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The Journal of Infectious Diseases Sep 2018Varicella-zoster virus (VZV) causes clinically significant illness during acute and recurrent infection accompanied by robust innate and acquired immune responses.... (Review)
Review
Varicella-zoster virus (VZV) causes clinically significant illness during acute and recurrent infection accompanied by robust innate and acquired immune responses. Innate immune cells in skin and ganglion secrete type I interferon (IFN-I) and proinflammatory cytokines to control VZV. Varicella-zoster virus subverts pattern recognition receptor sensing to modulate antigen presentation and IFN-I production. During primary infection, VZV hijacks T cells to disseminate to the skin and establishes latency in ganglia. Durable T- and B-cell memory formed within a few weeks of infection is boosted by reactivation or re-exposure. Antigen-specific T cells are recruited and potentially retained in VZV-infected skin to counteract reactivation. In latently VZV-infected ganglia, however, virus-specific T cells have not been recovered, suggesting that local innate immune responses control VZV latency. Antibodies prevent primary VZV infection, whereas T cells are fundamental to resolving disease, limiting severity, and preventing reactivation. In this study, we review current knowledge on the interactions between VZV and the human immune system.
Topics: Adaptive Immunity; Herpesvirus 3, Human; Humans; Immunity, Cellular; Immunity, Humoral; Immunity, Innate; Varicella Zoster Virus Infection
PubMed: 30247598
DOI: 10.1093/infdis/jiy403 -
Viruses May 2022The replication of varicella-zoster virus (VZV) in skin is critical to its pathogenesis and spread. Primary infection causes chickenpox, which is characterised by... (Review)
Review
The replication of varicella-zoster virus (VZV) in skin is critical to its pathogenesis and spread. Primary infection causes chickenpox, which is characterised by centrally distributed skin blistering lesions that are rich in infectious virus. Cell-free virus in the cutaneous blistering lesions not only spreads to cause further cases, but infects sensory nerve endings, leading to the establishment of lifelong latency in sensory and autonomic ganglia. The reactivation of virus to cause herpes zoster is again characterised by localised painful skin blistering rash containing infectious virus. The development of and models of VZV skin replication has revealed aspects of VZV replication and pathogenesis in this important target organ and improved our understanding of the vaccine strain vOKa attenuation. In this review, we outline the current knowledge on VZV interaction with host signalling pathways, the viral association with proteins associated with epidermal terminal differentiation, and how these interconnect with the VZV life cycle to facilitate viral replication and shedding.
Topics: Biology; Chickenpox; Herpes Zoster; Herpesvirus 3, Human; Humans; Skin
PubMed: 35632723
DOI: 10.3390/v14050982 -
Viruses Jul 2023Varicella-Zoster virus (VZV) is a pathogenic human alpha herpes virus that causes varicella (chicken pox) as a primary infection and, following a variable period of... (Review)
Review
Varicella-Zoster virus (VZV) is a pathogenic human alpha herpes virus that causes varicella (chicken pox) as a primary infection and, following a variable period of latency in different ganglionic neurons, it reactivates to produce herpes zoster (shingles). The focus of this review is on the wide spectrum of the possible neurological manifestations of VZV reactivation. While the most frequent reactivation syndrome is herpes zoster, this may be followed by the serious and painful post-herpetic neuralgia (PHN) and by many other neurological conditions. Prominent among these conditions is a VZV vasculopathy, but the role of VZV in causing giant cell arteritis (GCA) is currently controversial. VZV reactivation can also cause segmental motor weakness, myelitis, cranial nerve syndromes, Guillain-Barre syndrome, meningoencephalitis, and zoster sine herpete, where a neurological syndrome occurs in the absence of the zoster rash. The field is complicated by the relatively few cases of neurological complications described and by the issue of causation when a neurological condition is not manifest at the same time as the zoster rash.
Topics: Humans; Herpesvirus 3, Human; Herpes Zoster; Chickenpox; Neuralgia, Postherpetic; Alphavirus; Exanthema
PubMed: 37632006
DOI: 10.3390/v15081663 -
Veterinary Ophthalmology Jul 2016Feline herpesvirus type 1 (FHV-1) is a common and important cause of ocular surface disease, dermatitis, respiratory disease, and potentially intraocular disease in... (Review)
Review
Feline herpesvirus type 1 (FHV-1) is a common and important cause of ocular surface disease, dermatitis, respiratory disease, and potentially intraocular disease in cats. Many antiviral drugs developed for the treatment of humans infected with herpesviruses have been used to treat cats infected with FHV-1. Translational use of drugs in this manner ideally requires methodical investigation of their in vitro efficacy against FHV-1 followed by pharmacokinetic and safety trials in normal cats. Subsequently, placebo-controlled efficacy studies in experimentally inoculated animals should be performed followed, finally, by carefully designed and monitored clinical trials in client-owned animals. This review is intended to provide a concise overview of the available literature regarding the efficacy of antiviral drugs and other compounds with proven or putative activity against FHV-1, as well as a discussion of their safety in cats.
Topics: Animals; Antiviral Agents; Cat Diseases; Cats; Herpesviridae Infections; Humans; Varicellovirus
PubMed: 27091747
DOI: 10.1111/vop.12375 -
Journal of Virology Aug 2023Feline herpesvirus type 1 (FHV-1) is an enveloped dsDNA virus belonging to the family and is considered one of the two primary viral etiological factors of feline upper...
Feline herpesvirus type 1 (FHV-1) is an enveloped dsDNA virus belonging to the family and is considered one of the two primary viral etiological factors of feline upper respiratory tract disease. In this study, we investigated the entry of FHV-1 into host cells using two models: the AK-D cell line and primary feline skin fibroblasts (FSFs). We employed confocal microscopy, siRNA silencing, and selective inhibitors of various entry pathways. Our observations revealed that the virus enters cells via pH and dynamin-dependent endocytosis, as the infection was significantly inhibited by NHCl, bafilomycin A1, dynasore, and mitmab. Additionally, genistein, nystatin, and filipin treatments, siRNA knock-down of caveolin-1, as well as FHV-1 and caveolin-1 colocalization suggest the involvement of caveolin-mediated endocytosis during the entry process. siRNA knock-down of clathrin heavy chain and analysis of virus particle colocalization with clathrin indicated that clathrin-mediated endocytosis also takes part in the primary cells. This is the first study to systematically examine FHV-1 entry into host cells, and for the first time, we describe FHV-1 replication in AK-D and FSFs. IMPORTANCE Feline herpesvirus 1 (FHV-1) is one of the most prevalent viruses in cats, causing feline viral rhinotracheitis, which is responsible for over half of viral upper respiratory diseases in cats and can lead to ocular lesions resulting in loss of sight. Although the available vaccine reduces the severity of the disease, it does not prevent infection or limit virus shedding. Despite the clinical relevance, the entry mechanisms of FHV-1 have not been thoroughly studied. Considering the limitations of commonly used models based on immortalized cells, we sought to verify our findings using primary feline skin fibroblasts, the natural target for infection in cats.
Topics: Animals; Cats; Cat Diseases; Caveolin 1; Clathrin; Endocytosis; Herpesviridae Infections; RNA, Small Interfering; Varicellovirus
PubMed: 37493545
DOI: 10.1128/jvi.00681-23 -
Ugeskrift For Laeger Nov 2023This is a case report of a 3-year-old boy who presented with unilateral anterior uveitis and tonic pupil following varicella-zoster virus (VZV) Infection. The patient...
This is a case report of a 3-year-old boy who presented with unilateral anterior uveitis and tonic pupil following varicella-zoster virus (VZV) Infection. The patient had red and irritated eyes and photophobia. Ophthalmological findings included anterior uveitis and tonic pupil accompanied by reduced vision and accommodation. An MRI of the cerebrum was normal. To ease the symptoms the patient was prescribed photophobia glasses with correction of hyperopia. Tonic pupil due to VZV infection is a rare complication, but may have long-term consequences, why patients with eye-involving VZV infection need to be examined by an ophthalmologist.
Topics: Male; Humans; Child; Child, Preschool; Chickenpox; Tonic Pupil; Photophobia; Herpesvirus 3, Human; Uveitis, Anterior; Acute Disease
PubMed: 38018730
DOI: No ID Found -
Uirusu 2018Herpes zoster, or shingles, results from the reactivation of latent varicella- zoster virus (VZV) in the dorsal-root or cranial-nerve ganglia, usually decades after... (Review)
Review
Herpes zoster, or shingles, results from the reactivation of latent varicella- zoster virus (VZV) in the dorsal-root or cranial-nerve ganglia, usually decades after primary infection. Herpes zoster is characterized by a vesicular rash with a unilateral and dermatomal distribution and is almost always accompanied by pain. Herpes zoster is not only skin disease, but also sometimes affects other organs, including central nerve system, eye, and facial nerve. The most common complications, such as postherpetic neuralgia (PHN), are more frequent, severe and impair patients' quality of life. For more than 10 years, in US, EU, and Australia, a live-attenuated vaccine against herpes zoster (Zostavax) containing the Oka VZV strain is licensed for use in adults who are 50 years of age or older. In Japan, a live attenuated varicella vaccine is also licensed for preventing herpes zoster in 2016. Two large randomized multinational efficacy trials (ZOE-50 and ZOE-70) showed that the novel herpes zoster subunit vaccine (shinglix) candidate containing varicella-zoster virus glycoprotein E (gE) and the AS01B adjuvant system reduced the risk of herpes zoster and PHN by more than 90%. This article aimed to review the epidemiology, pathophysiology and complications of herpes zoster and mention the efficacies and problems of the live-attenuated and the new recombinant herpes zoster vaccines.
Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Child; Child, Preschool; Female; Herpes Zoster; Herpes Zoster Vaccine; Herpesvirus 3, Human; Humans; Infant; Male; Middle Aged; Vaccines, Subunit; Virus Replication; Young Adult
PubMed: 31105132
DOI: 10.2222/jsv.68.21 -
BMJ Case Reports Nov 2018
Topics: Child, Preschool; Female; Herpesvirus 3, Human; Humans; Pneumonia; Pneumoperitoneum
PubMed: 30567138
DOI: 10.1136/bcr-2018-227397 -
The EMBO Journal Jul 2022Varicella-Zoster virus (VZV) causes chickenpox and shingles. Although the infection is associated with severe morbidity in some individuals, molecular mechanisms that...
Varicella-Zoster virus (VZV) causes chickenpox and shingles. Although the infection is associated with severe morbidity in some individuals, molecular mechanisms that determine innate immune responses remain poorly defined. We found that the cGAS/STING DNA sensing pathway was required for type I interferon (IFN) induction during VZV infection and that recognition of VZV by cGAS restricted its replication. Screening of a VZV ORF expression library identified the essential VZV tegument protein ORF9 as a cGAS antagonist. Ectopically or virally expressed ORF9 bound to endogenous cGAS leading to reduced type I IFN responses to transfected DNA. Confocal microscopy revealed co-localisation of cGAS and ORF9. ORF9 and cGAS also interacted directly in a cell-free system and phase-separated together with DNA. Furthermore, ORF9 inhibited cGAMP production by cGAS. Taken together, these results reveal the importance of the cGAS/STING DNA sensing pathway for VZV recognition and identify a VZV immune antagonist that partially but directly interferes with DNA sensing via cGAS.
Topics: DNA; Herpesvirus 3, Human; Humans; Immunity, Innate; Interferon Type I; Membrane Proteins; Nucleotidyltransferases; Viral Proteins
PubMed: 35670106
DOI: 10.15252/embj.2021109217 -
Frontiers in Immunology 2023Induced by varicella zoster virus (VZV), postherpetic neuralgia (PHN) is one of the common complications of herpes zoster (HZ) with refractory pain. Animal models play... (Review)
Review
BACKGROUND
Induced by varicella zoster virus (VZV), postherpetic neuralgia (PHN) is one of the common complications of herpes zoster (HZ) with refractory pain. Animal models play pivotal roles in disclosing the pain mechanisms and developing effective treatments. However, only a few rodent models focus on the VZV-associated pain and PHN.
OBJECTIVE
To summarize the establishment and characteristics of popular PHN rodent models, thus offer bases for the selection and improvement of PHN models.
DESIGN
In this review, we retrospect two promising PHN rodent models, VZV-induced PHN model and HSV1-induced PHN model in terms of pain-related evaluations, their contributions to PHN pathogenesis and pharmacology.
RESULTS
Significant difference of two PHN models is the probability of virus proliferation; 2) Most commonly used pain evaluation of PHN model is mechanical allodynia, but pain-induced anxiety and other behaviours are worth noting; 3) From current PHN models, pain mechanisms involve changes in virus gene and host gene expression, neuroimmune-glia interactions and ion channels; 4) antiviral drugs and classical analgesics serve more on the acute stage of herpetic pain.
CONCLUSIONS
Different PHN models assessed by various pain evaluations combine to fulfil more comprehensive understanding of PHN.
Topics: Animals; Neuralgia, Postherpetic; Rodentia; Herpes Zoster; Herpesvirus 3, Human; Herpesviridae Infections
PubMed: 37020565
DOI: 10.3389/fimmu.2023.1026269