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Viruses Aug 2021The alphaherpesviruses are pathogens of the mammalian nervous system. Initial infection is commonly at mucosal epithelia, followed by spread to, and establishment of... (Review)
Review
The alphaherpesviruses are pathogens of the mammalian nervous system. Initial infection is commonly at mucosal epithelia, followed by spread to, and establishment of latency in, the peripheral nervous system. During productive infection, viral gene expression, replication of the dsDNA genome, capsid assembly and genome packaging take place in the infected cell nucleus, after which mature nucleocapsids emerge into the cytoplasm. Capsids must then travel to their site of envelopment at cytoplasmic organelles, and enveloped virions need to reach the cell surface for release and spread. Transport at each of these steps requires movement of alphaherpesvirus particles through a crowded and viscous cytoplasm, and for distances ranging from several microns in epithelial cells, to millimeters or even meters during egress from neurons. To solve this challenging problem alphaherpesviruses, and their assembly intermediates, exploit microtubule- and actin-dependent cellular motors. This review focuses upon the mechanisms used by alphaherpesviruses to recruit kinesin, myosin and dynein motors during assembly and egress.
Topics: Actins; Alphaherpesvirinae; Capsid; Dyneins; Host Microbial Interactions; Humans; Kinesins; Microtubules; Myosins; Virion; Virus Assembly; Virus Release
PubMed: 34452486
DOI: 10.3390/v13081622 -
Biomedicine & Pharmacotherapy =... Sep 2020The infections caused by Herpes simplex viruses (HSV-1 and -2) are seriously endangering the health of all human beings. Once infected with these two viruses, it will... (Review)
Review
The infections caused by Herpes simplex viruses (HSV-1 and -2) are seriously endangering the health of all human beings. Once infected with these two viruses, it will cause life-long latency in the host, and the continuous recurrence of the infection will seriously affect the quality of life. Moreover, infections with HSV-1 and HSV-2 have been reported to make the body susceptible to other diseases, such as Alzheimer's disease and HIV. Thus, more attention should be paid to the development of novel anti-HSV drugs. Polysaccharides obtained from medicinal plants and microorganism (both land and sea) are reported to be promising anti-herpes substances. However, their antiviral mechanisms are complex and diverse, which includes direct inhibition of virus life cycle (Adsorption, penetration, genetic material and protein synthesis) and indirectly through improving the body's immunity. And each step of the research processes from extraction to structural analysis contributes to the result in terms of antiviral activity. Therefore, The complex mechanisms involved in the treatment of Herpes simplex infections makes development of new antiviral compounds is difficult. In this paper, the mechanisms of polysaccharides in the treatment of Herpes simplex infections, the research processes of polysaccharides and their potential clinical applications were reviewed.
Topics: Animals; Antiviral Agents; Fungal Polysaccharides; Herpes Simplex; Herpesvirus 1, Human; Herpesvirus 2, Human; Humans; Plant Extracts; Plants, Medicinal; Polysaccharides; Polysaccharides, Bacterial
PubMed: 32768956
DOI: 10.1016/j.biopha.2020.110469 -
The Veterinary Quarterly Dec 2020Infectious laryngotracheitis (ILT) is a highly contagious upper respiratory tract disease of chicken caused by a Gallid herpesvirus 1 (GaHV-1) belonging to the genus... (Review)
Review
Infectious laryngotracheitis (ILT) is a highly contagious upper respiratory tract disease of chicken caused by a Gallid herpesvirus 1 (GaHV-1) belonging to the genus and subfamily within family. The disease is characterized by conjunctivitis, sinusitis, oculo-nasal discharge, respiratory distress, bloody mucus, swollen orbital sinuses, high morbidity, considerable mortality and decreased egg production. It is well established in highly dense poultry producing areas of the world due to characteristic latency and carrier status of the virus. Co-infections with other respiratory pathogens and environmental factors adversely affect the respiratory system and prolong the course of the disease. Latently infected chickens are the primary source of ILT virus (ILTV) outbreaks irrespective of vaccination. Apart from conventional diagnostic methods including isolation and identification of ILTV, serological detection, advanced biotechnological tools such as PCR, quantitative real-time PCR, next generation sequencing, and others are being used in accurate diagnosis and epidemiological studies of ILTV. Vaccination is followed with the use of conventional vaccines including modified live attenuated ILTV vaccines, and advanced recombinant vector vaccines expressing different ILTV glycoproteins, but still these candidates frequently fail to reduce challenge virus shedding. Some herbal components have proved to be beneficial in reducing the severity of the clinical disease. The present review discusses ILT with respect to its current status, virus characteristics, epidemiology, transmission, pathobiology, and advances in diagnosis, vaccination and control strategies to counter this important disease of poultry.
Topics: Animals; Chickens; Communicable Disease Control; Herpesviridae Infections; Herpesvirus 1, Gallid; Herpesvirus Vaccines; Iltovirus; Poultry Diseases
PubMed: 32315579
DOI: 10.1080/01652176.2020.1759845 -
Journal of Virology Apr 2016Many viruses have the capacity to prevent a cell from being infected by a second virus, often termed superinfection exclusion. Alphaherpesviruses, including the human...
UNLABELLED
Many viruses have the capacity to prevent a cell from being infected by a second virus, often termed superinfection exclusion. Alphaherpesviruses, including the human pathogen herpes simplex virus 1 (HSV-1) and the animal herpesvirus pseudorabies virus (PRV), encode a membrane-bound glycoprotein, gD, that can interfere with subsequent virion entry. We sought to characterize the timing and mechanism of superinfection exclusion during HSV-1 and PRV infection. To this end, we utilized recombinant viruses expressing fluorescent protein (FP) markers of infection that allowed the visualization of viral infections by microscopy and flow cytometry as well as the differentiation of viral progeny. Our results demonstrated the majority of HSV-1- and PRV-infected cells establish superinfection exclusion by 2 h postinfection. The modification of viral infections by virion inactivation and phosphonoacetic acid, cycloheximide, and actinomycin D treatments indicated new protein synthesis is needed to establish superinfection exclusion. Primary infection with gene deletion PRV recombinants identified that new gD expression is not required to establish superinfection exclusion of a secondary viral inoculum. We also identified the timing of coinfection events during axon-to-cell spread, with most occurring within a 2-h window, suggesting a role for cellular superinfection exclusion during neuroinvasive spread of infection. In summary, we have characterized a gD-independent mechanism of superinfection exclusion established by two members of the alphaherpesvirus family and identified a potential role of exclusion during the pathogenic spread of infection.
IMPORTANCE
Superinfection exclusion is a widely observed phenomenon initiated by a primary viral infection to prevent further viruses from infecting the same cell. The capacity for alphaherpesviruses to infect the same cell impacts rates of interviral recombination and disease. Interviral recombination allows genome diversification, facilitating the development of resistance to antiviral therapeutics and evasion of vaccine-mediated immune responses. Our results demonstrate superinfection exclusion occurs early, through a gD-independent process, and is important in the directed spread of infection. Identifying when and where in an infected host viral genomes are more likely to coinfect the same cell and generate viral recombinants will enhance the development of effective antiviral therapies and interventions.
Topics: Animals; Cell Line; Cells, Cultured; Chlorocebus aethiops; Herpesvirus 1, Human; Herpesvirus 1, Suid; Rats; Reassortant Viruses; Superinfection; Vero Cells; Viral Envelope Proteins
PubMed: 26842480
DOI: 10.1128/JVI.00089-16 -
Current Opinion in Virology Oct 2020Innate immune system is considered the first line of defense during viral invasion, with the wealth of the literature demonstrating innate immune control of diverse... (Review)
Review
Innate immune system is considered the first line of defense during viral invasion, with the wealth of the literature demonstrating innate immune control of diverse viruses during acute infection. What is far less clear is the role of innate immune system during chronic virus infections. This short review focuses on alphaherpesviruses and gammaherpesviruses, two highly prevalent herpesvirus subfamilies that, following a brief, once in a lifetime period of acute lytic infection, establish life-long latent infection that is characterized by sporadic reactivation in an immunocompetent host. In spite of many similarities, these two viral families are characterized by distinct cellular tropism and pathogenesis. Here we focus on the published in vivo studies to review known interactions of these two viral subfamilies with the innate immunity of the intact host, both during acute and, particularly, chronic virus infection.
Topics: Alphaherpesvirinae; Animals; Chronic Disease; Gammaherpesvirinae; Host-Pathogen Interactions; Humans; Immunity, Innate; Mice; Virus Latency; Virus Replication
PubMed: 32777757
DOI: 10.1016/j.coviro.2020.07.002 -
The Journal of Infectious Diseases Mar 2020Herpes simplex viruses (HSV-1 and HSV-2) are closely related alphaherpesviruses, with more than 80% identity at the deoxyribonucleic acid (DNA) sequence level [1]. More...
Herpes simplex viruses (HSV-1 and HSV-2) are closely related alphaherpesviruses, with more than 80% identity at the deoxyribonucleic acid (DNA) sequence level [1]. More than two thirds of the world’s population is estimated to have been infected with one or both viruses. The divergence of the common ancestor to these viruses is thought to have coincided with the separation of the human and chimpanzee lineages approximately 6 million years ago, leading to separate evolution of HSV-1 and HSV-2, respectively. Zoonotic transmission of HSV-2 to an extinct early hominid occurred approximately one and a half million years ago [2]. No other primate species are known to serve as common hosts for 2 distinct herpes simplex species.
Topics: Gene Transfer, Horizontal; Herpes Simplex; Herpesvirus 1, Human; Humans; Simplexvirus
PubMed: 31107962
DOI: 10.1093/infdis/jiz200 -
Epidemiology and Infection Feb 2023Herpes simplex virus type 1 (HSV-1) infection is a lifelong infection that is acquired primarily orally and during childhood. We aimed to characterise HSV-1 epidemiology... (Meta-Analysis)
Meta-Analysis Review
Herpes simplex virus type 1 (HSV-1) infection is a lifelong infection that is acquired primarily orally and during childhood. We aimed to characterise HSV-1 epidemiology in Australia and New Zealand. HSV-1-related data as recent as 6 December 2021 were systematically reviewed, synthesised and reported, following PRISMA guidelines. Pooled mean seroprevalence and proportions of HSV-1 detection in genital ulcer disease (GUD) and in genital herpes were calculated using random-effects meta-analyses. Meta-regressions were also conducted. HSV-1 measures were retrieved from 21 eligible publications. Extracted HSV-1 measures included 13 overall seroprevalence measures (27 stratified) in Australia, four overall proportions of HSV-1 detection in clinically diagnosed GUD (four stratified) in Australia, and ten overall proportions of HSV-1 detection in laboratory-confirmed genital herpes (26 stratified) in Australia and New Zealand. Pooled mean seroprevalence among healthy adults in Australia was 84.8% (95% confidence interval (CI) 74.3-93.1%). Pooled mean seroprevalence was 70.2% (95% CI 47.4-88.7%) among individuals <35 years of age and 86.9% (95% CI 79.3-93.0%) among individuals ≥35 years. Seroprevalence increased by 1.05-fold (95% CI 1.01-1.10) per year. Pooled mean proportion of HSV-1 detection in GUD was 8.2% (95% CI 0.4-22.9%). Pooled mean proportion of HSV-1 detection in genital herpes was 30.5% (95% CI 23.3-38.3%), and was highest in young individuals. Proportion of HSV-1 detection in genital herpes increased by 1.04-fold (95% CI 1.00-1.08) per year. Included studies showed heterogeneity, but 30% of the heterogeneity in seroprevalence and 42% of the heterogeneity in proportion of HSV-1 detection in genital herpes were explained in terms of epidemiological factors. HSV-1 seroprevalence is higher in Australia than in other Western countries. HSV-1 epidemiology in Australia and New Zealand appears to be transitioning towards less oral acquisition in childhood, but more genital acquisition among youth.
Topics: Adolescent; Adult; Aged, 80 and over; Humans; Australia; Herpes Genitalis; Herpes Simplex; Herpesvirus 1, Human; Herpesvirus 2, Human; New Zealand; Seroepidemiologic Studies
PubMed: 36750224
DOI: 10.1017/S0950268823000183 -
Viruses May 2022Primary simian varicella virus (SVV) infection and reactivation in nonhuman primates is a valuable animal model in the study of varicella zoster virus disease [varicella...
Primary simian varicella virus (SVV) infection and reactivation in nonhuman primates is a valuable animal model in the study of varicella zoster virus disease [varicella (chickenpox) and herpes zoster (shingles)]. To understand SVV pathogenesis in skin, we inoculated 10 rhesus macaques with SVV, resulting in varicella rash. After the establishment of latency, eight of the monkeys were immunosuppressed using tacrolimus with or without irradiation and prednisone and two monkeys were not immunosuppressed. Zoster rash developed in all immunosuppressed monkeys and in one non-immunosuppressed monkey. Five monkeys had recurrent zoster. During varicella and zoster, SVV DNA in skin scrapings ranged from 50 to 10 copies/100 ng of total DNA and 2-127 copies/100 ng of total DNA, respectively. Detection of SVV DNA in blood during varicella was more frequent and abundant compared to that of zoster. During varicella and zoster, SVV antigens colocalized with neurons expressing β-III tubulin in epidermis, hair follicles, and sweat glands, suggesting axonal transport of the virus. Together, we have demonstrated that both SVV DNA and antigens can be detected in skin lesions during varicella and zoster, providing the basis for further studies on SVV skin pathogenesis, including immune responses and mechanisms of peripheral spread.
Topics: Animals; Chickenpox; Exanthema; Herpes Zoster; Herpesvirus 3, Human; Macaca mulatta; Varicellovirus
PubMed: 35746639
DOI: 10.3390/v14061167 -
Journal of Virology Mar 2020β-Defensins protect the respiratory tract against the myriad of microbial pathogens entering the airways with each breath. However, this potentially hostile environment...
β-Defensins protect the respiratory tract against the myriad of microbial pathogens entering the airways with each breath. However, this potentially hostile environment is known to serve as a portal of entry for herpesviruses. The lack of suitable respiratory model systems has precluded understanding of how herpesvirus virions overcome the abundant mucosal β-defensins during host invasion. We demonstrate how a central alphaherpesvirus, equine herpesvirus type 1 (EHV1), actually exploits β-defensins to invade its host and initiate viral spread. The equine β-defensins (eBDs) eBD1, -2, and -3 were produced and secreted along the upper respiratory tract. Despite the marked antimicrobial action of eBD2 and -3 against many bacterial and viral pathogens, EHV1 virions were resistant to eBDs through the action of the viral glycoprotein M envelope protein. Pretreatment of EHV1 virions with eBD2 and -3 increased the subsequent infection of rabbit kidney (RK13) cells, which was dependent on viral N-linked glycans. eBD2 and -3 also caused the aggregation of EHV1 virions on the cell surface of RK13 cells. Pretreatment of primary equine respiratory epithelial cells (EREC) with eBD1, -2, and -3 resulted in increased EHV1 virion binding to and infection of these cells. EHV1-infected EREC, in turn, showed an increased production of eBD2 and -3 compared to that seen in mock- and influenza virus-infected EREC. In addition, these eBDs attracted leukocytes, which are essential for EHV1 dissemination and which serve as latent infection reservoirs. These novel mechanisms provide new insights into herpesvirus respiratory tract infection and pathogenesis. How herpesviruses circumvent mucosal defenses to promote infection of new hosts through the respiratory tract remains unknown due to a lack of host-specific model systems. We used the alphaherpesvirus equine herpesvirus type 1 (EHV1) and equine respiratory tissues to decipher this key event in general alphaherpesvirus pathogenesis. In contrast to several respiratory viruses and bacteria, EHV1 resisted potent antimicrobial equine β-defensins (eBDs) eBD2 and eBD3 by the action of glycoprotein M. Instead, eBD2 and -3 facilitated EHV1 particle aggregation and infection of rabbit kidney (RK13) cells. In addition, virion binding to and subsequent infection of respiratory epithelial cells were increased upon preincubation of these cells with eBD1, -2, and -3. Infected cells synthesized eBD2 and -3, promoting further host cell invasion by EHV1. Finally, eBD1, -2, and -3 recruited leukocytes, which are well-known EHV1 dissemination and latency vessels. The exploitation of host innate defenses by herpesviruses during the early phase of host colonization indicates that highly specialized strategies have developed during host-pathogen coevolution.
Topics: Alphaherpesvirinae; Animals; Anti-Infective Agents; Cell Line; Epithelial Cells; Herpesviridae Infections; Herpesvirus 1, Equid; Horse Diseases; Horses; Host-Pathogen Interactions; Immune Evasion; Rabbits; Respiratory Tract Infections; Viral Envelope Proteins; beta-Defensins
PubMed: 31996426
DOI: 10.1128/JVI.01676-19 -
Journal of Neurovirology Apr 2020Meeting Report on the 9th Annual Symposium of the Colorado Alphaherpesvirus Latency Society (CALS) held on May 8-11, 2019, in Vail, CO.
Meeting Report on the 9th Annual Symposium of the Colorado Alphaherpesvirus Latency Society (CALS) held on May 8-11, 2019, in Vail, CO.
Topics: Alphaherpesvirinae; Colorado; Herpesviridae Infections; Humans; Societies, Medical; Virus Latency
PubMed: 31502208
DOI: 10.1007/s13365-019-00798-z