promising results from a vaccine candidate

Caused by the Herpes Simplex virus (HSV), herpes is a common infectious disease that can affect many parts of the body, starting with the lips and genitals and, in severe cases, the eyes. In France, it is estimated that 10 million people suffer from cold sores, 2 million from genital herpes and 60,000 from ocular herpes.

Although it is possible to control the effects of herpes, especially with antiviral creams, our body never gets rid of the virus. The latter alternates the phases of sleep in nerve cells and exacerbations, generally caused by stress, during which it is particularly virulent. And, despite the prevalence of HSV, more than four decades of research have yet to produce a herpes vaccine.

A new study conducted by the University of Nebraska-Lincoln (United States) and published in the journal Vaccine these days rekindles the hope of a vaccine against the Herpes Simplex virus.

Counteracts immune difficulties

Researchers behind this new vaccine candidate have spent years studying how to prevent HSV from reaching the nervous system. They found that a certain protein in HSV, called pUL37, travels along nerve fibers to help them infiltrate nerve fibers and the sensory nucleus. Computer analyzes based on this architecture have suggested that three regions of the protein may be important for the process.

To prevent the virus from invading the nervous system, the researchers then removed and replaced five codons – the basic coding information of DNA – in the viral genome of each region. They then injected this modified virus into the mice. They then found that, instead of moving deep into the nervous system, the virus was stuck at the nerve end.

But, if the virus was unable to take refuge in the nervous system, this genetic modification of HSV would also have consequences on the immune response. “When you kill the virus to the point that it doesn’t replicate well, you’re not rewarded with a robust immune response that can protect you from future exposure.”explains Gary Pickard, co-author of the work.

Less replication and less viral shedding

However, it seems possible to get around this trap: by injecting the modified virus into region 2, or R2, of the pUL37 protein. Testing this alternative in mice, the researchers found that the modified R2 form of HSV-1 showed encouraging results. However, they weren’t sure that an HSV-1 vaccine would be up to the task of generating immunity against HSV-2.

Only one of twelve R2-vaccinated guinea pigs developed acute lesions after being injected with HSV-2. And unlike the guinea pigs that did not receive any vaccines or other vaccine candidates, those that received the R2 vaccine showed no signs of HSV-2 in the group of brain cells that normally harbor it. Neutralizing antibodies, on the other hand, were recorded about three times more often in guinea pigs vaccinated with the R2 vaccine than in those vaccinated with the other candidate vaccine.

“The fact that viral spread has also been reduced with the R2 vaccine is very important, because it is the viral spread – even if it does not cause harm – that can then transmit the virus. says Professor Pickard. S.If you have genital herpes, you can pass it on to loved ones without knowing you have it. It is very problematic. So the fact that the shedding was so heavy is a very good sign. “

Pending clinical trials in humans, researchers are now working on vaccines for livestock, particularly cattle and pigs, susceptible to HSV.

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