herpes simplex virus 1 (HSV-1) uses latency in peripheral ganglia to persist in its human host, however, recurrent reactivation from this reservoir can cause debilitating and potentially life-threatening disease. Most studies of latency use live-animal infection models, but these are complex, multilayered systems and can be difficult to by:.
Nested PCR was performed for each virus on ng of sample DNA using primers and conditions listed in Table -1 and VZV primers were verified previously in studies of DNA from fixed human trigeminal ganglia .HSV-2 external primers were obtained from published sequences, and nested primers were designed to be within this original –base Cited by: This chapter is devoted to the topics of not yet marketed HSV vaccine, which is still in the focus of interest, especially from the point of immunotherapeutic use.
To understand the principles of vaccination strategies (prophylactic and/or immunotherapeutic), the pathogenesis of herpes simplex virus 1 (HSV-1) and/or HSV-2 infections in animal models is briefly by: 2.literature surveys focusing on HSV-1 , HCMV , or EBV .
The systems used to study alpha- beta- and gamma-herpesvirus latency vary dramatically. A valuable animal model for HSV-1 latency exists, butin vitro models  receive less attention.
Thus the genetics of HSV-1 latency is established (i.e. which open reading framesCited by: