Subretinal Rather Than Intravitreal Adeno-Associated Virus-Mediated Delivery of a Complement Alternative Pathway Inhibitor Is Effective in a Mouse Model of RPE Damage
Open accessAbstract
Purpose: The risk for age-related macular degeneration has been tied to an overactive complement system. Despite combined attempts by academia and industry to develop therapeutics that modulate the complement response, particularly in the late geographic atrophy form of advanced AMD, to date, there is no effective treatment. We have previously demonstrated that pathology in the smoke-induced ocular pathology (SIOP) model, a model with similarities to dry AMD, is dependent on activation of the alternative complement pathway and that a novel complement activation site targeted inhibitor of the alternative pathway can be delivered to ocular tissues via an adeno-associated virus (AAV). Methods: Two different viral vectors for specific tissue targeting were compared: AAV5-VMD2-CR2-fH for delivery to the retinal pigment epithelium (RPE) and AAV2YF-smCBA-CR2-fH for delivery to retinal ganglion cells (RGCs). Efficacy was tested in SIOP (6 months of passive smoke inhalation), assessing visual function (optokinetic responses), retinal structure (optical coherence tomography), and integrity of the RPE and Bruch's membrane (electron microscopy). Protein chemistry was used to assess complement activation, CR2-fH tissue distribution, and CR2-fH transport across the RPE. Results: RPE- but not RGC-mediated secretion of CR2-fH was found to reduce SIOP and complement activation in RPE/choroid. Bioavailability of CR2-fH in RPE/choroid could be confirmed only after AAV5-VMD2-CR2-fH treatment, and inefficient, adenosine triphosphate-dependent transport of CR2-fH across the RPE was identified. Conclusions: Our results suggest that complement inhibition for AMD-like pathology is required basal to the RPE and argues in favor of AAV vector delivery to the RPE or outside the blood-retina barrier.
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Subretinal, but not intravitreal, administration of a CR2-FH fusion protein has been shown to reverse smoking-induced RPE damage in a mouse model.
“subretinal, but not intravitreal, administration of a CR2–FH fusion protein has been shown to reverse smoking-induced RPE damage in a mouse model [286].”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [286]
Subretinal gene delivery has been shown to be more effective and have a faster onset than intravitreal delivery in animal models.
“Subretinal gene delivery has been shown to be more effective and have a faster onset than intravitreal delivery in animal models [260,285,286].”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [286]
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Hammadi, S., Tzoumas, N., Ferrara, M., Meschede, I. P., Lo, K., Harris, C., Lako, M., & Steel, D. H. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12082870 · Cited by 44 · see citing works
- Authors
- Annamalai, B., Parsons, N., Nicholson, C., Obert, E., Jones, B., & Rohrer, B.
- Affiliations
- Medical University of South Carolina (US)
- University of Utah (US)
- Corresponding author
- Rohrer, Bärbel
- Venue
- Investigative Opthalmology & Visual Science
- Published
- 2021-04-08
- Volume
- 62
- Issue
- 4
- Pages
- 11
- ISSN
- 0146-0404 (ISSN-L)
- 1552-5783
- PMC
- PMC8039473
- OpenAlex
- W3149270267
- Cited by
- 16
- References
- 85
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 4
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Investigative Ophthalmology & Visual Science (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX003050, I01 RX000444, IK6 BX004858)
- National Eye Institute (R01EY030072, R01EY024581, R01EY015128, R01EY028927, P30EY014800)
- National Institute on Deafness and Other Communication Disorders (T32DC014435)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Keywords
- age-related macular degeneration, alternative complement pathway, adeno-associated virus vectors, subretinal gene delivery, retinal pigment epithelium, retinal ganglion cells, complement inhibition, dry age-related macular degeneration, Bruch's membrane, blood-retinal barrier, optokinetic response
- MeSH terms
- Animals, Choroid, Complement Activation, Disease Models, Animal, Macular Degeneration, Mice, Inbred C57BL, Retina, Tomography, Optical Coherence, Complement Inactivating Agents, Mice, Retinal Pigment Epithelium, Intravitreal Injections
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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