Evidence map›Paper›PMID 31852788›Full record

ArticleJournal of virology2020

Expression of Murine CD80 by Herpes Simplex Virus 1 in Place of Latency-Associated Transcript (LAT) Can Compensate for Latency Reactivation and Anti-apoptotic Functions of LAT.

Ujjaldeep Jaggi, Harry H Matundan, Kati Tormanen, Shaohui Wang, Jack Yu, Kevin R Mott, Homayon Ghiasi

Open access · greenAbstract 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
1.9field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

  1. Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.Investigative ophthalmology & visual science · 2026
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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

7 authors at 1 institution in 1 country.

Ujjaldeep Jaggi *Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Harry H Matundan *Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Kati TormanenCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Shaohui WangCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Jack YuCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Kevin R MottCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA.
Homayon GhiasiCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Burns & Allen Research Institute, Los Angeles, California, USA ghiasih@CSHS.org.
Cedars-Sinai Medical Center · US

Funding

Role of Macrophages in control of Ocular HSVR01EY024649 · NEI · CEDARS-SINAI MEDICAL CENTER · PI HOMAYON GHIASI · 2015 to 2026
$4.1M
Therapeutic control of HSK by CD80R01EY026944 · NEI · CEDARS-SINAI MEDICAL CENTER · PI GHIASI, HOMAYON · 2016 to 2025
$3.9M
Ocular HSV: Mechanism of virus reactivationR01EY029160 · NEI · CEDARS-SINAI MEDICAL CENTER · PI HOMAYON GHIASI · 2018 to 2026
$3.4M
NEI NIH HHS R01 EY024649NEI NIH HHS R01 EY026944NEI NIH HHS R01 EY029160
6 · The paper itself

Abstract

High rates of wild-type (WT) herpes simplex virus 1 (HSV-1) latency reactivation depend on the anti-apoptotic activities of latency-associated transcript (LAT). Replacing LAT with the baculovirus inhibitor of apoptosis protein (cpIAP) or cellular FLIP (FLICE-like inhibitory protein) gene restored the WT latency reactivation phenotype to that of a LAT-minus [LAT(-)] virus, while similar recombinant viruses expressing interleukin-4 (IL-4) or interferon gamma (IFN-γ) did not. However, HSV-1 recombinant virus expressing cpIAP did not restore all LAT functions. Recently, we reported that a similar recombinant virus expressing CD80 in place of LAT had higher latency reactivation than a LAT-null virus. The present study was designed to determine if this CD80-expressing recombinant virus can restore all LAT functions as observed with WT virus. Our results suggest that overexpression of CD80 fully rescues LAT function in latency reactivation, apoptosis, and immune exhaustion, suggesting that LAT and CD80 have multiple overlapping functions.

Indexed as

AnimalsApoptosisB7-1 AntigenHerpesvirus 1, HumanMiceMicroRNAsRNA, ViralVirus ActivationVirus LatencyB7-1 Antigenlatency associated transcript, herpes simplex virus-1MicroRNAsRNA, Viralapoptosiscorneal scarringexhaustionlatencyocular infectionprimary infectionreactivationT cells

Identifiers

PMID31852788
PMCPMC7158736
OpenAlexW2995964387

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.