Herpes simplex virus type 1 (HSV-1) causes recurrent mucocutaneous lesions, is an increasing cause of genital herpes, and is the primary source of infectious blindness and sporadic encephalitis in the United States 1 4. Several groups have used gene mapping methods to identify host genes influencing the severity of HSV-1 ocular disease. This study identified several virulence determinants, including UL41 (VHS), UL42 and US1 (ICP22), and suggested there was a complex interplay between viral genes since we obtained different disease phenotypes depending on which combinations of genes were transferred into the avirulent OD4 strain 6. The Herpes Simplex Virus 1 (HSV-1)-encoded ICP22 protein plays an important role in viral infection and affects expression of host cell genes. II and that ICP22 interacts directly with CDK9 to inhibit expression of host cell genes. Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that establishes a lifelong latent infection within the sensory nerve ganglia of humans, after it has been acquired by infection of the oral mucosa or eye. The HSV-1 UL20 gene is highly conserved in alphaherpesviruses, e.g., varicella-zoster virus (4), bovine herpesvirus 1 (29), and pseudorabies virus (15), as well as in the gammaherpesvirus Marek’s disease virus type 2 (12). The UL20 open reading frame, which is positionally conserved among alphaherpesvirus genomes, encodes a 222-amino-acid nonglycosylated membrane protein and is regulated as a 1 gene. In the absence of the UL20 protein, virions are trapped in the perinuclear space, as well as in cytoplasmic vesicles of the host cell, and therefore, infectious virions are not released to the extracellular space.
Herpes simplex virus type 1 (HSV-1) infection alters the phosphorylation of the large subunit of RNA polymerase II (RNAP II), resulting in the depletion of the hypophosphorylated and hyperphosphorylated forms of this polypeptide (known as IIa and IIo, respectively) and induction of a novel, alternatively phosphorylated form (designated IIi). DNA viruses regulate their genetic information during infection of host cells. Alternatively, HSV-1 may encode or induce additional factors which mediate changes to RNAP II. To determine whether d22-lacZ exhibits this host-range phenotype, single-cycle growth experiments were performed. Human herpes simplex viruses types 1 (HSV-1) and 2 (HSV-2), respectively, cause cold sores and genital lesions. FeHV-1 infection in cats is considered to be a good natural host model to study the comparative molecular pathogenesis of acute and latent alphaherpesvirus infections and to test novel immunization strategies. The size of FeHV-1 virions ranges from 120 to 180 nm. A better understanding of herpesvirus virulence factors is a prerequisite for the generation of safe and efficacious deletion mutant vaccines. Article: Using HSV-1 Genome Phylogenetics to Track Past Human Migrations.
Little is known about viral factors contributing to virulence, and there are currently only two genomic sequences available. A genome sequencer was used to sequence the HSV-1 ocular isolates TFT401, 134, CJ311, CJ360, CJ394, CJ970, and OD4, in a single lane. The herpes simplex virus type 1 (HSV-1) U(S)1 gene encodes host-range and ocular virulence determinants. Multiple determinants contribute to the virulence of HSV ocular and CNS infection and identification of serine 34 of the US1 gene as an ocular disease determinant. HSV displays a broad host cell range and its cellular receptors, heparan sulfate (HS), herpesvirus entry mediator (HVEM), and nectin-1 and 2, are widely expressed on the cell surface of numerous cell types. Almost half of the 84 known viral genes are nonessential for growth in tissue culture and then may be deleted to create genomic space for exogenous transgenes and to delete functions essential for virulence and toxicity in vivo. Attenuated, replication-competent herpes simplex virus type 1 mutant G207: safety evaluation of intracerebral injection in nonhuman primates. Herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) are two of the eight known viruses which comprise the human herpesvirus family. This results in considerable cross-reactivity between the HSV-1 and HSV-2 glycoproteins, although unique antigenic determinants exist for each virus.
Icp22 And The Ul13 Protein Kinase Are Both Required For Herpes Simplex Virus-induced Modification Of The Large Subunit Of Rna Polymerase Ii
The HSV-1 virion ranges from 180 to 300 nm in diameter. Herpes simplex virus (HSV) type-1 and type-2 HSV entry Receptors. Unlike many herpesviruses, HSV has low species specificity and a wide host range. Combined analyses of the TK gene and genotype of sequential isolates showed that acyclovir-sensitive isolates contained multiple acyclovir-resistant variants of the same virus and that an identical acyclovir-resistant HSV-1 strain reappeared in the patient’s cornea during RHK episodes. Herpes simplex virus type 1 (HSV-1) is a highly prevalent human pathogen infecting 60 80 of the human population worldwide 1. The clinical variables scored were age, sex, history of ocular disease, therapy regimen, and clinical picture at presentation of each recurrence and at the end of follow-up. Detailed analyses of the clinical and laboratory data available did not provide insight into the viral and host factors predisposing to the enrichment and persistence of either acyclovir phenotype during consecutive HK episodes (data not shown). Characterization of an essential HSV-1 protein encoded by the UL25 gene reported to be involved in virus penetration and capsid assembly. Viral replication is required for induction of ocular immunopathology by herpes simplex virus. The herpes simplex virus virulence factor ICP34.5 and the cellular protein MyD116 complex with proliferating cell nuclear antigen through the 63-amino-acid domain conserved in ICP34. Isolation and characterization of herpes simplex virus type 1 host range mutants defective in viral DNA synthesis. Granulocytes in Ocular HSV-1 Infection: Opposing Roles of Mast Cells and Neutrophils. Most alphaherpesviruses e.g., herpes simplex virus HSV; varicella-zoster virus, VZV; and pseudorabies virus, PRV) invade the peripheral nervous system (PNS) in their natural hosts. Our a-herpesvirus of choice is PRV, a broad host range herpesvirus that causes fatal encephalitis in a wide variety of animal species except its natural host, the adult pig. CDNA analyses coupled with gene array technology are being developed to understand the role of virus and host genes in virus replications in various cell types and tissues of infected animals. Cyclooxygenase-1 and -2 are required for production of infectious pseudorabies virus.