Evidence map›Paper›PMID 38240588›Full record

ArticleJournal of virology2024

Kaposi's sarcoma-associated herpesvirus (KSHV) LANA prevents KSHV episomes from degradation.

Ken-Ichi Nakajima, Tomoki Inagaki, Jonna Magdallene Espera, Yoshihiro Izumiya

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
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  7. Article
  8. Article
  9. Review
  10. Molecular Mechanisms of KSHV Latency Establishment and Maintenance.Current clinical microbiology reports · 2024
    Article
  11. Review
  12. Review
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Ken-Ichi NakajimaDepartment of Dermatology, School of Medicine, University of California Davis, Sacramento, California, USA.ORCID 0000-0002-5746-0951
Tomoki InagakiDepartment of Dermatology, School of Medicine, University of California Davis, Sacramento, California, USA.
Jonna Magdallene EsperaDepartment of Dermatology, School of Medicine, University of California Davis, Sacramento, California, USA.
Yoshihiro IzumiyaDepartment of Dermatology, School of Medicine, University of California Davis, Sacramento, California, USA.ORCID 0000-0002-9184-2603
University of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI PRIMO N. LARA · 2002 to 2026
$84.9M
Studies on Epigenetically Active Latent Chromatin MaintenanceR01AI167663 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Yoshihiro Izumiya · 2022 to 2026
$2.6M
NCI NIH HHS P30 CA093373NIAID NIH HHS R01 AI167663
6 · The paper itself

Abstract

Protein knockdown with an inducible degradation system is a powerful tool for studying proteins of interest in living cells. Here, we adopted the auxin-inducible degron (AID) approach to detail Kaposi's sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen (LANA) function in latency maintenance and inducible viral lytic gene expression. We fused the mini-auxin-inducible degron (mAID) tag at the LANA N-terminus with KSHV bacterial artificial chromosome 16 recombination, and iSLK cells were stably infected with the recombinant KSHV encoding mAID-LANA. Incubation with 5-phenyl-indole-3-acetic acid, a derivative of natural auxin, rapidly degraded LANA within 1.5 h. In contrast to our hypothesis, depletion of LANA alone did not trigger lytic reactivation but rather decreased inducible lytic gene expression when we stimulated reactivation with a combination of ORF50 protein expression and sodium butyrate. Decreased overall lytic gene induction seemed to be associated with a rapid loss of KSHV genomes in the absence of LANA. The rapid loss of viral genomic DNA was blocked by a lysosomal inhibitor, chloroquine. Furthermore, siRNA-mediated knockdown of cellular innate immune proteins, cyclic AMP-GMP synthase (cGAS) and simulator of interferon genes (STING), and other autophagy-related genes rescued the degradation of viral genomic DNA upon LANA depletion. Reduction of the viral genome was not observed in 293FT cells that lack the expression of cGAS. These results suggest that LANA actively prevents viral genomic DNA from sensing by cGAS-STING signaling axis, adding novel insights into the role of LANA in latent genome maintenance.IMPORTANCESensing of pathogens' components is a fundamental cellular immune response. Pathogens have therefore evolved strategies to evade such cellular immune responses. KSHV LANA is a multifunctional protein and plays an essential role in maintaining the latent infection by tethering viral genomic DNA to the host chromosome. We adopted the inducible protein knockdown approach and found that depletion of LANA induced rapid degradation of viral genomic DNA, which is mediated by innate immune DNA sensors and autophagy pathway. These observations suggest that LANA may play a role in hiding KSHV episome from innate immune DNA sensors. Our study thus provides new insights into the role of LANA in latency maintenance.

Indexed as

Antigens, ViralHerpesvirus 8, HumanPlasmidsSarcoma, KaposiDNAHumansIndoleacetic AcidsNuclear ProteinsNucleotidyltransferasesVirus LatencyAntigens, ViralDNAIndoleacetic Acidslatency-associated nuclear antigenNuclear ProteinsNucleotidyltransferasesepisomeKSHVlatencyprotein knockdown

Identifiers

PMID38240588
PMCPMC10878079
OpenAlexW4391025326

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.