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Journal of Clinical Virology : the... Aug 2023The recent mpox outbreak has highlighted the need to rapidly diagnose the causative agents of viral vesicular disease to inform treatment and control measures. Common...
BACKGROUND
The recent mpox outbreak has highlighted the need to rapidly diagnose the causative agents of viral vesicular disease to inform treatment and control measures. Common causes of vesicular disease include Monkeypox virus (MPXV), clades I and II, Herpes simplex viruses Type 1 and Type 2 (HSV-1, HSV-2), human herpes virus 6 (HHV-6), Varicella-zoster virus (VZV) and Enteroviruses (EVs). Here, we assessed a syndromic viral vesicular panel for rapid and simultaneous detection of these 7 targets in a single cartridge.
OBJECTIVE
The aim of this study was to evaluate the QIAStat-Dx ® viral vesicular (VV) panel and compare with laboratory developed tests (LDTs). Limit of detection, inter-run variability, cross-reactivity and specificity were assessed. Positive and negative percent agreement, and correlation between assays was determined using 124 clinical samples from multiple anatomical sites.
RESULTS
The overall concordance between the QIAstat and LDTs was 96%. Positive percent agreement was 82% for HHV-6, 89% for HSV-1 and 100% for MPXV, HSV-2, EV and VZV. Negative percent agreement was 100% for all targets assessed. There was no cross-reactivity with Vaccinia, Orf, Molluscum contagiosum viruses, and a pooled respiratory panel.
CONCLUSION
The QIAstat VV multi-target syndromic panel combine ease of use, rapid turnaround, good sensitivity and specificity for enhanced diagnosis, clinical care and public health responses.
Topics: Humans; Herpes Simplex; Herpesvirus 1, Human; Herpesvirus 2, Human; Herpesvirus 3, Human; Herpesvirus 6, Human; Virus Diseases; Viruses; Monkeypox virus
PubMed: 37364498
DOI: 10.1016/j.jcv.2023.105525 -
Dental and Medical Problems 2022Many complications can occur after the injection of local intraoral anesthetics (ILIA) before dental intervention. Facial paralysis (FP) is one of these complications.... (Review)
Review
Many complications can occur after the injection of local intraoral anesthetics (ILIA) before dental intervention. Facial paralysis (FP) is one of these complications. The purpose of this study was to systematically analyze the association between ILIA and FP. A systematic review was carried out taking into account the methodology of the Cochrane Handbook for Systematic Reviews of Interventions and the PRISMA statement. The search strategy used "Palsy AND Facial" and "Paralysis AND Facial" as search terms. The ScienceDirect, PubMed and Scopus databases were searched using the "dentistry journal" filter. The inclusion criteria included studies describing FP after or during ILIA that were published in dental journals. The CAse REports (CARE) checklist was applied in evaluating the methodological quality of case reports. A total of 2,462 articles (algorithm) were identified. After reviewing titles and abstracts, 18 articles were deemed relevant taking into account the objectives of this study. Only 13 of them, after reading the full text, met the inclusion criteria and were analyzed. Case reports on 18 cases of FP were analyzed, 12 of which described the early development of FP (onset within 24 h) and 6 the late development (onset after 24 h). Acceptable compliance with CARE guidelines was observed in the included studies . Early FP CRs presented the effect of the administered anesthetic on the facial nerve, and the vascular effect of the vasoconstrictor included in the anesthetic formula, while more recent FP CRs focused on the reactivation of herpes simplex virus type 1 (HSV-1), human herpesvirus 6 (HHV-6) or varicella-zoster virus (VZV).
Topics: Humans; Facial Paralysis; Herpesvirus 1, Human; Herpesvirus 3, Human; Face; Anesthetics
PubMed: 36583841
DOI: 10.17219/dmp/138910 -
Analytica Chimica Acta Apr 2023In the photoelectrochemical sensing, constant potential excitation to get the photoelectrochemical signal is the main excitation signal mode. Novel method for...
In the photoelectrochemical sensing, constant potential excitation to get the photoelectrochemical signal is the main excitation signal mode. Novel method for photoelectrochemical signal obtaining is needed. Inspired by this ideal, a photoelectrochemical strategy for Herpes simplex virus (HSV-1) detection with multiple potential step chronoamperometry (MUSCA) pattern was fabricated using CRISPR/Cas12a cleavage coupled with entropy-driven target recycling. In the presence of target, HSV-1, the Cas12a was activated by the H-H complex obtained by entropy-driven, then digesting the circular fragment of csRNA to expose single-stranded crRNA2 and alkaline phosphatase (ALP). The inactive Cas12a was self-assembled with crRNA2 and activated again with the help of assistant dsDNA. After multiple rounds of CRISPR/Cas12a cleavage and magnetic separation, MUSCA, as a signal amplifier, collected the enhanced photocurrent responses generated by catalyzed p-Aminophenol (p-AP). Different from the reported signal enhancement strategies based on photoactive nanomaterials and sensing mechanisms, MUSCA technique endowed the strategy with unique advantages of direct, fast and ultrasensitive. A superior detection limit of 3 aM toward HSV-1 was achieved. This strategy was successfully applied for HSV-1 detection in Human serum samples. The combination of MUSCA technique and CRISPR/Cas12a assay brings broader potential prospect for the detection of nucleic acids.
Topics: Humans; CRISPR-Cas Systems; Herpesvirus 1, Human; Alkaline Phosphatase; Biological Assay; Coloring Agents; Biosensing Techniques
PubMed: 36898814
DOI: 10.1016/j.aca.2023.340955 -
Viruses Aug 2021Diseases caused by human herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) affect millions of people worldwide and range from fatal encephalitis in neonates and... (Review)
Review
Diseases caused by human herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) affect millions of people worldwide and range from fatal encephalitis in neonates and herpes keratitis to orofacial and genital herpes, among other manifestations. The viruses can be shed efficiently by asymptomatic carriers, causing increased rates of infection. Viral transmission occurs through direct contact of mucosal surfaces followed by initial replication of the incoming virus in skin tissues. Subsequently, the viruses infect sensory neurons in the trigeminal and lumbosacral dorsal root ganglia, where they are primarily maintained in a transcriptionally repressed state termed "latency", which persists for the lifetime of the host. HSV DNA has also been detected in other sympathetic ganglia. Periodically, latent viruses can reactivate, causing ulcerative and often painful lesions primarily at the site of primary infection and proximal sites. In the United States, recurrent genital herpes alone accounts for more than a billion dollars in direct medical costs per year, while there are much higher costs associated with the socio-economic aspects of diseased patients, such as loss of productivity due to mental anguish. Currently, there are no effective FDA-approved vaccines for either prophylactic or therapeutic treatment of human herpes simplex infections, while several recent clinical trials have failed to achieve their endpoint goals. Historically, live-attenuated vaccines have successfully combated viral diseases, including polio, influenza, measles, and smallpox. Vaccines aimed to protect against the devastation of smallpox led to the most significant achievement in medical history: the eradication of human disease by vaccination. Recently, novel approaches toward developing safe and effective live-attenuated vaccines have demonstrated high efficacy in various preclinical models of herpetic disease. This next generation of live-attenuated vaccines has been tailored to minimize vaccine-associated side effects and promote effective and long-lasting immune responses. The ultimate goal is to prevent or reduce primary infections (prophylactic vaccines) or reduce the frequency and severity of disease associated with reactivation events (therapeutic vaccines). These vaccines' "rational" design is based on our current understanding of the immunopathogenesis of herpesviral infections that guide the development of vaccines that generate robust and protective immune responses. This review covers recent advances in the development of herpes simplex vaccines and the current state of ongoing clinical trials in pursuit of an effective vaccine against herpes simplex virus infections and associated diseases.
Topics: Animals; Drug Design; Herpes Simplex; Herpesvirus 1, Human; Herpesvirus 2, Human; Humans; Vaccines, Attenuated; Viral Vaccines
PubMed: 34452501
DOI: 10.3390/v13081637 -
Journal of Virology Mar 2023Type I interferon (IFN-I) response plays a prominent role in innate immunity, which is frequently modulated during viral infection. Here, we report DNA methylation...
Type I interferon (IFN-I) response plays a prominent role in innate immunity, which is frequently modulated during viral infection. Here, we report DNA methylation regulator UHRF1 as a potent negative regulator of IFN-I induction during alphaherpesvirus infection, whereas the viruses in turn regulates the transcriptional expression of UHRF1. Knockdown of UHRF1 in cells significantly increases interferon-β (IFN-β)-mediated gene transcription and viral inhibition against herpes simplex virus 1 (HSV1) and pseudorabies virus (PRV). Mechanistically, UHRF1 deficiency promotes IFN-I production by triggering dsRNA-sensing receptor RIG-I and activating IRF3 phosphorylation. Knockdown of UHRF1 in cells upregulates the accumulation of double-stranded RNA (dsRNA), including host endogenous retroviral sequence (ERV) transcripts, while the treatment of RNase III, known to specifically digest dsRNA, prevents IFN-β induction by siUHRF1. Furthermore, the double-knockdown assay of UHRF1 and DNA methyltransferase DNMT1 suggests that siUHRF1-mediated DNA demethylation may play an important role in dsRNA accumulation and subsequently IFN induction. These findings establish the essential role of UHRF1 in IFN-I-induced antiviral immunity and reveal UHRF1 as a potential antivrial target. Alphaherpesviruses can establish lifelong infections and cause many diseases in humans and animals, which rely partly on their interaction with IFN-mediated innate immune response. Using alphaherpesviruses PRV and HSV-1 as models, we identified an essential role of DNA methylation regulator UHRF1 in IFN-mediated immunity against virus replication, which unravels a novel mechanism employed by epigenetic factor to control IFN-mediated antiviral immune response and highlight UHRF1, which might be a potential target for antiviral drug development.
Topics: Animals; Humans; Antiviral Agents; CCAAT-Enhancer-Binding Proteins; Gene Expression; Herpesvirus 1, Human; Herpesvirus 1, Suid; Immunity, Innate; Interferon Regulatory Factor-3; Interferon Type I; Interferon-beta; Ubiquitin-Protein Ligases; Alphaherpesvirinae; Receptors, Immunologic
PubMed: 36916938
DOI: 10.1128/jvi.00134-23 -
Current Issues in Molecular Biology 2021Both the development of the mammalian innate immune system and the antagonistic strategies acquired by alphaherpesviruses to dismantle it have been shaped by co-evolving... (Review)
Review
Both the development of the mammalian innate immune system and the antagonistic strategies acquired by alphaherpesviruses to dismantle it have been shaped by co-evolving virus-host interactions over millions of years. Here, we review mechanisms employed by mammalian cells to detect pathogen molecules, such as viral glycoproteins and nucleic acids, and induce innate immune signaling upon infection with alphaherpesviruses. We further explore strategies acquired by these viruses to bypass immune detection and activation, thereby supporting virus replication and spread. Finally, we discuss the contributions of advanced 'omics' and microscopy methods to these discoveries in immune signaling and highlight emerging technologies that can help to further our understanding of the dynamic interplay between host innate immune responses and virus immune evasion.
Topics: Alphaherpesvirinae; Animals; Biological Evolution; DNA, Viral; Herpesviridae Infections; Host-Pathogen Interactions; Humans; Immune Evasion; Immunity, Innate; Signal Transduction; Viral Proteins; Virus Replication
PubMed: 33640867
DOI: 10.21775/cimb.042.635 -
Journal of Visualized Experiments : JoVE Nov 2021There are numerous published protocols for plaquing viruses, including references within primary literature for methodology. However, plaquing viruses can be difficult...
There are numerous published protocols for plaquing viruses, including references within primary literature for methodology. However, plaquing viruses can be difficult to perform, requiring focus on its specifications and refinement. It is an incredibly challenging method for new students to master, mainly because it requires meticulous attention to the most minute details. This demonstration of plaquing herpes simplex viruses should help those who have struggled with visualizing the method, especially its nuances, over the years. While this manuscript is based on the same principles of standard plaquing methodology, it differs in that it contains a detailed description of (1) how best to handle host cells to avoid disruption during the process, (2) a more useful viscous medium than agarose to limit the diffusion of virions, and (3) a simple fixation and staining procedure that produces reliably reproducible results. Furthermore, the accompanying video helps demonstrate the finer distinctions in the process, which are frequently missed when instructing others on conducting plaque assays.
Topics: Culture Media; Herpes Simplex; Humans; Simplexvirus; Virion
PubMed: 34806698
DOI: 10.3791/62962 -
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 -
Clinical Microbiology and Infection :... Oct 2022Herpes simplex virus (HSV) 1 and 2, varicella zoster virus (VZV), and human herpesvirus 6 (HHV-6) cause severe infections in immunocompromised hosts. Interventions to... (Review)
Review
BACKGROUND
Herpes simplex virus (HSV) 1 and 2, varicella zoster virus (VZV), and human herpesvirus 6 (HHV-6) cause severe infections in immunocompromised hosts. Interventions to optimize virus-specific adaptive immunity may have advantages over antivirals in the prophylaxis and treatment of these infections.
OBJECTIVES
We sought to review adaptive immune responses and methods for assessing and replenishing cellular and humoral immunity to HSV, VZV, and HHV-6 in solid organ transplant and hematopoietic cell transplant recipients.
SOURCES
We searched PubMed for relevant studies on immune responses to HSV, VZV, and HHV-6 as well as studies describing methods for evaluating and restoring cell-mediated immunity to other double-stranded DNA viruses in transplant recipients. Recent studies, randomized controlled trials, and investigations highlighting key concepts in clinical virology were prioritized for inclusion.
CONTENT
We describe the mechanisms of adaptive immunity to HSV, VZV, and HHV-6 and limitations of antivirals as prophylaxis and treatment for these infections in solid organ transplant and hematopoietic cell transplant recipients. We review methods for measuring and restoring cellular immunity to double-stranded DNA viruses; their potential applications to management of HSV, VZV, and HHV-6 in immunocompromised hosts; and barriers to clinical use. Vaccination and virus-specific T cell therapies are discussed in detail.
IMPLICATIONS
The growing repertoire of diagnostic and therapeutic techniques focused on virus-specific adaptive immunity provides a novel approach to management of viral infections in transplant recipients. Investigations to optimize such interventions specifically in HSV, VZV, and HHV-6 are needed.
Topics: Adaptive Immunity; Antiviral Agents; DNA; Hematopoietic Stem Cell Transplantation; Herpes Zoster; Herpesvirus 1, Human; Herpesvirus 3, Human; Herpesvirus 6, Human; Humans; Transplant Recipients
PubMed: 35150885
DOI: 10.1016/j.cmi.2022.02.001 -
Viruses Dec 2019The include the neurotropic pathogens herpes simplex virus and varicella zoster virus of humans and pseudorabies virus of swine. These viruses establish lifelong... (Review)
Review
The include the neurotropic pathogens herpes simplex virus and varicella zoster virus of humans and pseudorabies virus of swine. These viruses establish lifelong latency in the nuclei of peripheral ganglia, but utilize the peripheral tissues those neurons innervate for productive replication, spread, and transmission. Delivery of virions from replicative pools to the sites of latency requires microtubule-directed retrograde axonal transport from the nerve terminus to the cell body of the sensory neuron. As a corollary, during reactivation newly assembled virions must travel along axonal microtubules in the anterograde direction to return to the nerve terminus and infect peripheral tissues, completing the cycle. Neurotropic alphaherpesviruses can therefore exploit neuronal microtubules and motors for long distance axonal transport, and alternate between periods of sustained plus end- and minus end-directed motion at different stages of their infectious cycle. This review summarizes our current understanding of the molecular details by which this is achieved.
Topics: Alphaherpesvirinae; Animals; Axons; Biomarkers; Capsid; Cell Nucleus; Cytoplasm; Disease Susceptibility; Exocytosis; Herpesviridae Infections; Host-Pathogen Interactions; Humans; Life Cycle Stages; Microtubules; Nervous System Diseases; Neurons; Protein Transport
PubMed: 31861082
DOI: 10.3390/v11121165