Evolutionary studies of herpes simplex viruses (HSV) genomes provide evidences of HSV-2/HSV-1 interspecies recombination

2016 ◽  
Vol 82 ◽  
pp. S106
Author(s):  
S. Burrel ◽  
D. Boutolleau ◽  
D. Ryu ◽  
H. Agut ◽  
K. Merkel ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Herpes Simplex Viruses ◽  
Evolutionary Studies ◽  
Interspecies Recombination ◽  
Hsv 1

scholarly journals Herpes Simplex Virus Mistyping due to HSV-1 × HSV-2 Interspecies Recombination in Viral Gene Encoding Glycoprotein B

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 860
Author(s):  
Amanda M. Casto ◽  
Meei-Li W. Huang ◽  
Hong Xie ◽  
Keith R. Jerome ◽  
Anna Wald ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Recombination Event ◽  
Genomic Variation ◽  
Glycoprotein B ◽  
Viral Gene ◽  
Human Pathogens ◽  
Herpes Simplex Viruses ◽  
Single Nucleotide Change ◽  
Interspecies Recombination ◽  
Hsv 1

Human herpes simplex viruses (HSV) 1 and 2 are extremely common human pathogens with overlapping disease spectra. Infections due to HSV-1 and HSV-2 are distinguished in clinical settings using sequence-based “typing” assays. Here we describe a case of HSV mistyping caused by a previously undescribed HSV-1 × HSV-2 recombination event in UL27, the HSV gene that encodes glycoprotein B. This is the first documented case of HSV mistyping caused by an HSV-1 × HSV-2 recombination event and the first description of an HSV interspecies recombination event in UL27, which is frequently used as a target for diagnostics and experimental therapeutics. We also review the primer and probe target sequences for a commonly used HSV typing assay from nearly 700 HSV-1 and HSV-2 samples and find that about 4% of HSV-1 samples have a single nucleotide change in at least one of these loci, which could impact assay performance. Our findings illustrate how knowledge of naturally occurring genomic variation in HSV-1 and HSV-2 is essential for the design and interpretation of molecular diagnostics for these viruses.

scholarly journals Herpes Simplex Virus Mistyping due to HSV-1 x HSV-2 Interspecies Recombination in Viral Gene Encoding Glycoprotein B

2020 ◽  
Author(s):  
Amanda M. Casto ◽  
Meei-Li Huang ◽  
Hong Xie ◽  
Keith R. Jerome ◽  
Anna Wald ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Recombination Event ◽  
Glycoprotein B ◽  
Viral Gene ◽  
Human Herpes ◽  
Gene Encoding ◽  
Herpes Simplex Viruses ◽  
Simplex Virus ◽  
Interspecies Recombination ◽  
Hsv 1

AbstractHuman herpes simplex viruses (HSV) 1 and 2 are most often typed via molecular assays. Here we describe the first known case of HSV mistyping due to a previously undescribed HSV-1 x HSV-2 recombination event in UL27, the gene that encodes glycoprotein B. This is the first reported HSV interspecies recombination event impacting this gene, which is frequently used as a target for diagnostics and experimental therapeutics.

scholarly journals Characterization of Vesicular Stomatitis Virus Pseudotypes Bearing Essential Entry Glycoproteins gB, gD, gH, and gL of Herpes Simplex Virus 1

2016 ◽  
Vol 90 (22) ◽  
pp. 10321-10328 ◽  
Author(s):  
Henry B. Rogalin ◽  
Ekaterina E. Heldwein
Keyword(s):  
Herpes Simplex ◽  
Membrane Fusion ◽  
Viral Envelope ◽  
Herpes Simplex Virus 1 ◽  
Herpes Simplex Viruses ◽  
Systematic Exploration ◽  
Vesicular Stomatitis ◽  
Simplex Virus ◽  
First Time ◽  
Hsv 1

ABSTRACTHerpes simplex viruses (HSVs) are unusual in that unlike most enveloped viruses, they require at least four entry glycoproteins, gB, gD, gH, and gL, for entry into target cells in addition to a cellular receptor for gD. The dissection of the herpes simplex virus 1 (HSV-1) entry mechanism is complicated by the presence of more than a dozen proteins on the viral envelope. To investigate HSV-1 entry requirements in a simplified system, we generated vesicular stomatitis virus (VSV) virions pseudotyped with HSV-1 essential entry glycoproteins gB, gD, gH, and gL but lacking the native VSV fusogen G. These virions, referred to here as VSVΔG-BHLD virions, infected a cell line expressing a gD receptor, demonstrating for the first time that the four essential entry glycoproteins of HSV-1 are not only required but also sufficient for cell entry. To our knowledge, this is the first time the VSV pseudotyping system has been successfully extended beyond two proteins. Entry of pseudotyped virions required a gD receptor and was inhibited by HSV-1 specific anti-gB or anti-gH/gL neutralizing antibodies, which suggests that membrane fusion during the entry of the pseudotyped virions shares common requirements with the membrane fusion involved in HSV-1 entry and HSV-1-mediated syncytium formation. The HSV pseudotyping system established in this study presents a novel tool for systematic exploration of the HSV entry and membrane fusion mechanisms.IMPORTANCEHerpes simplex viruses (HSVs) are human pathogens that can cause cold sores, genital herpes, and blindness. No vaccines or preventatives are available. HSV entry into cells—a prerequisite for a successful infection—is a complex process that involves multiple viral and host proteins and occurs by different routes. Detailed mechanistic knowledge of the HSV entry is important for understanding its pathogenesis and would benefit antiviral and vaccine development, yet the presence of more than a dozen proteins on the viral envelope complicates the dissection of the HSV entry mechanisms. In this study, we generated heterologous virions displaying the four essential entry proteins of HSV-1 and showed that they are capable of cell entry and, like HSV-1, require all four entry glycoproteins along with a gD receptor. This HSV pseudotyping system pioneered in this work opens doors for future systematic exploration of the herpesvirus entry mechanisms.

scholarly journals Characterization of Herpes Simplex Viruses Selected in Culture for Resistance to Penciclovir or Acyclovir

2001 ◽  
Vol 75 (4) ◽  
pp. 1761-1769 ◽  
Author(s):  
Robert T. Sarisky ◽  
Matthew R. Quail ◽  
Philip E. Clark ◽  
Tammy T. Nguyen ◽  
Wendy S. Halsey ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Sequence Similarity ◽  
Cross Resistance ◽  
Phenotypic Analysis ◽  
Herpes Simplex Viruses ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT Penciclovir (PCV), an antiherpesvirus agent in the same class as acyclovir (ACV), is phosphorylated in herpes simplex virus (HSV)-infected cells by the viral thymidine kinase (TK). Resistance to ACV has been mapped to mutations within either the TK or the DNA polymerase gene. An identical activation pathway, the similarity in mode of action, and the invariant cross-resistance of TK-negative mutants argue that the mechanisms of resistance to PCV and ACV are likely to be analogous. A total of 48 HSV type 1 (HSV-1) and HSV-2 isolates were selected after passage in the presence of increasing concentrations of PCV or ACV in MRC-5 cells. Phenotypic analysis suggested these isolates were deficient in TK activity. Moreover, sequencing of the TK genes from ACV-selected mutants identified two homopolymeric G-C nucleotide stretches as putative hot spots, thereby confirming previous reports examining Acvr clinical isolates. Surprisingly, mutations identified in PCV-selected mutants were generally not in these regions but distributed throughout the TK gene and at similar frequencies of occurrence within A-T or G-C nucleotides, regardless of virus type. Furthermore, HSV-1 isolates selected in the presence of ACV commonly included frameshift mutations, while PCV-selected HSV-1 mutants contained mostly nonconservative amino acid changes. Data from this panel of laboratory isolates show that Pcvr mutants share cross-resistance and only limited sequence similarity with HSV mutants identified following ACV selection. Subtle differences between PCV and ACV in the interaction with viral TK or polymerase may account for the different spectra of genotypes observed for the two sets of mutants.

scholarly journals Cell-to-cell spread inhibiting antibodies constitute a correlate of protection against Herpes Simplex Virus Type 1 reactivations

2020 ◽  
Author(s):  
Susanne Wolf ◽  
Mira Alt ◽  
Robin Dittrich ◽  
Miriam Dirks ◽  
Leonie Schipper ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Blood Donors ◽  
Vaccine Development ◽  
Natural Infection ◽  
Herpes Simplex Viruses ◽  
Correlate Of Protection ◽  
Simplex Virus ◽  
Cell Spread ◽  
Hsv 1

AbstractHerpes simplex viruses (HSV) cause ubiquitous human infections. For vaccine development, knowledge concerning correlates of protection against HSV is essential. Therefore, we investigated if humans principally can produce highly protective cell-to-cell spread inhibiting antibodies upon natural infection and whether such antibody responses correlate with protection from HSV reactivation. We established a high-throughput HSV-1 GFP reporter virus-based assay and screened 2496 human plasma samples for HSV-1 cell-to-cell spread inhibiting antibodies. We conducted a survey among the blood donors to analyze the correlation between the presence of cell-to-cell spread inhibiting antibodies in plasma and the frequency of HSV reactivations. In total, 128 of 2496 blood donors (5.1 %) exhibited high levels of HSV-1 cell-to-cell spread inhibiting antibodies in the plasma. Such individuals showed a significantly lower frequency of HSV reactivations compared to subjects without sufficient levels of HSV-1 cell-to-cell spread inhibiting antibodies. This study provides two important findings: (I) a fraction of humans produce HSV cell-to-cell spread inhibiting antibodies upon natural infection and (II) such antibodies correlate with protection against recurrent HSV. Moreover, these elite neutralizers can provide promising material for hyperimmunoglobulin, the isolation of superior antiviral antibodies and information for the design of a vaccine against HSV.ImportanceHerpes simplex virus 1 infections can cause painful mucosal lesions at the oral or genital tract and severe, life threatening disease in immunosuppressed patients or neonates. There is no approved vaccine available, and the emergence of drug resistances especially in long time treated patients makes the treatment increasingly difficult. We tested 2496 people for HSV-1 cell-to-cell spread inhibiting antibodies. Five percent exhibited functional titers such antibodies and showed significantly lower risk of reactivations, uncovering cell-to-cell spread inhibiting antibodies as a correlate of protection against Herpes simplex virus reactivations. Isolation of the cell-to-cell spread inhibiting antibodies from B-cells of these donors may contribute to develop novel antibody-based interventions for prophylactic and therapeutic use and provide starting material for vaccine development.

MOLECULAR DETECTION OF VIRUS HERPES SIMPLEX TYPE 1(HSV-1) , VIRUS HERPES SIMPLEX TYPE 2(HSV-2), CYTOMEGALOVIRUS(HCMV) and EPSTEIN-BARRVIRUS (EBV) IN SUPRA-GI

2018 ◽  
Vol 28 (2) ◽  
pp. 415-422
Author(s):  
Marija Ivanovska- Stojanoska ◽  
Mirjana Popovska ◽  
Violeta Anastasovska ◽  
Lindita Zendeli Bedjeti ◽  
Sashka Todorovska
Keyword(s):  
Herpes Simplex ◽  
Periodontal Disease ◽  
Dental Plaque ◽  
Molecular Detection ◽  
Herpes Simplex Type ◽  
Advanced Stage ◽  
Negative Finding ◽  
Herpes Simplex Viruses ◽  
Significant Difference ◽  
Hsv 1

Introduction Chronic periodontitis is as an inflammatory disease of the supporting tissue of the teeth caused by periopatogens microorganisams. New concept about etiology of periodontal disease suggests that herpes viruses may play an important role in the pathogenesis of periodontal disease. The aim of this study was to analyze the presence of herpes simplex virus type 1and 2 (HSV-1, HSV-2) cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), in supra-gingival dental plaque .Materials and Methods The study comprised a total of 89 patients who were divided in two groups: patients who were diagnosed moderate stage of periodontal disease and patients who were diagnosed with advanced stage of periodontal disease. Clinical examinations included determination of plaque index, gingival index, sulcus bleeding index, probing depth, and clinical attachment level. Supra-gingival dental plaque samples were taken with sterile coton ball scrub on tooth enamel. Molecular detection of HSV1, HSV2 , EBV and CMV was analyzed using polymerase chain reaction (PCR).Results Molecular analysis of HSV-1 ,HSV-2, EBV and CMV in supra-gingival dental plaque in patients with chronic periodontal disease (a total of 89) showed the presence of EBV in 12,40% of patients , HSV-1 was found in 11,20% of patients, in 7,90% of patients was detected HSV-2, CMV was established in 9,00% of patients. In 3,40% patients in supra-gingival dental plaque was detected combination of viruses HSV1 and CMV, in 3,40% of patient combination of HSV1 and EBV ; and in 2,20% of patient combination ofHSV2,EBV was observed; in 2,20% of patients was found combination of 3 viruses HSV1; HSV2; EBV and in 49,50% patients we found negative finding. Patients with moderate stage of periodontal disease have a 0,78 times(OR = 0,78 / 0,33-1,84/)no significantly lower risk of probability of finding viruses in the supra-gingival plaque compared to patients who had advanced stage of periodontal disease. In the shown cross-culture of the presence of viruses in supra-gingival plaque in patients with moderate and advanced stage of periodontal disease for Fisher, s Exact Test = 5,19 and p >0.05 (p = 0.809 / Monte Carlo sig. (0.799-0.819)there is no significant difference.Conclusion We can associate the presence of herpes simplex viruses in supra-gingival dental plaque with periodontal disease. Our findings suggest that there is no significant difference in presence of viruses in supra-gingival plaque in patients with moderate and sereve stage of periodontal disease.

Herpes Simplex Virus Infections: The Genital Tract and the Newborn

1992 ◽  
Vol 13 (3) ◽  
pp. 107-111
Author(s):  
Ann M. Arvin ◽  
Charles G. Prober
Keyword(s):  
Herpes Simplex ◽  
Host Immune System ◽  
Virus Infections ◽  
Human Herpes ◽  
Neonatal Infections ◽  
Herpes Simplex Viruses ◽  
Barr Virus ◽  
Source Of Infection ◽  
Herpes Group ◽  
Hsv 1

There are six recognized members of the human herpes group of viruses. These include type 1 and type 2 herpes simplex viruses (HSV-1 and HSV-2), cytomegalovirus (CMV), Epstein-Barr virus (EBV), varicellazoster virus (VZV), and human herpes virus type 6 (HHV-6). These ubiquitous double-stranded DNA viruses are relatively large and lipid-enveloped. The capacity to induce a state of latency in the infected host has been proved for all of the herpes viruses. That is, after primary infection, the viruses remain forever with the host with the possibility for subsequent reactivations. The mechanisms of these reactivations are not understood completely. Both primary infections and recurrences may be associated with clinical illness or may be asymptomatic. To a large extent, the status of the host immune system determines the severity of the infection and the likelihood of recurrences. In general, infections are more severe and recurrences are more frequent in the most compromised hosts. This review focuses on HSV-1 and HSV-2, with emphasis on neonatal infections and maternal genital infections as a source of infection in the newborn. The clinical illnesses caused by HSV-1 and HSV-2 are usually quite distinct. HSV-1 is the predominant cause of oral, ocular, and central nervous system infections occurring after the neonatal period, and HSV-2 is the predominant cause of genital and neonatal infections.

scholarly journals Comparison of Herpes Simplex Virus 1 Strains Circulating in Finland Demonstrates the Uncoupling of Whole-Genome Relatedness and Phenotypic Outcomes of Viral Infection

2019 ◽  
Vol 93 (8) ◽  
Author(s):  
Christopher D. Bowen ◽  
Henrik Paavilainen ◽  
Daniel W. Renner ◽  
Jussi Palomäki ◽  
Jenni Lehtinen ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Herpes Simplex ◽  
Whole Genome ◽  
Cell Type ◽  
Phylogenetic Groups ◽  
Herpes Simplex Viruses ◽  
Phenotypic Differences ◽  
Gene Level ◽  
The Relationship ◽  
Hsv 1

ABSTRACTA majority of adults in Finland are seropositive carriers of herpes simplex viruses (HSV). Infection occurs at epithelial or mucosal surfaces, after which virions enter innervating nerve endings, eventually establishing lifelong infection in neurons of the sensory or autonomic nervous system. Recent data have highlighted the genetic diversity of HSV-1 strains and demonstrated apparent geographic patterns in strain similarity. Though multiple HSV-1 genomes have been sequenced from Europe to date, there is a lack of sequenced genomes from the Nordic countries. Finland’s history includes at least two major waves of human migration, suggesting the potential for diverse viruses to persist in the population. Here, we used HSV-1 clinical isolates from Finland to test the relationship between viral phylogeny, genetic variation, and phenotypic characteristics. We found that Finnish HSV-1 isolates separated into two distinct phylogenetic groups, potentially reflecting historical waves of human (and viral) migration into Finland. Each HSV-1 isolate harbored a distinct set of phenotypes in cell culture, including differences in the amount of virus production, extracellular virus release, and cell-type-specific fitness. Importantly, the phylogenetic clusters were not predictive of any detectable pattern in phenotypic differences, demonstrating that whole-genome relatedness is not a proxy for overall viral phenotype. Instead, we highlight specific gene-level differences that may contribute to observed phenotypic differences, and we note that strains from different phylogenetic groups can contain the same genetic variations.IMPORTANCEHerpes simplex viruses (HSV) infect a majority of adults. Recent data have highlighted the genetic diversity of HSV-1 strains and demonstrated apparent genomic relatedness between strains from the same geographic regions. We used HSV-1 clinical isolates from Finland to test the relationship between viral genomic and geographic relationships, differences in specific genes, and characteristics of viral infection. We found that viral isolates from Finland separated into two distinct groups of genomic and geographic relatedness, potentially reflecting historical patterns of human and viral migration into Finland. These Finnish HSV-1 isolates had distinct infection characteristics in multiple cell types tested, which were specific to each isolate and did not group according to genomic and geographic relatedness. This demonstrates that HSV-1 strain differences in specific characteristics of infection are set by a combination of host cell type and specific viral gene-level differences.

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