Varicella Zoster Virus Neuronal Latency and Reactivation Modeled in Vitro

Goldstein, Ronald S.; Kinchington, Paul R.

doi:10.1007/82_2021_244

Cited by 2 publications

(3 citation statements)

References 162 publications

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“…At present, there is evidence that the viruses that infect the ENS are mainly herpes simplex virus (HSV) and varicella-zoster virus (VZV), and the novel coronavirus that has become a global pandemic since 2019 can also infect the ENS [ 20 – 22 ]. Latent infection, lytic infection, and reactivation occur when viruses, such as VZV, reach enteric neurons through various pathways [ 23 – 25 ]. The distinction between lytic and latent infection can be determined by the presence or absence of cell-associated viral infection [ 26 , 27 ].…”

Section: Viral Infection Of the Intestinal Gangliamentioning

confidence: 99%

The mechanisms of nerve injury caused by viral infection in the occurrence of gastrointestinal motility disorder-related diseases

Li,

Chen,

Wang

et al. 2023

Virol J

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Gastrointestinal motility refers to the peristalsis and contractility of gastrointestinal muscles, including the force and frequency of gastrointestinal muscle contraction. Gastrointestinal motility maintains the normal digestive function of the human body and is a critical component of the physiological function of the digestive tract. At present, gastrointestinal motility disorder-related diseases are gradually affecting human production and life. In recent years, it has been consistently reported that the enteric nervous system has a coordinating and controlling role in gastrointestinal motility. Motility disorders are closely related to functional or anatomical changes in the gastrointestinal nervous system. At the same time, some viral infections, such as herpes simplex virus and varicella-zoster virus infections, can cause damage to the gastrointestinal nervous system. Therefore, this paper describes the mechanisms of viral infection in the gastrointestinal nervous system and the associated clinical manifestations. Studies have indicated that the means by which viruses can cause the infection of the enteric nervous system are various, including retrograde transport, hematogenous transmission and centrifugal transmission from the central nervous system. When viruses infect the enteric nervous system, they can cause clinical symptoms, such as abdominal pain, abdominal distension, early satiation, belching, diarrhea, and constipation, by recruiting macrophages, lymphocytes and neutrophils and regulating intestinal microbes. The findings of several case‒control studies suggest that viruses are the cause of some gastrointestinal motility disorders. It is concluded that one of the causes of gastrointestinal motility disorders is viral infection of the enteric nervous system. In such disorders, the relationships between viruses and nerves remain to be studied more deeply. Further studies are necessary to evaluate whether prophylactic antiviral therapy is feasible in gastrointestinal motility disorders.

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Section: Viral Infection Of the Intestinal Gangliamentioning

confidence: 99%

The mechanisms of nerve injury caused by viral infection in the occurrence of gastrointestinal motility disorder-related diseases

Li,

Chen,

Wang

et al. 2023

Virol J

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“…In the last 40 years, a variety of in vitro models have been used to study the mechanisms of α-HV latency and reactivation and are eloquently described in other reviews [9][10][11][12]. The different models can be organized into three broad categories depending on the neuronal cells they are built upon.…”

Section: Neuronal Latency Modelsmentioning

confidence: 99%

“…The ability to reactivate is an essential property of latency [83], and models based on the neuroblastoma line SH-SY5Y [12] or immortalized HD10.6 cells [20], have encountered difficulties achieving robust reactivation. While this is frustrating given the potential benefits of these more scalable platforms, there might be value in understanding why latent virus is not fully responsive.…”

Section: Mechanisms Of Reactivationmentioning

confidence: 99%

Impact of Cultured Neuron Models on α-Herpesvirus Latency Research

Wilson

2022

Viruses

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A signature trait of neurotropic α-herpesviruses (α-HV) is their ability to establish stable non-productive infections of peripheral neurons termed latency. This specialized gene expression program is the foundation of an evolutionarily successful strategy to ensure lifelong persistence in the host. Various physiological stresses can induce reactivation in a subset of latently-infected neurons allowing a new cycle of viral productive cycle gene expression and synthesis of infectious virus. Recurring reactivation events ensure transmission of the virus to new hosts and contributes to pathogenesis. Efforts to define the molecular basis of α-HV latency and reactivation have been notoriously difficult because the neurons harboring latent virus in humans and in experimentally infected live-animal models, are rare and largely inaccessible to study. Increasingly, researchers are turning to cultured neuron infection models as simpler experimental platforms from which to explore latency and reactivation at the molecular level. In this review, I reflect on the strengths and weaknesses of existing neuronal models and briefly summarize the important mechanistic insights these models have provided. I also discuss areas where prioritization will help to ensure continued progress and integration.

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Varicella Zoster Virus Neuronal Latency and Reactivation Modeled in Vitro

Cited by 2 publications

References 162 publications

The mechanisms of nerve injury caused by viral infection in the occurrence of gastrointestinal motility disorder-related diseases

The mechanisms of nerve injury caused by viral infection in the occurrence of gastrointestinal motility disorder-related diseases

Impact of Cultured Neuron Models on α-Herpesvirus Latency Research

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