Oncolytic virus platform

HSV-1-F-WT-mCherry

NDV, HSV-1 and VSV oncolytic platforms: natural tumor selectivity through the interferon axis. Catalog number FWT004, part of the Herpes Simplex Virus (HSV) range. Send the catalog number with your quantity and we will confirm availability, lead time and price.

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Vector map

FWT004

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The plasmid map for FWT004 is still being prepared. Contact us and we will send the vector map, sequence and QC data directly.

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How it works

Unlike the engineered adenoviruses, the NDV, HSV-1 and VSV platforms achieve tumor selectivity through a shared biological opening: most tumor cells have a blunted interferon response, while healthy cells mount a rapid antiviral state. A virus whose replication is normally suppressed by interferon therefore spares healthy tissue and replicates selectively where that brake is missing.

Newcastle disease virus is an avian paramyxovirus with a negative-sense RNA genome; lytic strains replicate efficiently in tumor cells with defective interferon signalling and kill them by fusion-driven lysis, independent of p53 status. Vesicular stomatitis virus is highly cytopathic, and its matrix protein shuts off host antiviral export; the M51R mutation restores interferon sensitivity so the virus is attenuated in healthy, interferon-competent cells while retaining full potency in interferon-defective tumors. Herpes simplex virus 1 brings the largest cargo capacity of any oncolytic platform — enough room for several therapeutic transgenes — and is the backbone of clinically advanced constructs in which virulence and latency functions are deleted to enforce tumor selectivity.

As with adenoviral oncolytics, lysis feeds an immunogenic cell death cascade: antigen plus adjuvant signals mature dendritic cells and prime tumor-specific CD8-positive T cells, which is what turns a local lytic infection into a systemic antitumor response.

Figure 1 · Interferon-axis selectivity and the immunogenic cell death cascade shared by NDV, HSV-1 and VSV platforms.
Figure 1 · Interferon-axis selectivity and the immunogenic cell death cascade shared by NDV, HSV-1 and VSV platforms.

Production & quality control

  • Each platform is produced in its permissive substrate — embryonated egg or cell culture for NDV, Vero or complementing lines for HSV-1 and VSV — then clarified, concentrated and purified.
  • Infectious titer is reported in PFU/mL or TCID50; sterility, mycoplasma and endotoxin are tested on every lot.
  • Interferon sensitivity — the safety attribute that underwrites tumor selectivity — is characterized during development and monitored between lots.
  • Strain identity and the selectivity data sheet are available on request when you ask for a quote.

Storage & handling

  • Ship on dry ice; store at -80 degrees Celsius.
  • Enveloped platforms (NDV, VSV, HSV) are freeze-thaw sensitive: aliquot after the first thaw and never re-freeze working stocks.
  • Avoid prolonged exposure to room temperature — infectivity decays measurably within hours.

Experimental protocol

  1. Map permissiveness first

    For each tumor model, run a viability curve across MOIs over 24 to 96 hours. Kill kinetics differ sharply between platforms: VSV is fastest, NDV acts through syncytium formation, HSV spreads cell to cell. Match the platform to the model, not the other way round.

  2. Test the interferon axis

    Confirm your tumor line is interferon-defective by pretreating a duplicate culture with interferon-alpha and showing the virus is restricted. This single control predicts selectivity far better than any single-dose assay.

  3. Infect and follow lysis

    Seed cells to 60 to 80 percent confluence, infect in a minimal volume for 1 to 2 hours, restore medium and monitor viability, progeny release and syncytium formation over 3 days. Collect supernatant for plaque assay to quantify the amplification cycle.

  4. Read the immune arm

    Harvest lysate for HMGB1, ATP and calreticulin exposure as the immunogenic cell death markers, then set up a dendritic cell co-culture if T cell priming is your endpoint.

Bench guidance only: these are replication-competent viruses. Confirm the biosafety classification your institution assigns to each platform before starting work.

Need the complete PDF manual with lot-specific parameters? Request the manual for FWT004.

Frequently asked questions

Why is interferon sensitivity the key safety attribute?

Healthy cells respond to infection by producing interferon, which shuts down viral replication in cells that are still sensitive to it. Tumor cells with defective interferon signalling lose that brake. A virus engineered to stay interferon-sensitive is therefore attenuated in healthy tissue and potent in tumors.

Which platform should I screen first?

Let the tumor model decide. VSV for fast, broad cytopathicity; NDV where syncytium-mediated spread suits the morphology; HSV-1 when you need large cargo capacity for arming transgenes.

Can these be armed with therapeutic genes?

Yes — that is a standard build, particularly on HSV-1 where the cargo budget is large. Cytokines, checkpoint modulators and prodrug convertases are the usual payloads; discuss the design with us.