ArticleVirology2009
Impairment in reactivation of a latency associated transcript (LAT)-deficient HSV-2 is not solely dependent on the latent viral load or the number of CD8(+) T cells infiltrating the ganglia.
Article in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Gene editing and elimination of latent herpes simplex virus in vivo.Nature communications · 2020Article
- [Mechanisms of herpes simplex virus latency and reactivation].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Review
- Herpes simplex virus-2 dynamics as a probe to measure the extremely rapid and spatially localized tissue-resident T-cell response.Immunological reviews · 2018Review
- Nasal Immunization Confers High Avidity Neutralizing Antibody Response and Immunity to Primary and Recurrent Genital Herpes in Guinea Pigs.Frontiers in immunology · 2016Article
- Influence of herpes simplex virus 1 latency-associated transcripts on the establishment and maintenance of latency in the ROSA26R reporter mouse model.Journal of virology · 2012Article
- The molecular basis of herpes simplex virus latency.FEMS microbiology reviews · 2012Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The HSV latency-associated transcript (LAT) is abundantly expressed during virus latency. Previous studies have shown that the latent viral load and CD8(+) T cells in ganglia influence the rate of reactivation of HSV. While LAT is important for efficient reactivation and establishment of latency, it is uncertain how LAT affects either the HSV latent viral load or CD8(+) T cell infiltration of ganglia. We infected mice with LAT-deficient or LAT-restored HSV-2 at a wide range of inocula. We found that the reduced rate of spontaneous ex-vivo reactivation of the LAT-deficient virus was not associated with a higher number of CD8(+) T cells in the ganglia. Reactivation rates were lower for LAT-deficient than LAT restored HSV-2 even when the latent viral loads were similar, indicating that differences in reactivation were not solely dependent on the latent viral load. Therefore, LAT likely has additional functions important for reactivation.
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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.