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An estimated 3.7 billion people are affected with Herpes Simplex 1 (HSV-1) under the age of 50 and roughly 417 million people between the ages of 15-49 are affected by the Herpes Simplex 2 (HSV-2) infection (Lafferty et al. 2015). That is more than half of the human population. With that being said, is there a way we can prevent these numbers in the future? Researchers at the Oregon Health and Science University are conducting a study using the CRISPR human genetic engineering system that can target and attack these cells that are responsible for these infections. The targeting of these sites have shown a significant decrease and, in some cases, even a complete vanishing of the infected cells. Experiments like this could be life changing for billions of people, or even for you.

As mentioned earlier, HSV-1 and HSV-2 virus combined affect almost four billion people. These infections can cause serious issues and even death sometimes. As of right now, herpes is an incurable infection. HSV-1 causes infections that mainly affect the oral region, while HSV-2 mainly affects the anogenital region. However, either of these viruses can affect either region. The virus attacks the epithelial cells of the oral mucosa (the membrane lining the inside of the mouth). Neonatal herpes is a version of this virus that is passed from mother to newborn and is extremely morbid (Lafferty et al. 2015). Those that do survive suffer from neurological deficits, leading to a significantly lower quality of life.

This study was conducted in 2016 by researchers at the Oregon Health and Science University, and is still an ongoing experiment. The specific researchers are not yet mentioned. The Netherlands Organization for Scientific Research and the Dutch Cancer Society funded this project. However, these organizations had nothing to do with the design of the research, the data, or this document that entails the details of their findings.

The whole purpose of this study is due to the fact that there are such limited treatment options for people who are affected by herpes. Therefore, scientists set out on the mission of figuring out a way that they can kill the herpes virus before it even has any effect on people. The hypothesis behind this study is that they could kill the herpes virus pathogens before they replicate in order to significantly reduce the chance of this infection occurring. This would be done by locating/targeting the cells and attacking them. These scientists are not necessarily responding to any previous studies or work, but more however, the lack thereof.

There is a period during the herpes virus called the latent state, where the cells are not replicating themselves. The goal here is to remove this latent area, which would prevent the occurrence of the cells reactivating in the future. To do this, the scientists came to the conclusion that the best way to combat this area is with the CRISPR method. CRISPR is a powerful tool that has been developed to edit genomes, which in simple terms, works by cutting strands of targeted DNA. The CRISPR system was forced to target the three prototypical members of the human herpes virus. Scientists decided that the most effective way to test out their method, was to split the process into two parts. The first test that the CRISPR system would be put to, is the tackling of the Epstein-Barr virus (EBV). Once the EBV was tested, the next step would be to put the same system up against the human cytomegalovirus (HCMV). Both of these steps are performed the same way, using the same technique and mimicking the CRISPR system the same way to cut the strands of DNA that produce HSV (Diemen et al. 2016). It is also important to note that the design protocol of this study definitely follows ethics and morals. The EBV and HCMV strands are simply mimicked in the laboratory setting and in no way are the researchers actually performing on humans.

With this, the CRISPR system did prove efficient at editing and clearing the latent state in EBV infections. Now the real test is to see if the CRISPR system can perform the same on human cells, as the goal is to impact the herpes virus replication. Results prove that this is possible; the CRISPR system was effective at inhibiting the HMCV replication as well as the EBV.

What does this mean for society? How is this beneficial to you? These findings are extremely important for the future of medicine and for the future of humanity and should be appreciated beyond words. If studies like this continue to develop and we continue to learn more information, then we can save millions of people. This would change the mortality rate in people with HSV-1 and HSV-2 at an incredible rate. As scientists continue to work with the CRISPR system and figure out how they can manipulate cells and attack them, then this information could be used not only to prevent HSV-1 and HSV-2 but other diseases as well.

Researchers that led this study claim that there is no bias that could interfere with the information that this experiment has brought us. I have to agree with this statement. The Netherlands Organization for Scientific Research and The Dutch Cancer Society had nothing to do with the study. Neither organization had any input on how the researchers should carry out their study or how they distribute information to readers. These reasons lead me to believe that in terms of the funding, there are no potential conflicts.

Scientists are at a good place with this research at the moment. Considering that this is an ongoing study, and yes there are years of research and experiments ahead of them, there is already so much to be learned. From now, there should be more scientists and researchers that want to get involved with the CRISPR system and figuring out how to improve the system. It is also possible that researchers will be broadening their research to more than just HSV, and now to other diseases. With the right dedication, and continuation of trial and error, the possibilities are endless. This is only the beginning of such ground breaking medical advancements.



Diemen FR, Kruse EM, Hooykaas MJG, Bruggeling CE, Schürch A,C., Ham PM, Imhof SM, Nijhuis M, Wiertz JH, Lebbink RJ. 2016. CRISPR/Cas9-mediated genome editing of herpesviruses limits productive and latent infections. PLoS Pathogens. 12(6): 5-29.

Lafferty W, Downey L, Celum C, Wald, A. 2015. Herpes Simplex Virus Type 1 as a Cause of Genital Herpes: Impact on Surveillance and Prevention, The Journal of Infectious Diseases. 181(4): 1454–1457.

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