The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Peter G E Kennedy - One of the best experts on this subject based on the ideXlab platform.
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a comparison of herpes simplex Virus type 1 and varicella zoster Virus Latency and reactivation
Journal of General Virology, 2015Co-Authors: Peter G E Kennedy, Joel Rovnak, Hussain Badani, Randall J CohrsAbstract:Herpes simplex Virus type 1 (HSV-1; human herpesVirus 1) and varicella-zoster Virus (VZV; human herpesVirus 3) are human neurotropic alphaherpesViruses that cause lifelong infections in ganglia. Following primary infection and establishment of Latency, HSV-1 reactivation typically results in herpes labialis (cold sores), but can occur frequently elsewhere on the body at the site of primary infection (e.g. whitlow), particularly at the genitals. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. Primary VZV infection causes varicella (chickenpox) following which latent Virus may reactivate decades later to produce herpes zoster (shingles), as well as an increasingly recognized number of subacute, acute and chronic neurological conditions. Following primary infection, both Viruses establish a latent infection in neuronal cells in human peripheral ganglia. However, the detailed mechanisms of viral Latency and reactivation have yet to be unravelled. In both cases latent viral DNA exists in an ‘end-less’ state where the ends of the Virus genome are joined to form structures consistent with unit length episomes and concatemers, from which viral gene transcription is restricted. In latently infected ganglia, the most abundantly detected HSV-1 RNAs are the spliced products originating from the primary Latency associated transcript (LAT). This primary LAT is an 8.3 kb unstable transcript from which two stable (1.5 and 2.0 kb) introns are spliced. Transcripts mapping to 12 VZV genes have been detected in human ganglia removed at autopsy; however, it is difficult to ascribe these as transcripts present during latent infection as early-stage Virus reactivation may have transpired in the post-mortem time period in the ganglia. Nonetheless, low-level transcription of VZV ORF63 has been repeatedly detected in multiple ganglia removed as close to death as possible. There is increasing evidence that HSV-1 and VZV Latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms of HSV-1 and VZV Latency hold much promise for our future understanding in this complex area. This review summarizes the molecular biology of HSV-1 and VZV Latency and reactivation, and also presents future directions for study.
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Herpes simplex Virus-1 and varicella-zoster Virus Latency in ganglia
Journal of NeuroVirology, 2003Co-Authors: Bradley M. Mitchell, Donald H. Gilden, Randall J Cohrs, David C Bloom, Peter G E KennedyAbstract:Two human alpha-herpesViruses, herpes simplex Virus (HSV)-1 and varicella zoster Virus (VZV), account for the most frequent and serious neurologic disease caused by any of the eight human herpesViruses. Both HSV-1 and VZV become latent in ganglia. In this review, the authors describe features of Latency for these Viruses, such as distribution, prevalence, abundance, and configuration of viral DNA in latently infected human ganglia, as well as transcription, translation, and cell type infected. Studies of viral Latency in animal models are also discussed. For each Virus, remaining questions and future studies to understand the mechanism of Latency are discussed with respect to prevention of serious cutaneous, ocular, and neurologic disease produced by Virus reactivation.
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Key issues in varicella-zoster Virus Latency.
Journal of NeuroVirology, 2002Co-Authors: Peter G E KennedyAbstract:The molecular mechanisms by which varicella-zoster Virus (VZV) causes a latent infection in human trigeminal and spinal ganglia are not well understood. It is known that VZV establishes Latency in ganglia following the primary infection causing varicella (chickenpox), and that the Virus may reactivate after years of dormancy to produce herpes zoster (shingles). Two key issues have been the cell-type localization of latent VZV in human ganglia, and the nature and extent of VZV gene expression during Latency. Although the cell specificity of latent VZV has been controversial for almost a decade, it is now widely accepted that the Virus is mainly latent in neuronal cells, with only a small proportion of non-neuronal cells infected. All of the studies carried out so far have indicated that VZV gene expression is highly restricted during ganglionic Latency. Although at least four VZV genes have been identified as being expressed, the possibility that latent gene expression is significantly greater than this cannot yet be excluded. There is also evidence for VZV gene‐encoded proteins being expressed during Latency, although the precise extent of this is unclear. Advances in this difficult field may be expected to arise from both newly developed molecular technology and more refined animal models of VZV Latency. Journal of NeuroVirology (2002) 8(suppl. 2), 80‐84.
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Varicella-zoster Virus Latency in human ganglia
Reviews in medical virology, 2002Co-Authors: Peter G E KennedyAbstract:Varicella-zoster Virus (VZV) is a human herpesVirus which causes varicella (chickenpox) as a primary infection, and, following a variable period during which it remains in latent form in trigeminal and dorsal root ganglia, reactivates in later life to cause herpes zoster (shingles). VZV is a significant cause of neurological disease including post-herpetic neuralgia which may be persistent and highly resistant to treatment, and small and large vessel encephalitis. VZV infections are more frequent with advancing age and in immunocompromised individuals. An understanding of the mechanisms of Latency is crucial in developing effective therapies for VZV infections of the nervous system. Such studies have been hampered by the difficulties in working with the Virus and also the lack of a good animal model of VZV Latency. It is known that the ganglionic VZV burden during Latency is low. Two of the key questions that have been addressed are the cellular site of latent VZV and the identity of the viral genes which are transcribed during Latency. There is now a consensus that latent VZV resides predominantly in ganglionic neurons with less frequent infection of non-neuronal satellite cells. There is considerable evidence to show that at least five viral genes are transcribed during Latency. Unlike herpes simplex Virus-1 Latency, viral protein expression has been demonstrated during VZV Latency. A precise knowledge of which viral genes are expressed is crucial in devising novel antiviral therapy using expressed genes as therapeutic targets. Whether gene expression at both the transcriptional and translational levels is more extensive than currently reported will require much more work and probably new molecular technology.
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Key issues in varicella-zoster Virus Latency.
Journal of neurovirology, 2002Co-Authors: Peter G E KennedyAbstract:The molecular mechanisms by which varicella-zoster Virus (VZV) causes a latent infection in human trigeminal and spinal ganglia are not well understood. It is known that VZV establishes Latency in ganglia following the primary infection causing varicella (chickenpox), and that the Virus may reactivate after years of dormancy to produce herpes zoster (shingles). Two key issues have been the cell-type localization of latent VZV in human ganglia, and the nature and extent of VZV gene expression during Latency. Although the cell specificity of latent VZV has been controversial for almost a decade, it is now widely accepted that the Virus is mainly latent in neuronal cells, with only a small proportion of non-neuronal cells infected. All of the studies carried out so far have indicated that VZV gene expression is highly restricted during ganglionic Latency. Although at least four VZV genes have been identified as being expressed, the possibility that latent gene expression is significantly greater than this cannot yet be excluded. There is also evidence for VZV gene-encoded proteins being expressed during Latency, although the precise extent of this is unclear. Advances in this difficult field may be expected to arise from both newly developed molecular technology and more refined animal models of VZV Latency.
Randall J Cohrs - One of the best experts on this subject based on the ideXlab platform.
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a comparison of herpes simplex Virus type 1 and varicella zoster Virus Latency and reactivation
Journal of General Virology, 2015Co-Authors: Peter G E Kennedy, Joel Rovnak, Hussain Badani, Randall J CohrsAbstract:Herpes simplex Virus type 1 (HSV-1; human herpesVirus 1) and varicella-zoster Virus (VZV; human herpesVirus 3) are human neurotropic alphaherpesViruses that cause lifelong infections in ganglia. Following primary infection and establishment of Latency, HSV-1 reactivation typically results in herpes labialis (cold sores), but can occur frequently elsewhere on the body at the site of primary infection (e.g. whitlow), particularly at the genitals. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. Primary VZV infection causes varicella (chickenpox) following which latent Virus may reactivate decades later to produce herpes zoster (shingles), as well as an increasingly recognized number of subacute, acute and chronic neurological conditions. Following primary infection, both Viruses establish a latent infection in neuronal cells in human peripheral ganglia. However, the detailed mechanisms of viral Latency and reactivation have yet to be unravelled. In both cases latent viral DNA exists in an ‘end-less’ state where the ends of the Virus genome are joined to form structures consistent with unit length episomes and concatemers, from which viral gene transcription is restricted. In latently infected ganglia, the most abundantly detected HSV-1 RNAs are the spliced products originating from the primary Latency associated transcript (LAT). This primary LAT is an 8.3 kb unstable transcript from which two stable (1.5 and 2.0 kb) introns are spliced. Transcripts mapping to 12 VZV genes have been detected in human ganglia removed at autopsy; however, it is difficult to ascribe these as transcripts present during latent infection as early-stage Virus reactivation may have transpired in the post-mortem time period in the ganglia. Nonetheless, low-level transcription of VZV ORF63 has been repeatedly detected in multiple ganglia removed as close to death as possible. There is increasing evidence that HSV-1 and VZV Latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms of HSV-1 and VZV Latency hold much promise for our future understanding in this complex area. This review summarizes the molecular biology of HSV-1 and VZV Latency and reactivation, and also presents future directions for study.
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Varicella zoster Virus Latency
Future virology, 2011Co-Authors: Emily M. Eshleman, Aamir Shahzad, Randall J CohrsAbstract:Primary infection by varicella zoster Virus (VZV) typically results in childhood chickenpox, at which time Latency is established in the neurons of the cranial nerve, dorsal root and autonomic ganglia along the entire neuraxis. During Latency, the histone-associated Virus genome assumes a circular episomal configuration from which transcription is epigenetically regulated. The lack of an animal model in which VZV Latency and reactivation can be studied, along with the difficulty in obtaining high-titer cell-free Virus, has limited much of our understanding of VZV Latency to descriptive studies of ganglia removed at autopsy and analogy to HSV-1, the prototype alphaherpesVirus. However, the lack of miRNA, detectable Latency-associated transcript and T-cell surveillance during VZV Latency highlight basic differences between the two neurotropic herpesViruses. This article focuses on VZV Latency: establishment, maintenance and reactivation. Comparisons are made with HSV-1, with specific attention to difference...
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Herpes simplex Virus-1 and varicella-zoster Virus Latency in ganglia
Journal of NeuroVirology, 2003Co-Authors: Bradley M. Mitchell, Donald H. Gilden, Randall J Cohrs, David C Bloom, Peter G E KennedyAbstract:Two human alpha-herpesViruses, herpes simplex Virus (HSV)-1 and varicella zoster Virus (VZV), account for the most frequent and serious neurologic disease caused by any of the eight human herpesViruses. Both HSV-1 and VZV become latent in ganglia. In this review, the authors describe features of Latency for these Viruses, such as distribution, prevalence, abundance, and configuration of viral DNA in latently infected human ganglia, as well as transcription, translation, and cell type infected. Studies of viral Latency in animal models are also discussed. For each Virus, remaining questions and future studies to understand the mechanism of Latency are discussed with respect to prevention of serious cutaneous, ocular, and neurologic disease produced by Virus reactivation.
Jimmy Kwang - One of the best experts on this subject based on the ideXlab platform.
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identification of white spot syndrome Virus Latency related genes in specific pathogen free shrimps by use of a microarray
Journal of Virology, 2003Co-Authors: Siti Khadijah, Soek Ying Neo, Mohammad Sorowar Hossain, Lance D Miller, Sinnakarupan Mathavan, Jimmy KwangAbstract:To investigate whether specific-pathogen-free (SPF) shrimps are asymptomatic carriers of white spot syndrome Virus (WSSV), we used a WSSV-specific DNA microarray to measure WSSV gene expression in SPF and WSSV-infected shrimps. Three WSSV genes were found to be relatively highly expressed in SPF shrimps. Reverse transcription-PCR using nested primers as well as real-time detection confirmed that these genes have no detectable counterparts in GenBank; structural analysis of the putative proteins revealed helix-loop-helix and leucine zipper motifs. Viral sequences could be PCR amplified from genomic DNA of SPF shrimp, further supporting the suggestion that these shrimps are asymptomatic carriers.
Donald H. Gilden - One of the best experts on this subject based on the ideXlab platform.
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Effect of Time Delay after Necropsy on Analysis of Simian Varicella-Zoster Virus Expression in Latently Infected Ganglia of Rhesus Macaques
Journal of Virology, 2010Co-Authors: Ravi Mahalingam, Vicki Traina-dorge, Eileen Deharo, Anjani Golive, Ilhem Messaoudi, Mary Wellish, Donald H. GildenAbstract:Studies of varicella-zoster Virus gene expression during Latency require the acquisition of human ganglia at autopsy. Concerns have been raised that the Virus might reactivate immediately after death. Because features of varicella-zoster Virus Latency are similar in primate and human ganglia, we examined Virus gene expression in tissues either processed immediately or kept at 4°C for 30 h before necropsy of two monkeys inoculated with simian varicella-zoster Virus and euthanized 117 days later. Virus transcription and the detection of open reading frame (ORF) 63 protein in the cytoplasm of neurons were comparable. Thus, a 30-h delay after death did not affect varicella-zoster Virus expression in latently infected ganglia.
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Herpes simplex Virus-1 and varicella-zoster Virus Latency in ganglia
Journal of NeuroVirology, 2003Co-Authors: Bradley M. Mitchell, Donald H. Gilden, Randall J Cohrs, David C Bloom, Peter G E KennedyAbstract:Two human alpha-herpesViruses, herpes simplex Virus (HSV)-1 and varicella zoster Virus (VZV), account for the most frequent and serious neurologic disease caused by any of the eight human herpesViruses. Both HSV-1 and VZV become latent in ganglia. In this review, the authors describe features of Latency for these Viruses, such as distribution, prevalence, abundance, and configuration of viral DNA in latently infected human ganglia, as well as transcription, translation, and cell type infected. Studies of viral Latency in animal models are also discussed. For each Virus, remaining questions and future studies to understand the mechanism of Latency are discussed with respect to prevention of serious cutaneous, ocular, and neurologic disease produced by Virus reactivation.
A. G. Ponniah - One of the best experts on this subject based on the ideXlab platform.
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Transcript Analysis of White spot syndrome Virus Latency and Phagocytosis Activating Protein Genes in Infected Shrimp (Penaeus monodon)
Indian Journal of Virology, 2012Co-Authors: M. S. Shekhar, M. Dillikumar, K. Vinaya Kumar, G. Gopikrishna, S. Rajesh, J. Kiruthika, A. G. PonniahAbstract:Viral Latency has been recently observed to be associated with White spot syndrome Virus (WSSV) infection in shrimp. In the present study, shrimp samples ( Penaeus monodon ) surviving WSSV infection were examined for presence of WSSV in latent phase. Virus Latency was observed in shrimp which were either experimentally challenged with WSSV and survived the infection or those which survived the natural infection. Three viral transcripts (ORFs 427, 151, 366) associated with Latency were analyzed by real-time PCR. The shrimp surviving the natural WSSV infection on estimation with RT-PCR were found to have low grade of WSSV infection (less than 56 copies of WSSV). All the shrimp samples were RT-PCR negative for structural protein genes of WSSV, VP24 and VP28, indicating that these samples were harboring latent phase Virus. RT-PCR of all the shrimp samples which survived WSSV infection revealed amplification of phagocytosis activating protein (PAP) gene (435 bp) with higher gene expression levels in experimentally challenged shrimp when compared to naturally infected shrimp. The expression of PAP in WSSV infected shrimp samples indicates its possible role in host response for resistance against WSSV infection. PAP was cloned and expressed as recombinant protein for protection studies. Shrimp were injected with three doses (5, 15 and 20 μg g^−1 body weight) of recombinant PAP. Relative percent survival of 10 % was observed in shrimp immunized with the dose of 15 μg g^−1 body weight of recombinant PAP. The expression of both WSSV Latency associated and PAP genes obtained from shrimp surviving the WSSV infection, indicates the possible role of these genes in host–pathogen interaction.
