Journal: Molecular Therapy Advances

Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

doi: 10.1016/j.omta.2026.201721

Figure Lengend Snippet: Identification of a heat-stable factor in human serum that competitively inhibits VSV-G-mediated entry (A) Inhibition of VSV by complement-deficient human serum. Vero cells were infected with VSV-Fluc (MOI = 0.01) in the presence of increasing concentrations of naive pooled complement-deficient human serum. After 16 h, luciferase activity was measured. Values represent mean luciferase (with SD) from 2 technical replicates. (B) Heat-inactivated serum inhibits VSV. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of medium alone, 25% human serum, or 25% HI human serum. After 24 h, GFP was imaged by fluorescent microscope. (C) Heat-inactivated serum inhibits VSV infectivity on multiple cell lines. The indicated human cell lines were infected with VSV-GFP (MOI = 0.05 for SKOV, HeLa, and HT1080, and 0005 for A549 and HEK) in the presence of medium alone (no serum) or 25% HI human serum. After 24 h, GFP was quantitated. Values represent the number of GFP-positive cells per well (with standard deviation) relative to the medium alone wells for each cell line ( n = 2 experimental replicates). (D) Analysis of individual human sera. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI sera from one of eighteen individual donors. After 24 h, GFP in each well was quantitated. Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells ( n = 2 technical replicates). A t test was performed comparing the average median relative GFP value of the individual HI sera to the media alone condition, ∗∗∗∗ p < 0.0001. (E) Timing of serum addition. K562 cells were infected with VSV-GFP (MOI = 0.1) in the presence of media alone or 25% HI human serum that was added either at the start of inoculation (0–24 h) or 4 h after initial inoculation (4–24 h). Values represent the number of GFP-positive cells per well (with SD) relative to the medium alone wells for each condition ( n = 8 from two experimental replicates). A one-way ANOVA was performed comparing medium to HI serum for each condition, ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

Techniques: Inhibition, Infection, Luciferase, Activity Assay, Microscopy, Standard Deviation

Journal: Molecular Therapy Advances

Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

doi: 10.1016/j.omta.2026.201721

Figure Lengend Snippet: Retargeted VSVs also escape competitive inhibition by serum from other pre-clinical animal models Parental K562 or K562-EGFR cells were infected with VSV-GFP containing a wild-type (WT) G (MOI = 0.1) or an EGFR-retargeted G (mEGF; MOI = 1) in the presence of medium alone or 25% HI serum from the indicated species. After 24 h, GFP-positive cells were quantitated. Values represent the number of GFP-positive cells (with SD) relative to the medium alone (in parental K562 cells for VSV-G-WT and in K562-EGFR cells for VSV-G-mEGF) ( n = 2 experimental replicates).

Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

Techniques: Inhibition, Infection

Journal: Molecular Therapy Advances

Article Title: Low-density lipoproteins in human serum competitively inhibit the binding and entry of vesicular stomatitis virus

doi: 10.1016/j.omta.2026.201721

Figure Lengend Snippet: Retargeted VSV-G-pseudotyped lentiviral vectors effectively transduce cells in the presence of serum lipoproteins Parental K562, K562-EGFR, or K562-cKit cells were transduced with LV-GFP containing wild-type (WT) G, EGFR-retargeted G (mEGF), or cKit-retargeted G (SCF), respectively, at 2.8 × 10 4 lentiviral particles/well, in the presence or absence of 60% heat-inactivated (HI) human serum. After 48 h, GFP-positive cells were imaged using a fluorescence microscope (A) and quantitated by Imaging Cytometry (B). Values represent the number of GFP-positive cells (with SD) relative to the medium alone for each LV ( n = 4 from 3 experimental replicates). A one-way ANOVA was performed on raw GFP + cell values comparing medium to serum for each LV. ns, not significant; ∗∗∗∗ p < 0.0001.

Article Snippet: Vyriad has several patents related to retargeting VSV-G glycoprotein for in vivo delivery of therapeutics.

Techniques: Transduction, Fluorescence, Microscopy, Imaging, Cytometry

Journal: Science Advances

Article Title: Functional interrogation of neuronal connections by chemoptogenetic presynaptic ablation

doi: 10.1126/sciadv.aeb6755

Figure Lengend Snippet: ( A ) Schematic of the construct used to make the UAS:syp-dL5-mNeonGreen transgenic line. ( B ) Horizontal confocal section through the spinal cord of 3-dpf y417-Gal4, UAS:syp-dL5-mNeonGreen embryo (green), stained with anti-sv2 (magenta). Scale bar, 20 μm. Arrows show synaptic puncta from y417 neurons. “A” and “D” denote anterior-dorsal orientation. The boxed region is shown at a higher magnification in the right panel. Scale bar, 5 μm. ( C and D ) Maximum projection from the confocal z -stack of GFP and differential interference contrast channels in 4 dpf y252-Gal4, UAS:syp-dL5-mNeonGreen larvae: untreated control larva (C) and an MG-2I–treated larva exposed for 20 min to wide-field illumination at 3 dpf (D). Scale bar, 100 μm. A square ROI was cropped from each panel in (C) and (D) and is shown at a higher magnification in (Ca) and (Da). ( E ) SLC [ n = 25 and 25 for ctl (dL5 − /Mg2I + ) and abl (dL5 + /Mg2I + )] and LLC ( n = 25 and 20) escape responsiveness and PPI ( n = 14 and 16) in control and wide-field light–exposed y252-Gal4, UAS:syp-dL5-mNeonGreen larvae. MWU, significant P value indicated and * P < 0.001. ( F ) Maximum projection of 80-μm confocal stacks from 4-dpf tph2:Gal4, UAS:syp-dL5, UAS:Kaede Red untreated larvae and in larvae exposed to NIR illumination in the indicated region of the left hindbrain at 3 dpf. Scale bars, 100 μm. Ra, raphe neurons. ( G ) Number of neurons in dorsal raphe 24 hours after photoablation of neuropil in the region indicated in (F) in untreated [ctl (dL5 − /Mg2I + ), n = 9] and photoablated larvae [abl (dL5 + /Mg2I + ), n = 8]. Welch t test, P = 0.50.

Article Snippet: Primary antibody incubation with a mouse anti–SV2 antibody (1:200, Developmental Studies Hybridoma Bank, Iowa City, IA) in PBS-T (PBS and 1% Triton) for 2 days at 4°C.

Techniques: Construct, Transgenic Assay, Staining, Control

Journal: Cell Reports

Article Title: The insertion of an ATTTC repeat in an Alu element hyperactivates a neurodevelopmental enhancer in spinocerebellar ataxia type 37

doi: 10.1016/j.celrep.2026.117146

Figure Lengend Snippet: DAB1 overexpression induces axonal defects during development (A) Schematic representation of cerebellar and cerebellar-like structures in zebrafish. Granule cell (GC) axons, named parallel fibers (PFs), innervate Purkinje cells (PCs) in the molecular cell layer. Axons from GCs in eminentia granularis (EG) innervate a type of Purkinje-like neuron called crest cells (CrCs). (B) Representative confocal images of zebrafish larvae, from a GFP + cerebellar granule cell line, microinjected with control or human DAB1 mRNA at 5 dpf; axonal tracts of GCs from EG are indicated with orange (absent) or gray (present) arrows. (C) Percentage of present or absent GC axonal tracts that innervate PC-like neurons (graphic representation of data by mean ± SD of at least 20 embryos/condition/replicate; three independent experiments; ꭕ 2 test for the percentage of GC axonal tracts, present or absent; ∗∗∗ p < 0.001). (D) Schematics of muscle innervation by PMN axon tracts in zebrafish larvae at 24 hpf. (E) Representative confocal images (40× objective) of PMN axon tracts from the 6-somites-spanning region anterior to the cloaca from control or DAB1 mRNA-injected embryos; whole-mounted immunofluorescence with SV2 antibody, representative z-projection images (maximum intensity). (F) Length of zebrafish PMN axon tracts in control and DAB1 mRNA-microinjected embryos ( n = 23 embryos for control and n = 24 embryos in DAB1 mRNA condition; four independent experiments; independent t test, ∗ p < 0.05; data are represented by the mean ± SD). (G) Proposed mechanistic model showing disruption of DRL function by the (ATTTC) n , which hyperactivates the neurodevelopmental enhancer, leading to DAB1 upregulation and DAB1 protein accumulation in axons, likely contributing to SCA37. See also .

Article Snippet: Embryos were incubated with anti-synaptic vesicle 2 (SV2) antibody (1:200, #AB2315387, Developmental Studies Hybridoma Bank) diluted in blocking solution overnight, at 4°C.

Techniques: Over Expression, Control, Injection, Immunofluorescence, Disruption

Journal: Cell Reports

Article Title: The insertion of an ATTTC repeat in an Alu element hyperactivates a neurodevelopmental enhancer in spinocerebellar ataxia type 37

doi: 10.1016/j.celrep.2026.117146

Figure Lengend Snippet: DAB1 overexpression induces axonal defects during development (A) Schematic representation of cerebellar and cerebellar-like structures in zebrafish. Granule cell (GC) axons, named parallel fibers (PFs), innervate Purkinje cells (PCs) in the molecular cell layer. Axons from GCs in eminentia granularis (EG) innervate a type of Purkinje-like neuron called crest cells (CrCs). (B) Representative confocal images of zebrafish larvae, from a GFP + cerebellar granule cell line, microinjected with control or human DAB1 mRNA at 5 dpf; axonal tracts of GCs from EG are indicated with orange (absent) or gray (present) arrows. (C) Percentage of present or absent GC axonal tracts that innervate PC-like neurons (graphic representation of data by mean ± SD of at least 20 embryos/condition/replicate; three independent experiments; ꭕ 2 test for the percentage of GC axonal tracts, present or absent; ∗∗∗ p < 0.001). (D) Schematics of muscle innervation by PMN axon tracts in zebrafish larvae at 24 hpf. (E) Representative confocal images (40× objective) of PMN axon tracts from the 6-somites-spanning region anterior to the cloaca from control or DAB1 mRNA-injected embryos; whole-mounted immunofluorescence with SV2 antibody, representative z-projection images (maximum intensity). (F) Length of zebrafish PMN axon tracts in control and DAB1 mRNA-microinjected embryos ( n = 23 embryos for control and n = 24 embryos in DAB1 mRNA condition; four independent experiments; independent t test, ∗ p < 0.05; data are represented by the mean ± SD). (G) Proposed mechanistic model showing disruption of DRL function by the (ATTTC) n , which hyperactivates the neurodevelopmental enhancer, leading to DAB1 upregulation and DAB1 protein accumulation in axons, likely contributing to SCA37. See also .

Article Snippet: Anti-Synaptic Vesicle 2 (SV2) primary antibody , Developmental Studies Hybridoma Bank , Cat #SV2;RRID:AB_2315387.

Techniques: Over Expression, Control, Injection, Immunofluorescence, Disruption