Evidence map›Paper›PMID 40937852›Full record

ArticlemBio2025

PARP14 is an interferon-induced host factor that promotes IFN production and affects the replication of multiple viruses.

Srivatsan Parthasarathy, Pradtahna Saenjamsai, Hongping Hao, Anna Ferkul, Jessica J Pfannenstiel, Daniel S Bejan, Yating Chen, Ellen L Suder, Nancy Schwarting, Masanori Aikawa and 7 more

Abstract read
In one paragraph

Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. NADThe Journal of general virology · 2026
    Review
  3. Article
  4. Article
  5. NADFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Mac1 ADP-ribosylhydrolase is a Therapeutic Target for SARS-CoV-2.bioRxiv : the preprint server for biology · 2025
    Article
  12. Review
  13. Article
  14. IFN-bioRxiv : the preprint server for biology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Srivatsan ParthasarathyDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.ORCID 0000-0003-0974-7269
Pradtahna SaenjamsaiDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Hongping HaoDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Anna FerkulDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Jessica J PfannenstielDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Daniel S BejanDepartment of Chemical Physiology and Biochemistry, Oregon Health Sciences University, Portland, Oregon, USA.
Yating ChenDepartment of Molecular Biosciences, University of Texas, Austin, Texas, USA.
Ellen L SuderDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.
Nancy SchwartingDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Masanori AikawaCenter for Excellence in Vascular Biology (P.K.J.E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Elke MuhlbergerDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.ORCID 0000-0003-3547-9376
Adam J HumeDepartment of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.ORCID 0000-0001-8454-3472
Robin C OrozcoDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.
Christopher S SullivanDepartment of Molecular Biosciences, University of Texas, Austin, Texas, USA.ORCID 0000-0002-1739-7417
Michael S CohenDepartment of Chemical Physiology and Biochemistry, Oregon Health Sciences University, Portland, Oregon, USA.
David J DavidoDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.ORCID 0000-0001-9102-083X
Anthony R FehrDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas, USA.ORCID 0000-0003-1560-1573

Funding

Whole Animal Imaging CoreUC7AI070088 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEVIN, JAMES L · 2006 to 2013
$57.9M
Women's Interagency HIV Study (WIHS) IV, Chicago ConsortiumU01AI034993 · NIAID · HEKTOEN INSTITUTE FOR MEDICAL RESEARCH · PI COHEN, MARDGE H, FRENCH, AUDREY · 1994 to 2018
$51.0M
Synthetic Chemical Biology CoreP20GM113117 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI JOHNSON, DAVID K · 2016 to 2025
$23.9M
Synthetic Chemical Biology CoreP30GM145499 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI Susan M Lunte · 2022 to 2026
$6.9M
Determining mechanisms of innate immune modulation by ADP-ribosylationR35GM138029 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI Anthony R Fehr · 2020 to 2026
$2.7M
Mechanisms of Marburg virus gene expressionR01AI133486 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FEARNS, RACHEL, MUHLBERGER, ELKE C · 2018 to 2022
$2.7M
PARP9 and PARP14 in atherosclerosisR01HL126901 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, MASANORI · 2016 to 2019
$2.4M
Non-coding RNA and ADP-ribosylation in Antiviral DefenseR01AI123231 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI SULLIVAN, CHRISTOPHER S. · 2017 to 2021
$1.9M
Elucidating the immune response of Schreiber's bats to Lloviu virus infection in vitro and in vivoR21AI169646 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MUHLBERGER, ELKE C · 2022 to 2023
$430k
Identifying the targets of virus-induced PARPs during SARS-CoV-2 infectionR21AI173781 · NIAID · UNIVERSITY OF KANSAS LAWRENCE · PI COHEN, MICHAEL S, FEHR, ANTHONY R · 2023 to 2024
$424k
Investigating How ADP-ribosylation Impacts Innate Immunity During Coronavirus InfectionK22AI134993 · NIAID · UNIVERSITY OF KANSAS LAWRENCE · PI FEHR, ANTHONY R · 2019 to 2020
$270k
Bill and Melinda Gates Foundation INV-048926National Institute of Allergy and Infectious Diseases K22AI34993National Institute of Allergy and Infectious Diseases R01AI123231National Institute of Allergy and Infectious Diseases R01AI133486National Institute of Allergy and Infectious Diseases R21AI169646National Institute of Allergy and Infectious Diseases UC7AI070088NHLBI NIH HHS R01 HL126901NHLBI NIH HHS R01HL126901NIAID NIH HHS K22 AI134993NIAID NIH HHS R01 AI123231NIAID NIH HHS R01 AI133486NIAID NIH HHS R21 AI169646NIAID NIH HHS R21 AI173781NIAID NIH HHS U01 AI034993NIAID NIH HHS UC7 AI070088NIGMS NIH HHS P20 GM113117NIGMS NIH HHS P20GM113117NIGMS NIH HHS P30 GM145499NIGMS NIH HHS R35 GM138029NIGMS NIH HHS R35GM138029
6 · The paper itself

Abstract

PARP14 is a 203 kDa multi-domain protein that is primarily known as an ADP-ribosyltransferase and is involved in a variety of cellular functions, including DNA damage, microglial activation, inflammation, and cancer progression. In addition, PARP14 is upregulated by interferon (IFN), indicating a role in the antiviral response. Furthermore, PARP14 has evolved under positive selection, again indicating that it is involved in host-pathogen conflict. We found that PARP14 is required for increased IFN-I production in response to coronavirus infection lacking ADP-ribosylhydrolase (ARH) activity and poly(I:C); however, whether it has a direct antiviral function remains unclear. Here, we demonstrate that the catalytic activity of PARP14 enhances IFN-β and IFN-γ responses and independently restricts ARH-deficient murine hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication. To determine if PARP14's antiviral functions extended beyond CoVs, we tested the ability of herpes simplex virus 1 (HSV-1), a DNA virus, vesicular stomatitis virus (VSV), a negative-sense RNA virus, and lymphocytic choriomeningitis virus (LCMV), an ambisense RNA virus, to infect A549 PARP14 knockout (KO) cells. While LCMV infection was unaffected, HSV-1 replication was increased in PARP14 KO cells, and VSV replication was decreased. These results indicate that PARP14 restricts HSV-1 replication but enhances the replication of VSV. A PARP14 active site inhibitor had no impact on HSV-1 or VSV replication, indicating that its effect on these viruses was independent of its catalytic activity. These data demonstrate that PARP14 promotes IFN production and has both proviral and antiviral functions targeting multiple viruses.IMPORTANCEThe antiviral response is largely regulated by post-translational modifications (PTM), including ADP-ribosylation. PARP14 is an ADP-ribosyltransferase that is upregulated by interferon and is under positive selection, indicating that it is involved in host-pathogen conflict. However, no anti-viral function has been described for PARP14. Here, we found that PARP14 represses both coronavirus and herpes simplex virus 1 (HSV-1) replication, demonstrating that PARP14 has antiviral functions. Surprisingly, we also found that PARP14 has pro-viral functions, as it was critical for the efficient replication of vesicular stomatitis virus (VSV). These data indicate that PARP14 has both proviral and antiviral functions. Defining the mechanisms used by PARP14 to both repress and promote virus replication will provide new insights into how PARPs regulate virus infection. .

Indexed as

Host-Pathogen InteractionsPoly(ADP-ribose) PolymerasesVirus ReplicationAnimalsCell LineHerpesvirus 1, HumanHumansInterferon-gammaMiceMurine hepatitis virusSARS-CoV-2Interferon-gammaPARP14 protein, humanPoly(ADP-ribose) PolymerasesADP-ribosylationcoronavirusHSV-1interferoninterferon-stimulated genesLCMVmacrodomainPARPVSV

Identifiers

PMID40937852
PMCPMC12505956

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Registered trials

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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.