Programs
Herpesvirus therapies
Developing therapeutic programs to remove herpesvirus-infected cells from their reservoirs throughout the body.
The rationale
Human herpesviruses are nearly universal and persist for life. Their broad cellular tropism and multiple routes of transmission allow them to establish latent and active reservoirs throughout the body — in neurons, immune cells, and the vasculature — where they can drive chronic disease; a growing body of evidence links them to Alzheimer’s disease.
Because so few infected cells can seed wide-reaching damage, and because those cells are distributed across many tissues, partial or single-tissue approaches are unlikely to be curative. Battle Biotech’s goal is a systemic therapy that reaches and removes herpesvirus-infected cells wherever they persist.
The challenge
The broad cellular tropism and transmission of human herpesviruses — and their ability to persist in reservoirs throughout the body — mean that clearing them demands an approach beyond anything currently disclosed. Battle Biotech is developing that approach: a systemic strategy designed to reach and remove infected cells from every reservoir at once.
Programs beyond those already protected by issued and published patents are held confidential pending further filings, and will be disclosed in more detail as that intellectual property is secured.
Pipeline
Battle Biotech is building a pipeline of therapies that clears herpesvirus-infected cells from their reservoirs. The first pipeline targets the gastrointestinal tract; the second pipeline targets latent reservoirs. The disclosed programs include RNA-interference and mRNA engineered-delivery, protected by a portfolio of issued and pending patents.
All programs are at the preclinical stage.
First pipeline
Gastrointestinal tract
Viral particles from all eight human herpesviruses are present in saliva, and a person swallows roughly 0.5 to 1.5 liters of it each day. This continually exposes the gastrointestinal enterocytes — and the dense immune presence surrounding them — to both infectious and non-infectious herpesvirus particles, which can infect enterocytes and provoke immunogenic inflammation. Sustained release of inflammatory factors in the gastrointestinal tract can, in turn, shift the balance between commensal and harmful bacteria.
The gastrointestinal pipeline comprises four preclinical programs that pair two delivery modalities — exosomes and recombinant commensal bacteria — against two targets: herpesvirus infection (GIHT) and the gastrointestinal inflammation it drives (GII).
GIHT-001E · Exosome delivery against herpesvirus infection
An orally administered exosome therapeutic that delivers short hairpin RNA (shRNA) to silence essential herpesvirus genes in infected enterocytes. Exosomes provide a naturally tolerated, membrane-bound vehicle able to carry their RNA cargo to target cells.
GIHT-001B · Recombinant commensal bacteria against herpesvirus infection
Commensal gut bacteria engineered to express antiviral mRNA together with shRNA directed at herpesvirus genes — establishing a resident, self-renewing source of antiviral payload within the gut that sustains local suppression of viral gene expression.
GII-001E · Exosome therapy against gastrointestinal inflammation
An exosome therapeutic carrying anti-inflammatory miRNA and mRNA, delivered to the gastrointestinal tract to resolve the chronic inflammation driven by herpesvirus exposure and to help restore the balance between commensal and harmful bacteria.
GII-001B · Recombinant commensal bacteria against gastrointestinal inflammation
Commensal gut bacteria engineered to express the same anti-inflammatory miRNA and mRNA payloads in situ — providing sustained, local resolution of inflammation while the antiviral programs (GIHT-001E and GIHT-001B) clear the infected-cell reservoir.
Protected intellectual property: these programs are claimed in issued U.S. Patent 12,428,643 and a pending continuation, U.S. 2026/0098267 A1.
Second pipeline
Latent reservoirs
The second pipeline delivers antisense oligonucleotides (ASOs) that suppress expression of the human cytomegalovirus (HCMV) pp150 and Epstein–Barr virus (EBV) gp350 mRNAs (pending U.S. national application No. 19/584,979, filed May 5, 2026 — the national phase of WO 2025/097185 A1).
HCMV pp150 binds BICD1 — and, likely, its paralog BICD2, which is highly expressed in immune cells and shares close sequence similarity at the BICD1–pp150 binding site — to disrupt the endosomal pathway that would otherwise present immunogenic viral proteins at the cell surface. BICD1, in turn, binds PTPN23, an accessory protein of the endosomal sorting complex required for transport (ESCRT) that sorts membrane proteins and drives vesicle formation. By engaging BICD1/BICD2, pp150 can thus reshape membrane-protein sorting and the multivesicular body to drive secretion of copious amounts of viral protein.
Each ASO is paired with the matching immunogenic vaccine — the pp150 ASO with the HCMV vaccine (pp150-IgG), and the gp350 ASO with the EBV vaccine (gp350-IgG). The ASO silences the viral protein that shields infected cells, while the vaccine — which alone has not cleared latent infection — primes the immune response. Together, this combination could expose and eliminate each virus in its latent reservoirs.
Intellectual property
Sole inventor: Dr. Richelle Cutler. Programmes are research-stage and investigational; nothing here describes an approved therapy or constitutes medical advice.
The science behind it
The full argument, its figures, and its evidence are set out in the Oskar Fischer Prize entry and its references, with an independent evaluation in the scientific analysis.