Latent/Quiescent Herpes Simplex Virus 1 Genome Detection by Fluorescence In Situ Hybridization (FISH)

Cohen, Camille; Corpet, Armelle; Maroui, Mohamed Ali; Juillard, Franceline; Lomonte, Patrick

doi:10.1007/978-1-4939-9814-2_10

Cited by 5 publications

(10 citation statements)

References 23 publications

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“…Both hDAXX and ATRX are recruited independently of PML to the genome and promote the maintenance of chromatin and viral gene repression ( 55 , 56 ), since depletion of any of these factors results in greatly increased infectivity of HSV-1 lacking ICP0 ( 57 , 58 ). Viral DNA and PML co-localize rapidly in cultured neurons of both murine and human origin ( 30 , 31 , 59 , 60 ), forming structures that have been called viral DNA containing PML-nuclear bodies (vDCP-NB) that are also DAXX/ATRX/SP100-positive in the absence of ICP0 expression. Neurons have PML-ND10 complexes, but recent work suggests ND10 form more cohesively when neurons are exposed to IFN-I, such as might occur when axons in peripherally infected tissues are exposed and there is subsequent signaling along the axon ( 61 ).…”

Section: Intrinsic Immunitymentioning

confidence: 99%

“…These changes follow PML association and the recruitment of chromatin remodeling components, such as the HIRA complex of histone H3.3 and its chaperone factors UBN-1, CABIN1 and ASFa1 ( 32 , 33 ). This occurs in epithelial cells infected at low multiplicity of infection that do not express ICP0 ( 30 , 31 ). Histone H3.3 becomes lysine 9 trimethylated at multiple sites of the genome, correlating with full silencing of HSV-1 gene expression ( 31 , 32 ).…”

Section: Intrinsic Immunitymentioning

confidence: 99%

“…Virion DNA is not histone-associated, but within an hour in epithelial cell nuclei, [and longer in neurons (29)], the HSV genome co-localizes with Pro Myelocytic Leukemia (PML) proteins, components of the nuclear domain 10 (ND10) complex and components of small ubiquitin like modification (SUMO) complex. The genome can then develop widespread repressive marks of facultative chromatinization (30)(31)(32)(33). The eventual fate of the default chromatinized viral genome differs for epithelial cells and neurons.…”

Section: Nuclear Restriction Factors and The Lytic/latent Decision Processmentioning

confidence: 99%

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Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man

et al. 2021

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Herpes simplex virus type 1 (HSV-1) is a prevalent human pathogen. HSV-1 genomes persist in trigeminal ganglia neuronal nuclei as chromatinized episomes, while epithelial cells are typically killed by lytic infection. Fluctuations in anti-viral responses, broadly defined, may underlay periodic reactivations. The ganglionic immune response to HSV-1 infection includes cell-intrinsic responses in neurons, innate sensing by several cell types, and the infiltration and persistence of antigen-specific T-cells. The mechanisms specifying the contrasting fates of HSV-1 in neurons and epithelial cells may include differential genome silencing and chromatinization, dictated by variation in access of immune modulating viral tegument proteins to the cell body, and protection of neurons by autophagy. Innate responses have the capacity of recruiting additional immune cells and paracrine activity on parenchymal cells, for example via chemokines and type I interferons. In both mice and humans, HSV-1-specific CD8 and CD4 T-cells are recruited to ganglia, with mechanistic studies suggesting active roles in immune surveillance and control of reactivation. In this review we focus mainly on HSV-1 and the TG, comparing and contrasting where possible observational, interventional, and in vitro studies between humans and animal hosts.

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Section: Intrinsic Immunitymentioning

confidence: 99%

Section: Intrinsic Immunitymentioning

confidence: 99%

Section: Nuclear Restriction Factors and The Lytic/latent Decision Processmentioning

confidence: 99%

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Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man

et al. 2021

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“…Currently, PCR constitutes the gold standard for the verification and diagnosis of HSV infection [ 54 ]. Besides, fluorescence in situ hybridization (FISH) and next-generation sequencing (NGS) are also applicable during HSV detection [ 55 , 56 ]. The presence of intranuclear eosinophilic inclusion bodies (Cowdry type A), that can be observed under a light microscope, provides a quick validation of the diagnosis.…”

Section: Herpesvirusesmentioning

confidence: 99%

Viral Infections in Burn Patients: A State-Of-The-Art Review

Baj

Korona-Głowniak

Buszewicz

et al. 2020

Viruses

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Infections that are triggered by the accompanying immunosuppression in patients with burn wounds are very common regardless of age. Among burn patients, the most frequently diagnosed infections include the bacterial ones primarily caused by Pseudomonas aeruginosa or Klebsiella pneumonia, as well as fungal infections with the etiology of Candida spp. or Aspergillus spp. Besides, burn wounds are highly susceptible to viral infections mainly due to the impaired immune responses and defective functions of the immune cells within the wound microenvironment. The most prevalent viruses that invade burn wounds include herpes simplex virus (HSV), cytomegalovirus (CMV), human papilloma virus (HPV), and varicella zoster virus (VZV). Likewise, less prevalent infections such as those caused by the orf virus or Epstein–Barr Virus (EBV) might also occur in immunosuppressed burn patients. Viral infections result in increased morbidity and mortality rates in severely burned patients. Additionally, a positive correlation between the hospitalization duration and the severity of the viral infection has been demonstrated. Viral infections trigger the occurrence of various complications, ranging from mild symptoms to even fatal incidents. Accurate detection of viral infection is of great clinical importance because of the possibility for a quicker introduction of proper treatment therapy and shortening of hospitalization time. The aim of this paper is to provide a comprehensive review of the literature and summarize the findings regarding the most common viral infections in immunosuppressed burn patients.

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“…As described for other herpesviruses [ 12 ], KHV establishes a lifelong latent infection. It has been demonstrated that peripheral blood leukocytes and other tissues (i.e., neurons) support KHV latency in carp [ 13 , 14 ], and that KHV can, asymptomatically or symptomatically, reactivate from the latency stage by temperature stress between 17–23 °C [ 14 , 15 ], which can lead to sporadic shedding episodes and outbreaks [ 16 ], subsequently sustaining high KHV-antibody titers on the population over time [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Seroconversion and Skin Mucosal Parameters during Koi Herpesvirus Shedding in Common Carp, Cyprinus carpio

Cano

Mulhearn

Akter

et al. 2020

IJMS

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Seroconversion and the mucosal lysozyme G (lysG), complement 3 (c3), and immunoglobulins M (IgMsec) and Z2 (IgZ2) were measured for up to 900 degree days (DD) in skin swabs from common carp exposed to koi herpesvirus (KHV or CyHV-3) at either a non-permissive temperature (12 °C) or permissive temperatures (17 and 22 °C), and in survivors subjected to temperature increase to 22 °C 500 DD after the initial exposure. The survival rate at 22 °C varied from 100% in fish initially exposed at 12 °C, to 20% at 17 °C and 0% at 22 °C. Viral shedding episodes lasted for up to 29 days (493 DD) for fish clinically infected at 17 °C, and up to 57 days (684 DD) for asymptomatic fish held at 12 °C. Up-regulation of lysG transcripts was measured at 17 and 22 °C. Down-regulation of c3 and IgMsec transcripts was measured independent of the water temperature, followed by up-regulation after the temperature increase coinciding with seroconversion and clearance of KHV from the skin mucus. IgZ2 mRNA showed a negative correlation with IgM transcripts. KHV subversion of the complement system at the mucosal site coupled with poor immunoglobulin secretion during the viral replication might contribute to the long window of viral shedding, thus facilitating viral transmission.

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Latent/Quiescent Herpes Simplex Virus 1 Genome Detection by Fluorescence In Situ Hybridization (FISH)

Cited by 5 publications

References 23 publications

Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man

Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man

Viral Infections in Burn Patients: A State-Of-The-Art Review

Seroconversion and Skin Mucosal Parameters during Koi Herpesvirus Shedding in Common Carp, Cyprinus carpio

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