Molecular Aspects of Varicella-Zoster Virus Latency

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herpes simplex 2 infectiousdiseases
herpes zoster 4 infectiousdiseases
rabies 2 infectiousdiseases
chickenpox 3 infectiousdiseases

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chickenpox 654 6/2018Publication date (collection): 7/2018AbstractPrimary varicella-zoster virus (VZV) infection causes varicella ( chickenpox ) and the establishment of a lifelong latent infection in ganglionic neurons. VZV reactivates in about
chickenpox 1896 causative agent of two distinct diseases: a generalized vesicular skin rash referred to as varicella ( chickenpox ), and a localized dermatomal skin rash referred to as herpes zoster (HZ; shingles) [[2]]. Although varicella
chickenpox 2556 literature regarding HZ. This led to his famous hypothesis that: “Following the primary infection ( chickenpox ), virus becomes latent in the sensory ganglia, where it can be reactivated from time to time (herpes
herpes simplex 19087 established are largely unknown and much of what is assumed is actually informed by studies of the related herpes simplex virus type 1 (HSV-1). Here, the key concept is that during the traversal of neuronal axons, the genome-containing
herpes simplex 43601 alphaherpesvirus latency transcript and encodes eleven distinct miRNAs within the spliced intron. (E) The 8.2 kb herpes simplex virus type 1 (HSV-1) LAT undergoes splicing which yields two highly stable intron lariats, approximately
herpes zoster 810 infection in ganglionic neurons. VZV reactivates in about one-third of infected individuals to cause herpes zoster , often accompanied by neurological complications. The restricted host range of VZV and, until recently,
herpes zoster 1961 skin rash referred to as varicella (chickenpox), and a localized dermatomal skin rash referred to as herpes zoster (HZ; shingles) [[2]]. Although varicella and HZ were known to be related [[3]], it was not until 1965
herpes zoster 2161 not until 1965 that the British general practitioner, Dr Robert E. Hope-Simpson, suggested that “ herpes zoster is a spontaneous manifestation of varicella infection”. This observation was based on a careful examination
herpes zoster 2661 (chickenpox), virus becomes latent in the sensory ganglia, where it can be reactivated from time to time ( herpes zoster )” [[4]]. Eighteen years later, this hypothesis was proven by Dr Donald Gilden’s crucial discovery
rabies 22498 all VZV-infected neurons. VLT appears to be structurally complex compared to the LATs of HSV-1, pseudo rabies virus (PRV) and bovine herpesvirus 1 (BHV-1), which are composed of only two exons and a single intron
rabies 43415 herpesvirus 1 encodes a 2.2 kb latency-related (LR) RNA and encodes two miRNAs in exon 1 (D) The pseudo rabies virus large latency transcript (LLT) is the largest characterized alphaherpesvirus latency transcript

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