FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1996041350> ?p ?o ?g. }

• W1996041350 abstract "Herpes simplex virus type-1 (HSV-1) establishes a life-long latent infection in peripheral neurons. This latent reservoir is the source of recurrent reactivation events that ensure transmission and contribute to clinical disease. Current antivirals do not impact the latent reservoir and there are no vaccines. While the molecular details of lytic replication are well-characterized, mechanisms controlling latency in neurons remain elusive. Our present understanding of latency is derived from in vivo studies using small animal models, which have been indispensable for defining viral gene requirements and the role of immune responses. However, it is impossible to distinguish specific effects on the virus-neuron relationship from more general consequences of infection mediated by immune or non-neuronal support cells in live animals. In addition, animal experimentation is costly, time-consuming, and limited in terms of available options for manipulating host processes. To overcome these limitations, a neuron-only system is desperately needed that reproduces the in vivo characteristics of latency and reactivation but offers the benefits of tissue culture in terms of homogeneity and accessibility. Here we present an in vitro model utilizing cultured primary sympathetic neurons from rat superior cervical ganglia (SCG) (Figure 1) to study HSV-1 latency and reactivation that fits most if not all of the desired criteria. After eliminating non-neuronal cells, near-homogeneous TrkA(+) neuron cultures are infected with HSV-1 in the presence of acyclovir (ACV) to suppress lytic replication. Following ACV removal, non-productive HSV-1 infections that faithfully exhibit accepted hallmarks of latency are efficiently established. Notably, lytic mRNAs, proteins, and infectious virus become undetectable, even in the absence of selection, but latency-associated transcript (LAT) expression persists in neuronal nuclei. Viral genomes are maintained at an average copy number of 25 per neuron and can be induced to productively replicate by interfering with PI3-Kinase / Akt signaling or the simple withdrawal of nerve growth factor(1). A recombinant HSV-1 encoding EGFP fused to the viral lytic protein Us11 provides a functional, real-time marker for replication resulting from reactivation that is readily quantified. In addition to chemical treatments, genetic methodologies such as RNA-interference or gene delivery via lentiviral vectors can be successfully applied to the system permitting mechanistic studies that are very difficult, if not impossible, in animals. In summary, the SCG-based HSV-1 latency / reactivation system provides a powerful, necessary tool to unravel the molecular mechanisms controlling HSV1 latency and reactivation in neurons, a long standing puzzle in virology whose solution may offer fresh insights into developing new therapies that target the latent herpesvirus reservoir." @default.
• W1996041350 created "2016-06-24" @default.
• W1996041350 creator A5019732653 @default.
• W1996041350 creator A5031710130 @default.
• W1996041350 creator A5034902241 @default.
• W1996041350 creator A5039444245 @default.
• W1996041350 creator A5054483003 @default.
• W1996041350 creator A5055851463 @default.
• W1996041350 creator A5083842270 @default.
• W1996041350 date "2012-04-02" @default.
• W1996041350 modified "2023-10-06" @default.
• W1996041350 title "A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation" @default.
• W1996041350 cites W1575731167 @default.
• W1996041350 cites W1898630910 @default.
• W1996041350 cites W1904975159 @default.
• W1996041350 cites W1942310387 @default.
• W1996041350 cites W1968848710 @default.
• W1996041350 cites W1973926432 @default.
• W1996041350 cites W2024824043 @default.
• W1996041350 cites W2028165101 @default.
• W1996041350 cites W2055798847 @default.
• W1996041350 cites W2057232864 @default.
• W1996041350 cites W2077023513 @default.
• W1996041350 cites W2102430810 @default.
• W1996041350 cites W2103851463 @default.
• W1996041350 cites W2121232238 @default.
• W1996041350 cites W2131117798 @default.
• W1996041350 cites W2131792187 @default.
• W1996041350 cites W2140408426 @default.
• W1996041350 cites W2141363673 @default.
• W1996041350 cites W2148710127 @default.
• W1996041350 cites W2155487534 @default.
• W1996041350 cites W2159334987 @default.
• W1996041350 cites W2163424373 @default.
• W1996041350 cites W2409736261 @default.
• W1996041350 cites W2477894406 @default.
• W1996041350 cites W2496202045 @default.
• W1996041350 cites W2497322117 @default.
• W1996041350 cites W2583369066 @default.
• W1996041350 doi "https://doi.org/10.3791/3823" @default.
• W1996041350 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3466666" @default.
• W1996041350 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22491318" @default.
• W1996041350 hasPublicationYear "2012" @default.
• W1996041350 type Work @default.
• W1996041350 sameAs 1996041350 @default.
• W1996041350 citedByCount "37" @default.
• W1996041350 countsByYear W19960413502012 @default.
• W1996041350 countsByYear W19960413502013 @default.
• W1996041350 countsByYear W19960413502014 @default.
• W1996041350 countsByYear W19960413502015 @default.
• W1996041350 countsByYear W19960413502016 @default.
• W1996041350 countsByYear W19960413502017 @default.
• W1996041350 countsByYear W19960413502018 @default.
• W1996041350 countsByYear W19960413502019 @default.
• W1996041350 countsByYear W19960413502020 @default.
• W1996041350 countsByYear W19960413502021 @default.
• W1996041350 countsByYear W19960413502022 @default.
• W1996041350 crossrefType "journal-article" @default.
• W1996041350 hasAuthorship W1996041350A5019732653 @default.
• W1996041350 hasAuthorship W1996041350A5031710130 @default.
• W1996041350 hasAuthorship W1996041350A5034902241 @default.
• W1996041350 hasAuthorship W1996041350A5039444245 @default.
• W1996041350 hasAuthorship W1996041350A5054483003 @default.
• W1996041350 hasAuthorship W1996041350A5055851463 @default.
• W1996041350 hasAuthorship W1996041350A5083842270 @default.
• W1996041350 hasBestOaLocation W19960413502 @default.
• W1996041350 hasConcept C140704245 @default.
• W1996041350 hasConcept C159047783 @default.
• W1996041350 hasConcept C169760540 @default.
• W1996041350 hasConcept C182615771 @default.
• W1996041350 hasConcept C203014093 @default.
• W1996041350 hasConcept C207001950 @default.
• W1996041350 hasConcept C2522874641 @default.
• W1996041350 hasConcept C2778794669 @default.
• W1996041350 hasConcept C2778852064 @default.
• W1996041350 hasConcept C2781196997 @default.
• W1996041350 hasConcept C2910737674 @default.
• W1996041350 hasConcept C41008148 @default.
• W1996041350 hasConcept C54355233 @default.
• W1996041350 hasConcept C76155785 @default.
• W1996041350 hasConcept C82876162 @default.
• W1996041350 hasConcept C86803240 @default.
• W1996041350 hasConcept C8891405 @default.
• W1996041350 hasConceptScore W1996041350C140704245 @default.
• W1996041350 hasConceptScore W1996041350C159047783 @default.
• W1996041350 hasConceptScore W1996041350C169760540 @default.
• W1996041350 hasConceptScore W1996041350C182615771 @default.
• W1996041350 hasConceptScore W1996041350C203014093 @default.
• W1996041350 hasConceptScore W1996041350C207001950 @default.
• W1996041350 hasConceptScore W1996041350C2522874641 @default.
• W1996041350 hasConceptScore W1996041350C2778794669 @default.
• W1996041350 hasConceptScore W1996041350C2778852064 @default.
• W1996041350 hasConceptScore W1996041350C2781196997 @default.
• W1996041350 hasConceptScore W1996041350C2910737674 @default.
• W1996041350 hasConceptScore W1996041350C41008148 @default.
• W1996041350 hasConceptScore W1996041350C54355233 @default.
• W1996041350 hasConceptScore W1996041350C76155785 @default.
• W1996041350 hasConceptScore W1996041350C82876162 @default.
• W1996041350 hasConceptScore W1996041350C86803240 @default.
• W1996041350 hasConceptScore W1996041350C8891405 @default.

• next