Evidence map›Paper›PMID 37292622›Full record

ArticleResearch square2023

A Novel Viral Assembly Inhibitor Blocks SARS-CoV-2 Replication in Airway Epithelial Cells.

Satish Pillai, Li Du, Fred Deiter, Mohamed Bouzidi, Jean-Noel Billaud, Simmons Graham, Dabral Prerna, Suganya Selvarajah, Anuradha Lingappa, Maya Michon and 5 more

Open access · greenAbstract readPreprint
In one paragraph

Article in Research square, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Satish PillaiVitalant Research Institute / UCSF.
Li DuVitalant Research Institute/UCSF.
Fred DeiterVeterans Administration Health Care System/UCSF.
Mohamed BouzidiVitalant Research Institute.
Jean-Noel BillaudQIAGEN Digital Insights.
Simmons GrahamVitalant Research Institute / UCSF.
Dabral PrernaVitalant Research Institute / UCSF.
Suganya SelvarajahProsetta Biosciences Inc.
Anuradha LingappaProsetta Biosciences Inc.
Maya MichonProsetta Biosciences Inc.
Shao YuProsetta Biosciences Inc.
Kumar PaulvannanProsetta Biosciences Inc.
Vishwanath LingappaProsetta Biosciences Inc.
Homer BousheyUniversity of California San Francisco.
John GreenlandUniversity of California, San Francisco.ORCID 0000-0003-1422-8367
Vitalant · USUniversity of California, San Francisco · USDigital Insight (Norway) · NOUnited States Department of Veterans Affairs · US

Funding

Effects of Human Galectin-9 on the CNS HIV ReservoirR01MH112457 · NIMH · VITALANT · PI NDHLOVU, LISHOMWA C, PILLAI, SATISH KUMAR · 2016 to 2020
$2.0M
Telomere Dysfunction as a cause of Chronic Lung Allograft DysfunctionR01HL151552 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GREENLAND, JOHN · 2020 to 2024
$1.6M
Cytomegalovirus Immune Responses in Chronic Lung Allograft Dysfunction PathogenesisI01CX002011 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI GREENLAND, JOHN · 2020 to 2025
–
CSRD VA I01 CX002011NHLBI NIH HHS R01 HL151552NIMH NIH HHS R01 MH112457
6 · The paper itself

Abstract

The ongoing evolution of SARS-CoV-2 to evade vaccines and therapeutics underlines the need for novel therapies with high genetic barriers to resistance. The small molecule PAV-104, identified through a cell-free protein synthesis and assembly screen, was recently shown to target host protein assembly machinery in a manner specific to viral assembly. Here, we investigated the capacity of PAV-104 to inhibit SARS-CoV-2 replication in human airway epithelial cells (AECs). Our data demonstrate that PAV-104 inhibited > 99% of infection with diverse SARS-CoV-2 variants in primary and immortalized human AECs. PAV-104 suppressed SARS-CoV-2 production without affecting viral entry or protein synthesis. PAV-104 interacted with SARS-CoV-2 nucleocapsid (N) and interfered with its oligomerization, blocking particle assembly. Transcriptomic analysis revealed that PAV-104 reversed SARS-CoV-2 induction of the Type-I interferon response and the 'maturation of nucleoprotein' signaling pathway known to support coronavirus replication. Our findings suggest that PAV-104 is a promising therapeutic candidate for COVID-19.

Identifiers

PMID37292622
PMCPMC10246244
OpenAlexW4376868244

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.