RESEARCH ON HSV1 AND HSV2 -(3 BILLION PEOPLE AFFECTED)cure by 2035

 today we discuss how to destroy hsv hiding in nerveand ganglia

is there research going on?what is present result?how soon can hsv be destroyed from nerves and nerve ganglia and SAVE 3 BILLION PEOPLE

Yes, there is active, high-priority research focused exactly on destroying latent HSV (both HSV-1 and HSV-2) hiding in sensory nerve ganglia — the trigeminal ganglia (oral/eye), dorsal root/sacral ganglia (genital), and others. This is the root cause of lifelong infection and recurrences, since standard antivirals (acyclovir, valacyclovir, etc.) only suppress active replication and cannot touch the dormant episomal viral DNA inside neurons. The leading strategy is gene editing (meganucleases or CRISPR) delivered via AAV vectors to cut the viral DNA in latently infected neurons. The body’s repair machinery then destroys the damaged viral genomes. Other approaches (new antivirals like pritelivir, therapeutic vaccines, nanobodies, or 3D neuron-inclusive skin models) improve symptom control or reduce shedding but do not eradicate latency from ganglia. Key Research & Present Results (as of March 2026)

1. Fred Hutchinson Cancer Center (Keith Jerome & Martine Aubert labs) – AAV-meganuclease gene therapy
   • Most advanced for systemic/oral/genital HSV.
   • 2024 mouse studies (oral + genital models): One optimized vector + one meganuclease (dual cuts in HSV DNA) eliminated ≥90–97% of latent virus from ganglia, sharply reduced viral shedding (and thus transmission). Earlier versions reached similar results; the latest is safer (minimal liver/nerve side effects).
   • HSV-2 adaptation is underway.
   • Status: Still preclinical (mice). Human trials are the #1 lab priority, but safety/IND-enabling studies are still required — no Phase 1 start announced yet. Community fundraising continues to speed this up.
2. Excision BioTherapeutics – EBT-104 (CRISPR-SaCas9)
   • Targets HSV-1 (ICP0 + ICP27 genes) for ocular keratitis (cornea/trigeminal ganglia latency).
   • Rabbit latent-infection model: 92% of treated eyes showed complete elimination of viral shedding; large deletions in latent viral DNA.
   • Status: Preclinical data presented May 2025 (ASGCT). No human trial started as of March 2026 (speculation about Q1 2026 Phase 1b for keratitis exists in community forums, but no official confirmation).
3. Small human proof-of-concept (China, 2023 investigator-initiated trial, NCT04560790)
   • CRISPR formulation (HELP) injected into cornea during transplant in 3 patients with severe refractory HSV-1 stromal keratitis.
   • Results (18–21 months follow-up): No off-target edits (GUIDE-seq), no systemic side effects, HSV-1 became undetectable, no relapses. Visual acuity improved in some. This is the first in-human evidence that direct in-vivo gene editing can safely clear HSV genomes.
   • A follow-on Chinese Phase 1 (NCT06474416, BD111 CRISPR) for HSV-1 stromal keratitis is recruiting (corneal injection, n=16).

NIH/NIAID’s 2023–2028 Strategic Plan explicitly prioritizes “strategies to target latent HSV” via gene editing (CRISPR or meganucleases) for a functional or sterilizing cure. Vaccines (e.g., Moderna mRNA-1608 Phase 1/2, BioNTech BNT163) and newer antivirals (pritelivir Phase 3) are advancing but only control, not destroy, latency. How Soon Can HSV Be Destroyed from Nerves/Ganglia?

• Ocular/keratitis-specific (trigeminal ganglia): Earliest human data already exists (2023 small trial); next Phase 1 trials could report safety/efficacy 2026–2028. A limited therapy might reach approval in the early 2030s if successful.
• Systemic (oral + genital, full ganglia eradication): Fred Hutch and similar programs are still in late preclinical. First-in-human trials likely 2027–2030 at earliest (safety testing is rigorous because AAV delivery reaches neurons). Full approval (after Phase 2/3) realistically 5–10+ years from now — optimistic scenario ~2035 or later.
• No one can guarantee success or exact dates; off-target risks, immune responses to AAV, and delivery efficiency are the main hurdles. But preclinical results are the strongest ever seen for latency eradication.

Saving ~3–4 Billion People?HSV-1 alone infects 67% of the global adult population (3.7–4 billion carriers today); HSV-2 adds hundreds of millions more. A true ganglia-eradicating cure would be one of the biggest public-health breakthroughs in history — stopping transmission, recurrences, neonatal herpes, and links to Alzheimer’s risk (HSV-1 hypothesis). Vaccines could prevent new infections faster, but for the already-infected billions, gene editing is the only path to actual destruction of the hidden virus.Bottom line: Research is moving faster than ever (thanks to NIH priority + advocacy), with real proof in animals and tiny human ocular cases that it is possible. But we are still years away from a broadly available cure that could reach billions. Current management remains daily or episodic antivirals + safer-sex practices.

 

3.6.2. Aspirin and SARS-CoV-2 Infection

The global pandemic caused by SARS-CoV-2 has over 260 million confirmed cases and 5.2 million deaths worldwide (November 2021) [137]. The clinical presentation of SARS-CoV-2 infection is variable, ranging from totally asymptomatic cases up to mild, severe or life-threatening manifestations related to the disease named COVID-19. Severe lung and systemic inflammation may develop in COVID-19 patients, with potential to induce respiratory failure, multi-organ dysfunction and finally, death. Although still largely unknown, the mechanisms underlying the most severe clinical manifestations involve hyperinflammation (the so-called cytokine storm) and a prothrombotic status, with relevant platelet activation, microvascular thrombosis and embolization. Therefore, a strong pathophysiological rationale for a potential therapeutic role for ASA in COVID-19 has been advocated because of its anti-inflammatory, antiplatelet aggregation and anticoagulant effects, as well as its modulation of the immune system and possible inhibition of viral replication and/or entry [138,139,140].

Since ASA is largely prescribed worldwide for the primary prevention of cardiovascular diseases, several studies retrospectively analyzed the effects of antiplatelet action of low-dose (81–100 mg/day) ASA in COVID-19. Based on this literature, a total of five systematic reviews with meta-analysis were published [140,141,142,143,144]. The most recent was conducted by Martha et al. and included six studies comprising 13,993 patients [141]. Overall, the meta-analysis agreed in finding that the use of low-dose ASA was significantly associated with a reduced risk of mortality compared with patients not undergoing this therapy. Only Martha’s study distinguished between individuals taking ASA routinely and those receiving low-dose ASA during hospitalization and reported that in both cases, ASA was significantly and independently associated with reduced mortality (pre-infection ASA: RR 0.46, 95% CI 0.35–0.61, p < 0.001; in-hospital ASA: RR 0.39, 95% CI 0.16–0.96, p < 0.001) [141]. However, the meta-analysis also agreed that a low certainty of evidence for the mortality-reducing effect of low-dose ASA can be assumed, mainly because of the retrospective design of the most included studies, with a possibility of relevant biases. For example, the meta-analysis included studies involving from 5 to more than 40,000 patients: only one study performed a separate meta-analysis after excluding such outliers, not confirming the effect of ASA on mortality [144].

Subsequently, two prospective clinical trials were published between October and November 2021. The first included symptomatic clinically stable outpatients with COVID-19 who were treated with ASA 81 mg/day compared to a placebo; unfortunately, this study was interrupted early, having documented an event rate lower than expected [145]. The second was a large multicentric RCT realized by the RECOVERY Collaborative Group, exploring the effect of 150 mg ASA (daily until discharge) compared to usual care in hospitalized COVID-19 patients, finding that ASA did not reduce neither the risk of invasive mechanical ventilation, nor 28-day mortality (RR 0.96, 95% CI 0.89–1.04; p = 0.35); conversely, in the ASA group, a statistically significant increase in major bleeding events was documented (1.6% vs. 1.0%; p = 0.003) [146].

In conclusion, regarding the potential effects of ASA in patients with COVID-19, the available literature reports conflicting results with low-level evidence, and the only available RCT has not confirmed the positive role of ASA. It should be noted that all the above studies explored essentially the antithrombotic effect of ASA, since at the low doses administered, the anti-inflammatory effects are limited [147]. Therefore, further RCTs are needed to prove a positive role of ASA in relevant outcomes in COVID-19 patients.