Evidence map›Paper›PMID 38435130›Full record

ArticleMolecular therapy. Methods & clinical development2024

Rationally engineered novel AAV capsids for intra-articular gene delivery.

Wenjun Li, Susi Liu Feng, Lizette Herrschaft, R Jude Samulski, Chengwen Li

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Navigating the Hurdles of Intra-Articular AAV Gene Therapy.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. 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

5 authors at 1 institution in 1 country.

Wenjun LiGene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Susi Liu FengGene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Lizette HerrschaftGene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
R Jude SamulskiGene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Chengwen LiGene Therapy Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
University of North Carolina at Chapel Hill · US

Funding

Novel strategy to block Nabs for AAV gene deliveryR01AI168242 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Chengwen Li, Timothy Charles Nichols · 2022 to 2026
$3.0M
Optimization of AAV vector to deliver FVa for hemophilia with inhibitorsR01HL144661 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, CHENGWEN, NICHOLS, TIMOTHY CHARLES · 2019 to 2022
$2.2M
Development of AAV vectors for CF therapyR01HL151348 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LI, CHENGWEN, SAMULSKI, RICHARD J · 2021 to 2024
$1.6M
NHLBI NIH HHS R01 HL144661NHLBI NIH HHS R01 HL151348NIAID NIH HHS R01 AI168242
6 · The paper itself

Abstract

Intra-articular adeno-associated virus (AAV) gene therapy has been explored as a potential strategy for joint diseases. However, concerns of low transduction efficacy, off-target expression, and neutralizing antibodies (Nabs) still need to be addressed. In this study, we demonstrated that AAV6 was the best serotype to transduce joints after screening serotypes 1 to 9. To develop a more effective AAV vector, a set of novel AAV capsids were rationally engineered. The mutant AAV62 created by swapping variable region I (VRI) of AAV2 into AAV6 induced a higher transduction efficiency per AAV genome copy number. To further investigate the roles of specific amino acids in the transduction of AAV62 and AAV6, we found out that AAV6D with the deletion of threonine at residue 265 induced a 2-fold higher transduction than AAV6, while the transduction efficiency from AAV6M with the mutation of alanine to glutamine at residue 263 was 10-fold lower. AAV6D efficiently transduced both synoviocytes and chondrocytes with low AAV genome copy numbers in other tissues and less Nab formation. This study demonstrates that novel AAV mutants with rational engineering may enhance joint transduction after intra-articular administration in mice, with the potential to evade AAV Nabs and minimize off-target effects in the liver.

Indexed as

AAVengineeringjointNabrational designtransduction

Identifiers

PMID38435130
PMCPMC10907215
OpenAlexW4391832016

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.