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Journal of General Internal Medicine Feb 2017
Topics: Cost-Benefit Analysis; Herpes Zoster; Herpes Zoster Vaccine; Herpesvirus 3, Human; Humans; Vaccination
PubMed: 27730484
DOI: 10.1007/s11606-016-3885-x -
Anais Da Academia Brasileira de Ciencias 2020EHV-1 infection is responsible for huge economic losses in equines due to abortion and neonatal mortality. In this study, we describe 4 cases of abortion and neonatal...
EHV-1 infection is responsible for huge economic losses in equines due to abortion and neonatal mortality. In this study, we describe 4 cases of abortion and neonatal deaths from pregnant mares and a she-donkey from different localities in Egypt during the period from May 2015 to October 2017. Attempts were made to isolate and identify EHV-1, in addition to compare the different pathological lesions in various tissues of the necropsied cases. EHV-1 was successfully isolated from two aborted fetuses and one dead neonatal foal from mares, beside one aborted fetus from a she-donkey. The positive cases showed cytopathic effect on embryonated chicken eggs scattered on chorioallantoic membrane. Moreover, PCR was applied for the pock lesions and revealed positive results for EHV-1. Interstitial pneumonia, bronchopneumonia and necrosis of hepatic, myocardial, microcotyledonary tissues besides disseminated thrombi were the main encountered lesions. Intranuclear inclusion bodies were demonstrated in brain, liver, placenta and pulmonary tissues. Here, we describe EHV-1 induced brain lesions represented by degenerated neurons, vascular endotheliosis with intranuclear inclusion bodies in the aborted she-donkey fetus. Lesions were more sever in the aborted fetuses from mares than the one from the she-donkey. EHV-1 antigen was detected by immunohistochemistry staining.
Topics: Abortion, Veterinary; Animals; Equidae; Female; Fetus; Herpesviridae Infections; Herpesvirus 1, Equid; Horse Diseases; Horses; Pregnancy
PubMed: 32965312
DOI: 10.1590/0001-3765202020180837 -
The American Journal of Tropical... Mar 2023The first manifestation of a viral infection may be conjunctivitis. There are limited data on the etiology of viral conjunctivitis in Vanuatu, a country in the South...
The first manifestation of a viral infection may be conjunctivitis. There are limited data on the etiology of viral conjunctivitis in Vanuatu, a country in the South Pacific Ocean. Patients presenting to one of two Vanuatu health centers with presumed infectious conjunctivitis were eligible if symptom onset was within 14 days of screening. Conjunctival and anterior nasal swabs were obtained and subjected to unbiased RNA deep sequencing (RNA-seq) to identify DNA and RNA viruses. For samples collected from May to November 2021, RNA-seq identified a viral etiology in 12/48 patients. Human adenovirus species were the most common viruses (58%) detected, followed by human herpes viruses (cytomegalovirus, varicella zoster virus, and human herpes 7 virus). Rhinovirus C, Epstein-Barr virus, and bocavirus were also detected. In summary, the etiology for viral conjunctivitis in Vanuatu appears broad. Unbiased testing may be useful for disease surveillance.
Topics: Humans; Epstein-Barr Virus Infections; Vanuatu; Herpesvirus 4, Human; Herpesvirus 3, Human; Conjunctivitis; Conjunctivitis, Viral
PubMed: 36646076
DOI: 10.4269/ajtmh.22-0600 -
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 -
Viruses Mar 2022The non-specific innate immunity can initiate host antiviral innate immune responses within minutes to hours after the invasion of pathogenic microorganisms. Therefore,... (Review)
Review
The non-specific innate immunity can initiate host antiviral innate immune responses within minutes to hours after the invasion of pathogenic microorganisms. Therefore, the natural immune response is the first line of defense for the host to resist the invaders, including viruses, bacteria, fungi. Host pattern recognition receptors (PRRs) in the infected cells or bystander cells recognize pathogen-associated molecular patterns (PAMPs) of invading pathogens and initiate a series of signal cascades, resulting in the expression of type I interferons (IFN-I) and inflammatory cytokines to antagonize the infection of microorganisms. In contrast, the invading pathogens take a variety of mechanisms to inhibit the induction of IFN-I production from avoiding being cleared. Pseudorabies virus (PRV) belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus. PRV is the causative agent of Aujeszky's disease (AD, pseudorabies). Although the natural host of PRV is swine, it can infect a wide variety of mammals, such as cattle, sheep, cats, and dogs. The disease is usually fatal to these hosts. PRV mainly infects the peripheral nervous system (PNS) in swine. For other species, PRV mainly invades the PNS first and then progresses to the central nervous system (CNS), which leads to acute death of the host with serious clinical and neurological symptoms. In recent years, new PRV variant strains have appeared in some areas, and sporadic cases of PRV infection in humans have also been reported, suggesting that PRV is still an important emerging and re-emerging infectious disease. This review summarizes the strategies of PRV evading host innate immunity and new targets for inhibition of PRV replication, which will provide more information for the development of effective inactivated vaccines and drugs for PRV.
Topics: Animals; Antiviral Agents; Cattle; Dogs; Herpesvirus 1, Suid; Immunity, Innate; Mammals; Pseudorabies; Sheep; Swine; Virus Replication
PubMed: 35336954
DOI: 10.3390/v14030547 -
Viruses May 2023Pseudorabies virus (PRV) variants have caused substantial economic losses in the swine industry in China since 2011. To surveil the genetic variation in PRV field...
Pseudorabies virus (PRV) variants have caused substantial economic losses in the swine industry in China since 2011. To surveil the genetic variation in PRV field strains, here, two novel variant strains of PRV were isolated from Shanxi Province in central China and were designated SX1910 and SX1911. To identify the genetic characteristics of the two isolates, their complete genomes were sequenced, and phylogenetic analysis and sequence alignment revealed that field PRV variants have undergone genetic variations; notably, the protein-coding sequences UL5, UL36, US1 and IE180 exhibited extensive variation and contained one or more hypervariable regions. Furthermore, we also found that the glycoproteins gB and gD of the two isolates had some novel amino acid (aa) mutations. Importantly, most of these mutations were located on the surface of the protein molecule, according to protein structure model analysis. We constructed a mutant virus of SX1911 with deletion of the gE and gI genes via CRISPR/Cas9. When tested in mice, SX1911-ΔgE/gI-vaccinated mice were protected within a comparable range to Bartha-K61-vaccinated mice. Additionally, a higher dose of inactivated Bartha-K61 protected the mice from lethal SX1911 challenge, while a lower neutralization titer, higher viral load and more severe microscopic lesions were displayed in Bartha-K61-vaccinated mice. These findings highlight the need for continuous monitoring of PRV and novel vaccine development or vaccination program design for PRV control in China.
Topics: Swine; Animals; Mice; Herpesvirus 1, Suid; Pseudorabies; Phylogeny; Genomics; China; Swine Diseases
PubMed: 37376537
DOI: 10.3390/v15061237 -
Viruses Feb 2023Bovine alphaherpesvirus 1 (BoHV-1) is a persistent and recurring disease that affects cattle worldwide. It is a major contributor to bovine respiratory disease and... (Review)
Review
Bovine alphaherpesvirus 1 (BoHV-1) is a persistent and recurring disease that affects cattle worldwide. It is a major contributor to bovine respiratory disease and reproductive failure in the US. A major complication of BoHV-1 arises from the lifelong latent infection established in the sensory ganglia of the peripheral nervous system following acute infection. Lifelong latency is marked by periodic reactivation from latency that leads to virus transmission and transient immunosuppression. Physiological and environmental stress, along with hormone fluctuations, can drive virus reactivation from latency, allowing the virus to spread rapidly. This review discusses the mechanisms of the latency/reactivation cycle, with particular emphasis on how different hormones directly regulate BoHV-1 gene expression and productive infection. Glucocorticoids, including the synthetic corticosteroid dexamethasone, are major effectors of the stress response. Stress directly regulates BoHV-1 gene expression through multiple pathways, including β-catenin dependent Wnt signaling, and the glucocorticoid receptor. Related type 1 nuclear hormone receptors, the androgen and progesterone receptors, also drive BoHV-1 gene expression and productive infection. These receptors form feed-forward transcription loops with the stress-induced Krüppel-like transcription factors KLF4 and KLF15. Understanding these molecular pathways is critical for developing novel therapeutics designed to block reactivation and reduce virus spread and disease.
Topics: Animals; Cattle; Cattle Diseases; Glucocorticoids; Herpesvirus 1, Bovine; Immunosuppression Therapy; Kruppel-Like Transcription Factors; Virus Latency
PubMed: 36851767
DOI: 10.3390/v15020552 -
International Journal of Medical... 2020Both the herpes zoster virus and suid herpesvirus type 1 (SuHV-1) belong to the Varicellovirus genus of the α-herpesviridae subfamily. They may cause opportunistic... (Review)
Review
Both the herpes zoster virus and suid herpesvirus type 1 (SuHV-1) belong to the Varicellovirus genus of the α-herpesviridae subfamily. They may cause opportunistic infections especially in patients with kidney diseases, varying from latent illness to overt lethality. Under these circumstances, impaired renal function is both the culprit for and victim of the infection. However, fulminant eruption of severe skin herpes zoster in lupus nephritis (LN) patients under prolonged immunosuppressive therapy is rare and even more rarely seen is the SuHV-1 encephalitis in human. Facing the evolution of these rare infections, we hence chose to review the clinical pathogenicity of these two viruses which were cognate in origin but distinct in virulence. As such, we began with the first of the two above viral diseases and proceeded with peculiar renal involvement, unique clinical symptoms and pertinent lethal risk. Of importance, LN was used to exemplify the reciprocally detrimental interactions between impaired renal function and suppressed immune response. Then in a manner similar to the gradient overlay, SuHV-1 encephalitis was discussed focusing on its neurotropic features, specific MRI findings and exclusive test of high throughput sequencing. Our report highlighted novel presentations of the Varicellovirus genus infection by providing a productive multidisciplinary communication with pointed disclosure of the renal involvement. It may therefore be of great medical relevance and educational value for clinicians, especially the unseasoned ones, to foresee and manage similar cases in susceptible patients.
Topics: Animals; Herpes Zoster; Herpesviridae Infections; Herpesvirus 1, Suid; Humans; Infectious Encephalitis; Kidney Diseases; Lupus Nephritis; Opportunistic Infections; Swine; Varicellovirus
PubMed: 32218696
DOI: 10.7150/ijms.41952 -
PLoS Pathogens Oct 2022Interferon-stimulated gene 15 (ISG15) is strongly upregulated during viral infections and exerts pro-viral or antiviral actions. While many viruses combat host antiviral...
Interferon-stimulated gene 15 (ISG15) is strongly upregulated during viral infections and exerts pro-viral or antiviral actions. While many viruses combat host antiviral defenses by limiting ISG expression, PRV infection notably increases expression of ISG15. However, studies on the viral strategies to regulate ISG15-mediated antiviral responses are limited. Here, we demonstrate that PRV-induced free ISG15 and conjugated proteins accumulation require viral gene expression. Conjugation inhibition assays showed that ISG15 imposes its antiviral effects via unconjugated (free) ISG15 and restricts the viral release. Knockout of ISG15 in PK15 cells interferes with IFN-β production by blocking IRF3 activation and promotes PRV replication. Mechanistically, ISG15 facilitates IFNα-mediated antiviral activity against PRV by accelerating the activation and nuclear translocation of STAT1 and STAT2. Furthermore, ISG15 facilitated STAT1/STAT2/IRF9 (ISGF3) formation and ISGF3-induced IFN-stimulated response elements (ISRE) activity for efficient gene transcription by directly interacting with STAT2. Significantly, ISG15 knockout mice displayed enhanced susceptibility to PRV, as evidenced by increased mortality and viral loads, as well as more severe pathology caused by excessive production of the inflammatory cytokines. Our studies establish the importance of free ISG15 in IFNα-induced antiviral immunity and in the control of viral infections.
Topics: Mice; Animals; Herpesvirus 1, Suid; Mice, Knockout; Antiviral Agents; Interferon-alpha; Virus Diseases
PubMed: 36315588
DOI: 10.1371/journal.ppat.1010921