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Uirusu Dec 2010Varicella-zoster virus (VZV) causes varicella in primary infection and zoster after reactivation from latency. Both herpes simplex virus (HSV) and VZV are classified... (Review)
Review
Varicella-zoster virus (VZV) causes varicella in primary infection and zoster after reactivation from latency. Both herpes simplex virus (HSV) and VZV are classified into the same alpha-herpesvirus subfamily. Although most VZV genes have their HSV homologs, VZV has many unique biological characteristics. In this review, we summarized recent studies on 1) animal models for VZV infection and outcomes from studies using the models, including 2) viral dissemination processes from respiratory mucosa, T cells, to skin, 3) cellular receptors for VZV entry, 4) functions of viral genes required uniquely for in vivo growth and for establishment of latency, 5) host immune responses and viral immune evasion mechanisms, and 6) varicella vaccine and anti-VZV drugs.
Topics: Animals; Antiviral Agents; Chickenpox Vaccine; Disease Models, Animal; Drug Design; Herpes Zoster; Herpesvirus 3, Human; Humans; Immunity, Cellular; Nervous System; Receptors, Virus; Respiratory System; Skin; T-Lymphocytes; Vaccines, Attenuated; Virus Latency
PubMed: 21488333
DOI: 10.2222/jsv.60.197 -
Virology Journal May 2023Felid herpesvirus 1 (FHV-1) is a major pathogenic agent of upper respiratory tract infections and eye damage in felines worldwide. Current FHV-1 vaccines offer limited...
BACKGROUND
Felid herpesvirus 1 (FHV-1) is a major pathogenic agent of upper respiratory tract infections and eye damage in felines worldwide. Current FHV-1 vaccines offer limited protection of short duration, and therefore, do not reduce the development of clinical signs or the latency of FHV-1.
METHODS
To address these shortcomings, we constructed FHV ∆gIgE-eGFP, FHV ∆TK mCherry, and FHV ∆gIgE/TK eGFP-mCherry deletion mutants (ΔgI/gE, ΔTK, and ΔgIgE/TK, respectively) using the clustered regularly interspaced palindromic repeats (CRISPR)/CRISP-associated protein 9 (Cas9) system (CRISPR/Cas9), which showed safety and immunogenicity in vitro. We evaluated the safety and efficacy of the deletion mutants administered with intranasal (IN) and IN + subcutaneous (SC) vaccination protocols. Cats in the vaccination group were vaccinated twice at a 4-week interval, and all cats were challenged with infection 3 weeks after the last vaccination. The cats were assessed for clinical signs, nasal shedding, and virus-neutralizing antibodies (VN), and with postmortem histological testing.
RESULTS
Vaccination with the gI/gE-deleted and gI/gE/TK-deleted mutants was safe and resulted in significantly lower clinical disease scores, fewer pathological changes, and less nasal virus shedding after infection. All three mutants induced virus-neutralizing antibodies after immunization.
CONCLUSIONS
In conclusion, this study demonstrates the advantages of FHV-1 deletion mutants in preventing FHV-1 infection in cats.
Topics: Cats; Animals; Virulence; Varicellovirus; Vaccination; Antibodies, Neutralizing; Herpesviridae Infections; Cat Diseases
PubMed: 37143065
DOI: 10.1186/s12985-023-02053-8 -
Viruses Jun 2022Pseudorabies virus (PRV) can cause neurological, respiratory, and reproductive diseases in pigs and establish lifelong latent infection in the peripheral nervous system... (Review)
Review
Pseudorabies virus (PRV) can cause neurological, respiratory, and reproductive diseases in pigs and establish lifelong latent infection in the peripheral nervous system (PNS). Latent infection is a typical feature of PRV, which brings great difficulties to the prevention, control, and eradication of pseudorabies. The integral mechanism of latent infection is still unclear. Latency-associated transcripts (LAT) gene is the only transcriptional region during latent infection of PRV which plays the key role in regulating viral latent infection and inhibiting apoptosis. Here, we review the characteristics of PRV latent infection and the transcriptional characteristics of the LAT gene. We also analyzed the function of non-coding RNA (ncRNA) produced by the LAT gene and its importance in latent infection. Furthermore, we provided possible strategies to solve the problem of latent infection of virulent PRV strains in the host. In short, the detailed mechanism of PRV latent infection needs to be further studied and elucidated.
Topics: Animals; Herpesvirus 1, Suid; Latent Infection; Pseudorabies; Swine; Swine Diseases
PubMed: 35891360
DOI: 10.3390/v14071379 -
Mayo Clinic Proceedings May 2019
Topics: Exanthema; Herpes Zoster; Herpesvirus 3, Human; Humans
PubMed: 31054599
DOI: 10.1016/j.mayocp.2019.03.020 -
Viruses May 2019Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce... (Review)
Review
Varicella-zoster virus (VZV), an exclusively human herpesvirus, causes chickenpox and establishes a latent infection in ganglia, reactivating decades later to produce zoster and associated neurological complications. An understanding of VZV neurotropism in humans has long been hampered by the lack of an adequate animal model. For example, experimental inoculation of VZV in small animals including guinea pigs and cotton rats results in the infection of ganglia but not a rash. The severe combined immune deficient human (SCID-hu) model allows the study of VZV neurotropism for human neural sub-populations. Simian varicella virus (SVV) infection of rhesus macaques (RM) closely resembles both human primary VZV infection and reactivation, with analyses at early times after infection providing valuable information about the extent of viral replication and the host immune responses. Indeed, a critical role for CD4 T-cell immunity during acute SVV infection as well as reactivation has emerged based on studies using RM. Herein we discuss the results of efforts from different groups to establish an animal model of VZV neurotropism.
Topics: Animals; Chickenpox; Disease Models, Animal; Ganglia; Guinea Pigs; Herpes Zoster; Herpesviridae Infections; Herpesvirus 3, Human; Macaca mulatta; Sigmodontinae; Viral Load; Viral Tropism; Virus Replication
PubMed: 31159224
DOI: 10.3390/v11060502 -
Current Topics in Microbiology and... 2010Simian varicella virus (SVV) is a primate herpesvirus that is closely related to varicella-zoster virus (VZV), the causative agent of varicella (chickenpox) and herpes... (Review)
Review
Simian varicella virus (SVV) is a primate herpesvirus that is closely related to varicella-zoster virus (VZV), the causative agent of varicella (chickenpox) and herpes zoster (shingles). Epizootics of simian varicella occur sporadically in facilities housing Old World monkeys. This review summarizes the molecular properties of SVV. The SVV and VZV genomes are similar in size, structure, and gene arrangement. The 124.5 kilobase pair (kbp) SVV genome includes a 104.7 kbp long component covalently linked to a short component, which includes a 4.9 kbp unique short segment flanked by 7.5 kbp inverted repeat sequences. SVV DNA encodes 69 distinct open reading frames, three of which are duplicated within the viral inverted repeats. The viral genome is coordinately expressed, and immediate early (IE), early, and late genes have been characterized. Genetic approaches have been developed to create SVV mutants, which will be used to study the role of SVV genes in viral pathogenesis, latency, and reactivation. In addition, SVV expressing foreign genes are being investigated as potential recombinant varicella vaccines.
Topics: Animals; Cercopithecidae; DNA, Viral; Gene Expression Regulation, Viral; Genome, Viral; Herpesviridae Infections; Monkey Diseases; Mutagenesis, Site-Directed; Open Reading Frames; Varicellovirus
PubMed: 20369316
DOI: 10.1007/82_2010_27 -
Experimental Neurology May 2022It has become widely appreciated that the spinal cord has significant neuroplastic potential, is not hard-wired, and that with traumatic injury and anatomical... (Review)
Review
It has become widely appreciated that the spinal cord has significant neuroplastic potential, is not hard-wired, and that with traumatic injury and anatomical plasticity, the networks that we once understood now comprise a new anatomy. Harnessing advances in neuroanatomical tracing to map the neuronal networks of the intact and injured spinal cord has been crucial to elucidating this new spinal cord anatomy. Many new techniques have been developed to identify these networks using a variety of retrograde and anterograde tracers. One method of tracing that has become more widely used to map anatomical changes is transneuronal tracing. Viral tracers are being increasingly used to map spinal networks, leading to an advanced understanding of spinal circuitry and host-donor-host interactions between the injured spinal cord and neural transplants. This review will highlight advances in neuronal tracing, specifically using pseudorabies virus (PRV), and its use in the intact, injured, and transplanted spinal cord.
Topics: Animals; Herpesvirus 1, Suid; Neuronal Plasticity; Neurons; Spinal Cord; Spinal Cord Injuries
PubMed: 35085573
DOI: 10.1016/j.expneurol.2022.113990 -
American Journal of Obstetrics and... Aug 2023
Topics: Female; Humans; Herpes Zoster; Herpesvirus 3, Human; Vulva
PubMed: 36828295
DOI: 10.1016/j.ajog.2023.02.013 -
Cleveland Clinic Journal of Medicine Nov 2021
Topics: Chickenpox; Gastrointestinal Tract; Herpes Zoster; Herpesvirus 3, Human; Humans
PubMed: 34728482
DOI: 10.3949/ccjm.88a.20151 -
Viruses Jan 2021Felid herpesvirus-1 (FeHV-1) is an important respiratory and ocular pathogen of cats and current vaccines are limited in duration and efficacy because they do not...
Felid herpesvirus-1 (FeHV-1) is an important respiratory and ocular pathogen of cats and current vaccines are limited in duration and efficacy because they do not prevent infection, viral nasal shedding and latency. To address these shortcomings, we have constructed FeHV-1 gE-TK- and FeHV-1 PK- deletion mutants (gE-TK- and PK-) using bacterial artificial chromosome (BAC) mutagenesis and shown safety and immunogenicity in vitro. Here, we compare the safety and efficacy of a prime boost FeHV-1 gE-TK- and FeHV-1 PK- vaccination regimen with commercial vaccination in cats. Cats in the vaccination groups were vaccinated at 3-week intervals and all cats were challenge infected 3 weeks after the last vaccination. Evaluations included clinical signs, nasal shedding, virus neutralizing antibodies (VN), cytokine mRNA gene expression, post-mortem histology and detection of latency establishment. Vaccination with gE-TK- and PK- mutants was safe and resulted in significantly reduced clinical disease scores, pathological changes, viral nasal shedding, and viral DNA in the trigeminal ganglia (the site of latency) following infection. Both mutants induced VN antibodies and interferons after immunization. In addition, after challenge infection, we observed a reduction of IL-1β expression, and modulation of TNFα, TGFβ and IL10 expression. In conclusion, this study shows the merits of using FeHV-1 deletion mutants for prevention of FeHV-1 infection in cats.
Topics: Animals; Antibodies, Neutralizing; Antibodies, Viral; Cat Diseases; Cats; Cell Line; Cytokines; Gene Deletion; Herpesviridae Infections; Immunity, Innate; Immunization, Secondary; Male; Varicellovirus; Viral Envelope Proteins; Viral Vaccines; Virulence; Virus Replication; Virus Shedding
PubMed: 33499363
DOI: 10.3390/v13020163