Insights into the Pathogenesis of Varicella Viruses

Purpose of Review Varicella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older...

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Published in:Current clinical microbiology reports Vol. 6; no. 3; pp. 156 - 165
Main Authors: Sorel, Océane, Messaoudi, Ilhem
Format: Journal Article
Language:English
Published: Cham Springer International Publishing 15-09-2019
Springer Nature B.V
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Abstract Purpose of Review Varicella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older individuals and those who are immune-suppressed. Given that VZV infection is highly specific to humans, developing a reliable in vivo model that recapitulates the hallmarks of VZV infection has been challenging. Simian varicella virus (SVV) infection in non-human primates reproduces the cardinal features of VZV infections in humans and allows the study of varicella virus pathogenesis in the natural host. In this review, we summarize our current knowledge about genomic and virion structure of varicelloviruses as well as viral pathogenesis and antiviral immune responses during acute infection, latency, and reactivation. We also examine the immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster. Recent Findings Data from recent studies suggest that infected T cells are important for viral dissemination to the cutaneous sites of infection as well as the site of latency and that a viral latency-associated transcript might play a role in the transition from lytic infection to latency and then reactivation. Summary Recent studies have provided exciting insights into mechanisms of varicelloviruses pathogenesis such as the critical role of T cells in VZV/SVV dissemination from the respiratory mucosa to the skin and the sensory ganglia; the ability of VZV/SVV to interfere with host defense; and the identification of VLT transcripts in latently infected ganglia. However, our understanding of these phenomena remains poorly understood. Therefore, it is critical that we continue to investigate host-pathogen interactions during varicelloviruses infection. These studies will lead to a deeper understanding of VZV biology as well as novel aspects of cell biology.
AbstractList PURPOSE OF REVIEWVaricella zoster virus (VZV) is a highly contagious, neurotropic alpha herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older individuals and those who are immune-suppressed. Given that VZV infection is highly specific to humans, developing a reliable in vivo model that recapitulates the hallmarks of VZV infection has been challenging. Simian Varicella Virus (SVV) infection in nonhuman primates reproduces the cardinal features of VZV infections in humans and allows the study of varicella virus pathogenesis in the natural host. In this review, we summarize our current knowledge about genomic and virion structure of varicelloviruses as well as viral pathogenesis and antiviral immune responses during acute infection, latency and reactivation. We also examine the immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster. RECENT FINDINGSData from recent studies suggest that infected T cells are important for viral dissemination to the cutaneous sites of infection as well as site of latency and that a viral latency-associated transcript might play a role in the transition from lytic infection to latency and then reactivation. SUMMARYRecent studies have provided exciting insights into mechanisms of varicelloviruses pathogenesis such as the critical role of T cells in VZV/SVV dissemination from the respiratory mucosa to the skin and the sensory ganglia; the ability of VZV/SVV to interfere with host defense; and the identification of VLT transcripts in latently infected ganglia. However, our understanding of these phenomena remains poorly understood. Therefore, it is critical that we continue to investigate host-pathogen interactions during varicelloviruses infection. These studies will lead to a deeper understanding of VZV biology as well as novel aspects of cell biology.
Purpose of ReviewVaricella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older individuals and those who are immune-suppressed. Given that VZV infection is highly specific to humans, developing a reliable in vivo model that recapitulates the hallmarks of VZV infection has been challenging. Simian varicella virus (SVV) infection in non-human primates reproduces the cardinal features of VZV infections in humans and allows the study of varicella virus pathogenesis in the natural host. In this review, we summarize our current knowledge about genomic and virion structure of varicelloviruses as well as viral pathogenesis and antiviral immune responses during acute infection, latency, and reactivation. We also examine the immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster.Recent FindingsData from recent studies suggest that infected T cells are important for viral dissemination to the cutaneous sites of infection as well as the site of latency and that a viral latency-associated transcript might play a role in the transition from lytic infection to latency and then reactivation.SummaryRecent studies have provided exciting insights into mechanisms of varicelloviruses pathogenesis such as the critical role of T cells in VZV/SVV dissemination from the respiratory mucosa to the skin and the sensory ganglia; the ability of VZV/SVV to interfere with host defense; and the identification of VLT transcripts in latently infected ganglia. However, our understanding of these phenomena remains poorly understood. Therefore, it is critical that we continue to investigate host-pathogen interactions during varicelloviruses infection. These studies will lead to a deeper understanding of VZV biology as well as novel aspects of cell biology.
Purpose of Review Varicella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older individuals and those who are immune-suppressed. Given that VZV infection is highly specific to humans, developing a reliable in vivo model that recapitulates the hallmarks of VZV infection has been challenging. Simian varicella virus (SVV) infection in non-human primates reproduces the cardinal features of VZV infections in humans and allows the study of varicella virus pathogenesis in the natural host. In this review, we summarize our current knowledge about genomic and virion structure of varicelloviruses as well as viral pathogenesis and antiviral immune responses during acute infection, latency, and reactivation. We also examine the immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster. Recent Findings Data from recent studies suggest that infected T cells are important for viral dissemination to the cutaneous sites of infection as well as the site of latency and that a viral latency-associated transcript might play a role in the transition from lytic infection to latency and then reactivation. Summary Recent studies have provided exciting insights into mechanisms of varicelloviruses pathogenesis such as the critical role of T cells in VZV/SVV dissemination from the respiratory mucosa to the skin and the sensory ganglia; the ability of VZV/SVV to interfere with host defense; and the identification of VLT transcripts in latently infected ganglia. However, our understanding of these phenomena remains poorly understood. Therefore, it is critical that we continue to investigate host-pathogen interactions during varicelloviruses infection. These studies will lead to a deeper understanding of VZV biology as well as novel aspects of cell biology.
Varicella zoster virus (VZV) is a highly contagious, neurotropic alpha herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the sensory ganglia from which it can reactivate to induce herpes zoster (HZ), a painful disease that primarily affects older individuals and those who are immune-suppressed. Given that VZV infection is highly specific to humans, developing a reliable model that recapitulates the hallmarks of VZV infection has been challenging. Simian Varicella Virus (SVV) infection in nonhuman primates reproduces the cardinal features of VZV infections in humans and allows the study of varicella virus pathogenesis in the natural host. In this review, we summarize our current knowledge about genomic and virion structure of varicelloviruses as well as viral pathogenesis and antiviral immune responses during acute infection, latency and reactivation. We also examine the immune evasion mechanisms developed by varicelloviruses to escape the host immune responses and the current vaccines available for protecting individuals against chickenpox and herpes zoster. Data from recent studies suggest that infected T cells are important for viral dissemination to the cutaneous sites of infection as well as site of latency and that a viral latency-associated transcript might play a role in the transition from lytic infection to latency and then reactivation. Recent studies have provided exciting insights into mechanisms of varicelloviruses pathogenesis such as the critical role of T cells in VZV/SVV dissemination from the respiratory mucosa to the skin and the sensory ganglia; the ability of VZV/SVV to interfere with host defense; and the identification of VLT transcripts in latently infected ganglia. However, our understanding of these phenomena remains poorly understood. Therefore, it is critical that we continue to investigate host-pathogen interactions during varicelloviruses infection. These studies will lead to a deeper understanding of VZV biology as well as novel aspects of cell biology.
Author Messaoudi, Ilhem
Sorel, Océane
Author_xml – sequence: 1
  givenname: Océane
  surname: Sorel
  fullname: Sorel, Océane
  organization: Department of Molecular Biology and Biochemistry, University of California Irvine
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  givenname: Ilhem
  surname: Messaoudi
  fullname: Messaoudi, Ilhem
  email: imessaou@uci.edu
  organization: Department of Molecular Biology and Biochemistry, University of California Irvine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32999816$$D View this record in MEDLINE/PubMed
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Issue 3
Keywords Varicella
Viral latency
Herpes zoster
Varicella-zoster virus
Simian varicella virus
Herpesvirus
varicella zoster virus
herpes zoster
viral latency
simian varicella virus
herpesvirus
varicella
Language English
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Snippet Purpose of Review Varicella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes...
Varicella zoster virus (VZV) is a highly contagious, neurotropic alpha herpes virus that causes varicella (chickenpox). VZV establishes lifelong latency in the...
Purpose of ReviewVaricella-zoster virus (VZV) is a highly contagious, neurotropic alpha-herpes virus that causes varicella (chickenpox). VZV establishes...
PURPOSE OF REVIEWVaricella zoster virus (VZV) is a highly contagious, neurotropic alpha herpes virus that causes varicella (chickenpox). VZV establishes...
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SubjectTerms Biomedical and Life Sciences
Biomedicine
Chicken pox
Herpes zoster
Host-pathogen interactions
Infections
Latency
Latent infection
Lymphocytes T
Medical Microbiology
Mucosa
Pathogenesis
Section Editor
Sensory neurons
Skin
Topical Collection on Virology
Transcription
Vaccines
Varicella
Virions
Virology (A Nicola
Viruses
Title Insights into the Pathogenesis of Varicella Viruses
URI https://link.springer.com/article/10.1007/s40588-019-00119-2
https://www.ncbi.nlm.nih.gov/pubmed/32999816
https://www.proquest.com/docview/2276012190
https://search.proquest.com/docview/2447839444
https://pubmed.ncbi.nlm.nih.gov/PMC7523919
Volume 6
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