OPENVIRUS — Open Science Framework for Eradicating Latent Viruses

A Global Open-Source Initiative to Accelerate Cures for HSV, EBV, and CMV

Why OpenVirus Exists

For decades, cures for latent viruses such as HSV-1/2, EBV, and CMV have progressed slowly.

Not because science is impossible—

but because data, experiments, and failures remain locked behind institutional walls, patents, and fragmented funding models.

Patients fund research through donations, yet they cannot see:

• what was tried

• what failed

• what succeeded

• why clinical trials stalled

• how money was allocated

• what scientific obstacles remain

This “black box” structure slows global progress and prevents real cures from emerging.

OpenVirus exists to break this pattern.

Our Vision

To build the first global open-science framework for eradicating latent herpesviruses, by releasing:

• open-source mechanistic models

• open-access viral target maps

• transparent experiment logs

• computational off-target predictions

• immune interaction models

• delivery-system blueprints

• failure datasets (the most valuable part of science)

Our purpose is not to replace existing labs—but to accelerate the entire field, force scientific clarity, and build a shared roadmap that no single institution can monopolize.

Why Open Science Matters

Today’s HSV/EBV/CMV research is siloed:

• universities protect data

• biotech companies protect patents

• philanthropies restrict access

• early discoveries get locked inside institutional boundaries

But latent viruses are not a business problem.

They are a species-level biological burden.

Humanity deserves a transparent path to eradication.

OpenVirus provides that path.

What OpenVirus Is Building

1. Open-Source Viral Eradication Models

We create computational frameworks that map:

• latent reservoir structure

• essential survival genes

• immune evasion circuits

• nerve ganglion biology

• reactivation triggers

• candidate editing sites (UL30, UL52, EBNA1, UL122/123, etc.)

• risk assessment layers

These models are released openly, allowing any researcher to build upon them.

2. Preclinical Blueprint That Anyone Can Replicate

We publish:

• in-vitro experiment protocols

• organoid and neuronal model guidance

• predicted editing strategies

• delivery systems (exosomes, LNP candidates)

• off-target analysis frameworks

• toxicity prediction matrices

No paywall. No secrecy.

The world deserves access to the full logic of eradication science.

3. Transparent Failure Reporting

Science advances by learning what does not work.

OpenVirus will openly publish:

• negative results

• incomplete trials

• abandoned approaches

• models that fail safety thresholds

• reasons for experimental collapse

This prevents the global community from wasting years repeating the same hidden failures.

4. A Competitive Ecosystem that Accelerates Cures

Open-source science creates healthy pressure:

• If OpenVirus identifies a promising target,

  → biotech companies will independently validate it.

• If we publish a safer editing route,

  → pharmaceutical groups will race to optimize delivery.

• If we show a breakthrough model,

  → multiple institutions will compete to produce drug candidates.

Competition shortens the time-to-cure dramatically.

Concerns About Patents

Some worry that open-source work may be “stolen” and patented.

Here is the truth:

OpenVirus produces foundational scientific models,

not commercialized drug formulations.

Foundations of science cannot be patented.

Multiple companies competing on top of open foundations

→ reduces drug prices

→ increases accessibility

→ accelerates innovation

Our mission is not to control ownership.

Our mission is to force progress.

Why Start From Zero?

OpenVirus does not request private data from labs.

We respect:

• institutional investment

• paid research

• proprietary datasets

Therefore, the only ethical and powerful path is:

Build new open-source foundations from scratch.

This ensures:

• no secrecy walls

• no ownership conflicts

• no intellectual property disputes

• no dependency on gatekeepers

By reconstructing the entire scientific logic tree openly,

OpenVirus allows humanity to participate in the cure race together.

What OpenVirus Is Not

OpenVirus does not:

• run human clinical trials

• manufacture drugs

• engage in unsafe self-experimentation

• violate any scientific or regulatory laws

• attack existing research groups

We complement—not replace—traditional biomedical systems.

What OpenVirus Is

A global patient-driven initiative that:

• gathers open data

• builds computational models

• designs preclinical frameworks

• encourages replication

• invites multi-institution collaboration

• accelerates the discovery pipeline

• democratizes access to scientific logic

Our goal is simple:

Produce the scientific foundation upon which the world’s first herpesvirus cure will be built.

Long-Term Goal: Viral Eradication Program

Once foundational models mature, OpenVirus will advocate for:

• early compassionate-use programs

• transparent clinical trial design

• patient-access equity

• multi-national regulatory collaboration

When clinical trials become available,

OpenVirus will support pathways for patient participation worldwide.

Call for Collaborators

We invite:

• computational biologists

• immunologists

• virologists

• data scientists

• clinicians

• lab owners

• philanthropies

• biotech founders

• patient communities

Anyone with expertise—or motivation—to join the effort to end latent viral disease.

Core Philosophy

Data should serve humanity.

Science should be transparent.

Cures should be universal.

OpenVirus is not a company.

It is a movement, a scientific stance, and a global coordination framework.

My name is not important.

My face is not important.

My identity is not important.

But my voice is — because today, I am not speaking only for myself. Today, I am speaking for millions of us.

We — the chronic virus community — have no voice. We have no unified organization. No global alliance. No public representation. No funding pipeline. No pressure on the scientific system. No roadmap toward real solutions wait HSV EBV CMV Herpesvirus 6/7/8 in our body turn into Parkinson, leukemia, heart disease, vascular disease, cancer. We suffer alone.

There is no functional cure anywhere in this world right now. AVV is way to deliver gene editing that could position the liver and kidneys to get our cure. This fund will span target discovery, delivery system engineering (LNP/Exosomes), CK2 and genome editing platforms.

In this group, we are going to monitor preclinical research, including small-animal and non-human primate studies.

GMP-grade manufacturing and IND enabling toxicology packages.

Early phase human trials(Phase I/II) under FDA-compliant pathways, including expanded-access or compassionate-use programs for eligible members.

Founding members receive:

priority enrollment in early-phase clinical programs.

voting rights on research direction and resource allocation.

If you do not wanna to carry those viruses for the rest of your life and quickly eradicate them, get a functional cure. Please contact us and join this world-first Herpes Cure Alliance.

Come to this community, HSV IgG positive? EBV VCA IgM high? EBNA positive? CMV IgG high? HSV functional cure? CMV chronic fatigue? This community is going to answer all questions.

HSV Therapeutic Pipeline — Full English Summary (2025 Edition)

Tier-1 = Potential Cure | Tier-2 = Strong Suppression | Tier-3 = Weak Benefit

TIER 1 — Potential Cure (Gene Editing / Gene Deletion / Eradication-Level Technologies)

1. Excision Bio — CRISPR/Meganuclease HSV Gene Editing (EBT-104 / EBT-101 class)

Mechanism:

Cuts latent HSV genomes inside neurons using CRISPR or meganucleases, aiming to permanently disable replication.

Side Effects:

Off-target editing, potential neuronal toxicity, immune response to AAV vector.

Availability:

Preclinical for HSV. HIV version (EBT-101) in Phase 1. HSV timeline ~3–7 years.

2. ΔgD-2 Live-attenuated Cure Vaccine (gD-deleted HSV vaccine)

Mechanism:

Deletes the viral gD gene so the vaccine virus cannot replicate. Generates exceptionally strong CD4/CD8 responses capable of clearing latent reservoirs in animal models.

Side Effects:

Typical vaccine inflammation; theoretical risk of reactivation (designed to be replication-incompetent).

Availability:

Preclinical. Considered one of the most promising future cures.

3. Prime Editing / Base Editing Anti-HSV Programs

Mechanism:

Uses genome editing without DNA double-strand breaks to disable viral genes inside neurons more safely than CRISPR.

Side Effects:

Unknown; technology still early.

Availability:

Experimental, not in clinical development yet.

TIER 2 — Strong Immune Control (Near-Zero Shedding, Not a Cure)

4. RVx201 / RVx202 — Replication-defective Live HSV Vaccines (Rational Vaccines)

Mechanism:

A live HSV vaccine engineered to replicate only once or not at all. Produces strong TRM (tissue-resident memory) CD8+ responses, reducing shedding 70–95% in early data.

Side Effects:

Local redness, mild fever, theoretical safety concerns with live-attenuated approaches.

Availability:

Preparing for human trials; previously administered in limited compassionate-use settings.

5. NanoVax Mucosal Vaccine (NanoSTIM / mucosal IgA vaccine)

Mechanism:

Delivers antigen into nasal/oral mucosa to build a strong IgA + TRM immune shield at the entry site.

Blocks shedding and reactivation at mucosal surfaces.

Side Effects:

Nasal irritation, sore throat, fatigue.

Availability:

Human trials ongoing for other viruses; HSV-specific version in pipeline.

6. Helocyte / Theravax — ICP8 or Helicase-Primase Targeted Immunotherapy

Mechanism:

Targets HSV replication machinery (helicase–primase and ICP8), producing robust T-cell responses capable of suppressing reactivation.

Side Effects:

Typical vaccine-type reactions; not steroid-based and not hormonal.

Availability:

In development; considered promising but not yet in Phase 3.

TIER 3 — Weak or Limited Benefit

7. GEN-003 (Agenus) — Subunit Vaccine (Discontinued)

Mechanism:

gD2 + ICP4 protein vaccine, induces moderate T-cell response. Reduced shedding ~40–60%.

Side Effects:

Injection-site pain, fatigue; waning efficacy within 6–12 months.

Availability:

Terminated after Phase 2. Scientific data remains important but product unavailable.

8. Traditional Protein Subunit Vaccines

Mechanism:

Uses isolated HSV proteins to induce immunity; historically weak immunogenicity.

Side Effects:

Mild; requires repeated boosters.

Availability:

Not considered viable for true HSV control; outdated.

9. Standard Antivirals (acyclovir, valacyclovir, famciclovir)

Mechanism:

Inhibit viral DNA polymerase, suppressing replication but not affecting latency.

Side Effects:

Renal burden, headaches, drug rashes.

Acyclovir allergy = cannot use these.

Availability:

Standard of care, not curative.

TIER X — Technologies Misunderstood as HSV Therapies

10. RV201 / RV202 (Revolo Bio — Immune Modulation Drugs)

Mechanism:

Targets immune tolerance pathways, not HSV viral genes.

Side Effects:

Dependent on indication; not HSV-directed.

Availability:

Not part of HSV cure pipeline.

Notes on current HSV-1 / HSV-2 vaccine & “not cure” pipelines (late 2025 snapshot)

GEN-003 (Genocea Biosciences) – therapeutic HSV-2 vaccine that actually worked… then died for financial reasons

• GEN-003 was a therapeutic protein vaccine for genital HSV-2.

• In Phase 2 trials it significantly reduced viral shedding and lesion rates for up to 12 months after a 3-dose series. 

• The antigens (like gD2) are highly homologous to HSV-1, so in theory there’s cross-reactive T and B cell immunity to HSV-1 as well, not just HSV-2.

• Problem: Genocea ran out of money. The company halted development of GEN-003 in 2017 and fully wound down operations by 2022. The program died because of capital, not because the vaccine failed scientifically. 

So: proof of principle that a therapeutic HSV vaccine can reduce shedding for at least a year. The company is gone, but the data are real.

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Rational Vaccines – live-attenuated HSV-1 / HSV-2 vaccines (RVx201 / VC2 platform)

• Rational Vaccines is an investigational-stage company focused on diseases caused by HSV-1 and HSV-2. 

• Their pipeline includes:

  
  

  • RVx201 – a therapeutic live-attenuated vaccine for genital HSV-1 / HSV-2, still in preclinical development. 

  • VC2 – a live-attenuated HSV-1 strain engineered so it cannot enter neuronal axons, i.e., designed not to establish latency in neurons. It’s immunogenic and protective in animal models. 

  
  

• Some early human use (Theravax) was controversial and ran outside standard FDA pathways; that’s a regulatory/ethics mess, but the scientific idea (strong live-virus-like immunity without new latency) is very interesting.

So: high-risk, high-reward live vaccine approach. Early data are promising in animals; human development is still early and complicated.

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BlueWillow Biologics – intranasal NanoVax HSV-1/HSV-2 mucosal vaccine

• BlueWillow has a patented intranasal NanoVax HSV vaccine, designed to protect against both HSV-1 and HSV-2. 

• It uses a nanoemulsion adjuvant (NE01) plus HSV glycoproteins. Preclinical studies suggest:

  
  

  • strong systemic + mucosal immunity,

  • potential to both prevent and treat genital HSV infections in animal models. 

  
  

• As of now, this program is still preclinical for HSV; BlueWillow has pushed other intranasal vaccines (e.g., anthrax) further into the clinic first. 

So: very interesting for mucosal HSV-1 (oral) and HSV-2 (genital) in the long run, but still preclinical for herpes.

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Excision BioTherapeutics – CRISPR gene-editing for HSV-1 (EBT-104)

• Excision is a CRISPR gene-editing company going after latent viral infections. 

• EBT-104 is their HSV-1 program: a CRISPR-based gene therapy aiming to inactivate latent HSV-1 in its reservoirs (e.g., in HSV-1 keratitis models). 

• It uses multiplexed CRISPR/Cas9 to cut two essential HSV-1 genes (e.g., ICP0 and ICP27) and has shown the ability to reduce or prevent reactivation in animal models, including latent keratitis models. 

• This is one of the few programs that explicitly markets itself as a potential “cure” strategy for HSV-1, not just symptom control.

So: true “cure-attempt” technology – still preclinical, but very aligned with the idea of removing latent HSV-1 from neurons/eye tissue.

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Other directions & why this matters for HSV-1 (not just HSV-2)

From the broader literature on HSV vaccine development: 

• Many vaccine candidates target HSV-2 genital disease, but HSV-1 and HSV-2 share a lot of antigens (especially glycoproteins and T-cell epitopes).

• That means a well-designed HSV-2 vaccine often has immune cross-reactivity against HSV-1 as well.

• On the “cure” side, the serious approaches include:

  
  

  • Live-attenuated vaccines like VC2 to train strong tissue-resident T cells without establishing new latency.

  • Gene-editing (CRISPR/AAV, etc.) to physically damage or delete HSV-1 genomes in neurons.

  • Future engineered T-cell therapies (HSV-specific CAR-T or TCR-T) plus antivirals.

  
  

We’re not at a consumer-ready cure yet, but the science has clearly shifted from “acyclovir forever” to vaccines + gene therapy to attack latency itself.

Again:

None of this is medical advice.

Everything here is still experimental / in trials / in animals.

This is just a 2025 snapshot of where the serious HSV-1 / HSV-2 work is happening.

You may join anonymously.

Please contact: herpesalliance@proton.me

Call: +1 650-460-3094 to push our cure