ReviewProteomics2015
Investigating the biology of alpha herpesviruses with MS-based proteomics.
Review in Proteomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Transneuronal Circuit Analysis with Pseudorabies Viruses.Current protocols · 2023Review
- Putative targeting by BX795 causes decrease in protein kinase C protein levels and inhibition of HSV1 infection.Antiviral research · 2022Article
- Characterization of BoHV-1 gG-/tk-/gE- Mutant in Differential Protein Expression, Virulence, and Immunity.Veterinary sciences · 2021Article
- Article
- Article
- An Integrated Sequencing Approach for Updating the Pseudorabies Virus Transcriptome.Pathogens (Basel, Switzerland) · 2021Article
- Differential CircRNA Expression Profiles in PK-15 Cells Infected with Pseudorabies Virus Type II.Virologica Sinica · 2021Article
- The Roles of Envelope Glycoprotein M in the Life Cycle of Some Alphaherpesviruses.Frontiers in microbiology · 2021Review
- Typical gene expression profile of pseudorabies virus reactivation from latency in swine trigeminal ganglion.Journal of neurovirology · 2020Article
- Article
- Host BAG3 Is Degraded by Pseudorabies Virus pUL56 C-TerminalInternational journal of molecular sciences · 2020Article
- A GFP-tagged version of the pseudorabies virus protein UL56 localizes to the Golgi and trans-Golgi network through a predicted C-terminal leucine-rich helix in transfected cells.Virology journal · 2019Article
- Qualitative Differences in Capsidless L-Particles Released as a By-Product of Bovine Herpesvirus 1 and Herpes Simplex Virus 1 Infections.Journal of virology · 2018Article
- Expression of pseudorabies virus-encoded long noncoding RNAs in epithelial cells and neurons.Journal of neurovirology · 2018Article
- Article
- Cloning and sequencingVeterinary world · 2018Article
- Glycomics and Proteomics Approaches to Investigate Early Adenovirus-Host Cell Interactions.Journal of molecular biology · 2018Review
- Experimental Dissection of the Lytic Replication Cycles of Herpes Simplex VirusesFrontiers in microbiology · 2018Review
- Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins.Journal of visualized experiments : JoVE · 2017Article
- iTRAQ-based Proteomic Analysis of Porcine Kidney Epithelial PK15 cells Infected with Pseudorabies virus.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Viruses are intracellular parasites that can only replicate and spread in cells of susceptible hosts. Alpha herpesviruses (α-HVs) contain double-stranded DNA genomes of at least 120 kb, encoding for 70 or more genes. The viral genome is contained in an icosahedral capsid that is surrounded by a proteinaceous tegument layer and a lipid envelope. Infection starts in epithelial cells and spreads to the peripheral nervous system. In the natural host, α-HVs establish a chronic latent infection that can be reactivated and rarely spread to the CNS. In the nonnatural host, viral infection will in most cases spread to the CNS with often fatal outcome. The host response plays a crucial role in the outcome of viral infection. α-HVs do not encode all the genes required for viral replication and spread. They need a variety of host gene products including RNA polymerase, ribosomes, dynein, and kinesin. As a result, the infected cell is dramatically different from the uninfected cell revealing a complex and dynamic interplay of viral and host components required to complete the virus life cycle. In this review, we describe the pivotal contribution of MS-based proteomics studies over the past 15 years to understand the complicated life cycle and pathogenesis of four α-HV species from the alphaherpesvirinae subfamily: Herpes simplex virus-1, varicella zoster virus, pseudorabies virus and bovine herpes virus-1. We describe the viral proteome dynamics during host infection and the host proteomic response to counteract such pathogens.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.