Evidence map›Paper›PMID 31694948›Full record

ArticleJournal of virology2020

Kaposi's Sarcoma-Associated Herpesvirus ORF66 Is Essential for Late Gene Expression and Virus Production via Interaction with ORF34.

Tadashi Watanabe, Mayu Nishimura, Taisuke Izumi, Kazushi Kuriyama, Yuki Iwaisako, Kohei Hosokawa, Akifumi Takaori-Kondo, Masahiro Fujimuro

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Tadashi WatanabeDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.
Mayu NishimuraDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.
Taisuke IzumiDepartment of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kazushi KuriyamaDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.
Yuki IwaisakoDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.
Kohei HosokawaDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan.
Akifumi Takaori-KondoDepartment of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masahiro FujimuroDepartment of Cell Biology, Kyoto Pharmaceutical University, Kyoto, Japan fuji2@mb.kyoto-phu.ac.jp.
Kyoto Pharmaceutical University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is closely associated with B-cell and endothelial cell malignancies. After the initial infection, KSHV retains its viral genome in the nucleus of the host cell and establishes a lifelong latency. During lytic infection, KSHV-encoded lytic-related proteins are expressed in a sequential manner and are classified as immediate early, early, and late (L) gene transcripts. The transcriptional initiation of KSHV late genes is thought to require the complex formation of the viral preinitiation complex (vPIC), which may consist of at least 6 transcription factors (ORF18, -24, -30, -31, -34, and -66). However, the functional role of ORF66 in vPIC during KSHV replication remains largely unclear. Here, we generated ORF66-deficient KSHV using a bacterial artificial chromosome (BAC) system to evaluate its role during viral replication. While ORF66-deficient KSHV demonstrated mainly attenuated late gene expression and decreased virus production, viral DNA replication was unaffected. Chromatin immunoprecipitation analysis showed that ORF66 bound to the promoters of a late gene (K8.1) but did not bind to those of a latent gene (ORF72), an immediate early gene (ORF16), or an early gene (ORF46/47). Furthermore, we found that three highly conserved C-X-X-C sequences and a conserved leucine repeat in the C-terminal region of ORF66 were essential for the interaction with ORF34, the transcription of K8.1, and virus production. The interaction between ORF66 and ORF34 occurred in a zinc-dependent manner. Our data support a model in which ORF66 serves as a critical vPIC component to promote late viral gene expression and virus production.

Indexed as

Gene Expression Regulation, ViralOpen Reading FramesVirus ReplicationCell LineHerpesvirus 8, HumanHumansViral ProteinsViral ProteinsGammaherpesvirinaeherpesvirusKSHVlytic replication

Identifiers

PMID31694948
PMCPMC6955251
OpenAlexW2985794614

What OpenQuestion holds

Textmetadata
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.