Could this jab STOP genital herpes? Scientists create ‘most effective ever’ vaccine to control spread of the STI

Home / Pharmaceutical Updates / Could this jab STOP genital herpes? Scientists create ‘most effective ever’ vaccine to control spread of the STI

 

  • More than 500 million people have genital herpes, or HSV2
  • But no vaccine candidate has ever stood up to pre-clinical trials
  • Now a new three-pronged formula has protected monkeys from transmission 
  • It means human trials are likely, paving the way to a publicly-available vaccine 

The first ever effective genital herpes vaccine has succeeded in pre-clinical trials.

The three-dose injection, administered over six months, is the most promising formula ever created to target HSV2, the strain that causes infectious genital warts.

Around 500 million people have genital herpes, leading health experts to call it a global pandemic. But no experimental jab has ever achieved strong or consistent results in a clinical trial.

However, a new formula has provided powerful protection in guinea pig and money models at the University of Pennsylvania’s Perelman School of Medicine.

It means human trials will likely start in the coming months – paving the way to a publicly-available vaccine within years.

The University of Pennsylvania's three-dose injection, administered over six months, is the most promising formula ever to target HSV2, the strain that causes infectious genital warts

WHY THIS HERPES VACCINE IS THE ‘BEST TO DATE’

This is far from the first attempt at a herpes vaccine.

However, most of the jabs up to this point were built to target a glycoprotein called gD2.

This protein, covered in molecules quite similar to sugar, is part of the virus’s armor.

It helps it attack and enter host cells.

However, when it came down to trials, this approach didn’t prove very effective in blocking the virus.

The new vaccine takes aim at two other glycoproteins as well (gC2 and gE2) which hamper the immune system while HSV2 runs amok through the body.

The new ‘trivalent’ vaccine induces antibodies against three different parts of the virus.

This includes two key components that normally help HSV2 escape attack from the immune system.

‘It’s a novel strategy, and it works beautifully,’ said lead investigator Dr Harvey Friedman.

‘I know of no other HSV2 vaccine candidate with published results that are as promising as this study.’

This is far from the first attempt at a herpes vaccine.

However, most of the jabs up to this point were built to target a glycoprotein called gD2.

This protein, covered in molecules quite similar to sugar, is part of the virus’s armor.

It helps it attack and enter host cells.

However, when it came down to trials, this approach didn’t prove very effective in blocking the virus.

The new vaccine takes aim at two other glycoproteins as well (gC2 and gE2) which hamper the immune system while HSV2 runs amok through the body.

‘In essence, we’re stimulating the immune system to attack the virus and at the same time preventing the virus from using some of the tools it has to thwart that immune attack,’ Dr Friedman, a professor of Infectious Diseases at Penn, said.

Current treatments for the virus include medications which are taken to treat outbreaks and to reduce the risk of sexual transmission.

But there is no cure – despite the staggering number of sufferers.

One in six Americans aged between 15 and 49 have HSV2. In Africa, close to 50 percent of adults are infected.

Studies show the virus can be fatal for children born to infected mothers.

It also increases the risk of HIV transmission, and a recent study showed some strains of herpes can cause cancer.

To prove the new formula’s stealth, Dr Friedman tested it on HSV2-infected macaque monkeys, who have a similar immune response to humans.

Though macaque monkeys do not develop genital warts, they show vaginal inflammation when exposed to the virus.

The vaccinated monkeys, however, had no reaction.

Next, testing wart-prone guinea pigs, barely any of the vaccinated rodents got genital lesions.

It did not eliminate the risk of transmission – scientists were still able to detect a small amount of the virus in their discharge.

But it was barely enough to spread and replicate in cells.

‘We are pleased to have demonstrated such a potent and durable immune response to the vaccine,’ said lead author, Dr Sita Awasthi.

‘If found effective in clinical trials, the vaccine will have a huge impact on reducing the overall prevalence of genital herpesinfections and could reduce new HIV infections as well, especially in high-burden regions of sub-Saharan Africa.’

Dr Friedman added: ‘If the vaccine behaves like this in people, it would limit lesions to appearing only about one day in 100, and the virus would be potentially contagious only about two in every 1,000 days.’