Worry! Oral herpes and genital herpes virus seem to be merging

Studies have shown that the “sexual” relationship between herpes simplex virus and genital herpes virus is more frequent and more frequent than scientists originally envisioned.

In this study, the scientists found that the two herpes simplex viruses (numbered HSV-1 and HSV-2, respectively) fused each other’s genetic material, or “recombined” at a frequency that was originally conceived by scientists. Higher. Normally, HSV-1 causes an oral infection, while HSV-2 causes a genital infection.

Genital herpes

One of the co-authors of the relevant research paper, Dr. Alex Greninger, assistant professor of experimental medicine at the University of Washington, USA, said: “In short, in this latest study, scientists realized that these two The ‘reorganization’ phenomenon between viruses is much more frequent than originally thought.

It’s not over yet: although scientists know that in the distant past, the two viruses have merged in the far past, but this latest research shows that this process of convergence may continue today. In the words of Gleninger: “These two viruses are still undergoing a ‘sexual relationship’.”

However, such a fusion mechanism seems to be a single mode, in which the HSV-2 virus acquires new genes from the HSV-1 virus, but not vice versa.

Thus, the genital herpes virus, HSV-2, will continue to evolve, and this is definitely not good news for public health-related departments. For example, the HSV-2 virus may have evolved the ability to completely disable the antiviral drugs we use today, which is entirely possible. The fusion of these two types of viruses may also expose people who have been vaccinated against herpes to a protective effect and thus be exposed to risk.

History of herpes

Scientists have learned that these two herpes simplex viruses were separated from each other about 6 million years ago; HSV-1 evolved the ability to infect human ancestors, while HSV-2 evolved to be able to infect primates Ability. But about 1.6 million years ago, HSV-2 began to have the ability to infect humans. Since then, HSV-2 has been adapting to the human environment.

In recent years, scientists have found that most of the HSV-2 strains actually contain part of the HSV-1 virus gene, indicating that the exchange between the two viruses has been around for a long time. But scientists are not aware that there is no such exchange between the two viruses today.

In a recent study led by Dr. Amanda Casto, a senior fellow at the University of Washington School of Medicine, scientists gained more than 250 patients with herpes in the Seattle area from 1994 to 2016. A sample of the herpes simplex virus strain was sequenced and sequenced. At the same time, they also obtained genetic information from 230 previously strained strains from published literature and databases.

Analysis of the relevant data revealed evidence of communication between HSV-1 and HSV-2 strains. For example, in some cases, scientists have noticed that HSV-2 has obtained a large number of gene fragments from HSV-1, even 10 times more than previously observed.

One case has attracted the attention of scientists in particular because in this case, the patient’s genital infection was a “mixed infection”: he was infected with both HSV-1 and HSV-2. The patient’s physically infected HSV-2 strain contains a large fragment of the gene from HSV-1. In this case, the mixing and communication between the two strains may be achieved through infection in such a patient. This shows that communication and integration between the two viruses continue to occur.

The researchers suggest that such mixed infections may accelerate the mixing and communication between the two different strains. Interestingly, although HSV-1 is generally infected with the oral cavity, it has also been increasingly causing genital infections in recent years, greatly increasing the chances of mixed infections.

Immunization challenges

The mutual fusion between HSV-2 and HSV-1 strains will pose significant challenges in the development of vaccines against herpes. For example, if scientists develop a vaccine against HSV-2, in the face of HSV-2 strains that change their genes so rapidly, they may be able to flexibly avoid the blow by quickly discarding some of the gene fragments targeted by the drug. To make the vaccine invalid.

In addition, the principle of vaccine development, in many cases, is actually to cultivate some life but weakened HSV-2 strain, which is introduced into the human body to stimulate the antibody response of the immune system. However, there is now a foreseeable potential risk: Are these treated HSV-2 strains likely to suddenly mutate after acquiring a portion of the gene from HSV-1, becoming a more toxic super-virus?

However, scientists also acknowledge that this latest study has some flaws, that is, its strains are mainly collected from the Seattle area. Such research is likely to be local and imperfect, and its representativeness may be very problematic. Therefore, scientists have called on scientists around the world to conduct research and expand their scope to gain a deeper understanding of the issue in the near future.

The herpes patients have been saved, and the herpes vaccine has made a breakthrough!

herpes

Scientists have discovered a new infection mechanism for herpesvirus EBV. In addition, two antibodies have been discovered that prevent the virus from entering the cell. The findings, published in the Proceedings of the National Academy of Sciences (PNAS), are likely to lead to new ideas for developing new vaccines against herpesviruses and other human herpesviruses.

The study worked for Bertha Spears researchers and researchers at Stanford University, where human herpesviruses can cause infectious mononucleosis and infect humans with nine types of herpes. The vast majority of humans are at risk of contracting this virus in adulthood. Usually, there are no serious medical problems. However, this infection can also lead to a variety of cancers, including Burkitt’s lymphoma and Hodgkin’s disease.

There is currently no cure and no vaccine to prevent infection and spread of EBV. Earlier, a study published in Nature said that a study of the structural proteins of EBV can help regulate the fusion of the virus into the host cell membrane. These proteins also protect antibodies, which play a key role in the development of vaccines.

In the current study, scientists have established a previous discovery to expand the EBV protein and discover other proteins that regulate the process of human herpesvirus infection. Importantly, the team also analyzed the role of binding sites that neutralize EBV infection and describe the mechanisms by which these antibodies block the virus. At the same time that the antibody is blocked, the fusion of epithelial cells and B cells is the process by which EBV infects human cells.

The researchers said in the report: “These studies may lead to antibody production, protect humans from EBV infection, and provide new ideas for the development of vaccine candidates to prevent EBV and other human herpesvirus infections.”