Explainers
Plain-language background on the science behind HSV vaccine research — what the platforms are, how prophylactic and therapeutic goals differ, and what each trial phase does and doesn't tell you.
- How mRNA herpes vaccines work
Several of the most-watched herpes vaccine candidates use mRNA — the same technology behind the COVID-19 vaccines. This explainer covers how an mRNA vaccine delivers instructions for a cell to make selected viral proteins, why several HSV programs chose the approach, and why a platform that works for one disease is not proof it will work for another.
- HSV-1 vs HSV-2: what's the difference?
Herpes simplex virus comes in two types. HSV-1 has traditionally caused oral herpes and HSV-2 genital herpes, but that line has blurred, and either type can infect either site. The distinction still matters for vaccines: a vaccine can protect against one type and not the other, as the Phase 3 Herpevac trial showed. Neither type has an approved vaccine as of 2026.
- Prophylactic vs therapeutic: two very different herpes vaccines
"A herpes vaccine" can mean two different things. A prophylactic (preventive) vaccine is given to people who are not infected, to stop them getting herpes simplex virus (HSV) at all. A therapeutic vaccine is given to people who are already infected, to reduce outbreaks and viral shedding. The two use different trials, endpoints, and populations — so the first question to ask of any candidate is which goal it targets. Neither type is approved.
- What each clinical trial phase does and doesn't prove
A plain-language guide to reading herpes (HSV) vaccine news by trial phase. Each phase answers a different question, and early-phase results say nothing about whether a vaccine prevents disease. A trial existing or finishing is not the same as a vaccine working — the Phase 3 Herpevac trial ran to completion but missed its main goal, and as of 2026 no HSV vaccine has cleared Phase 3 to approval.
- Why gC2, gD2, and gE2? The trivalent vaccine rationale
Several leading HSV-2 vaccine candidates combine three viral surface proteins — gC2, gD2, and gE2 — to do two jobs at once: block the virus from entering cells and disable two of the tricks it uses to evade the immune system. The rationale is well supported by animal data; whether it protects people is still being tested in an early-stage (Phase 1) human trial of the candidate BNT163.
- Why is HSV so hard to vaccinate against?
Herpes simplex virus establishes a lifelong dormant infection in nerve cells and carries genes that actively blunt the immune response, so even natural infection does not stop reinfection or recurrences — a vaccine has to outperform what the body manages on its own. This explainer walks through the four obstacles researchers keep hitting: latency, active immune evasion, unknown correlates of protection, and animal models that do not fully mirror human disease. As of 2026, no HSV vaccine is approved.