The ongoing study for the cure of Herpes Virus
The herpes virus is mostly present in adults. Just like AIDS and cancer, there is no known cure to herpes infections. It is a lifelong disease, and once contracted the virus will stay in your cell for life.
Being conscious with your lifestyle is important and practicing an acceptable norms with regards to dating and relationship will likely help in avoiding this irritating, lifetime disease. As we know, the herpes virus is commonly spreads by means of sexual contact. It’s no wonder why most adults get infected by herpes simplex.
An ongoing study about herpesvirus has long been started up to this day. The most recent is the study made with CRISPR/Cas9 targeting the infection. The article below is packed of the latest information about the cure towards herpes viruses.
First seen on: (https://www.sciencedaily.com/releases/2016/06/160630144357.htm)
Most adults carry multiple herpes viruses. Following the initial acute infection, these viruses establish life-long infections in their hosts and cause cold sores, keratitis, genital herpes, shingles, infectious mononucleosis, and other diseases. Some herpes viruses can cause cancer in man. During the latent phase of infection, the viruses remain dormant for long periods of time, but retain the capacity to cause occasional reactivation, that may lead to disease. A study published on June 30th in PLOS Pathogens suggests that attacking herpes virus DNA with CRISPR/Cas9 genome editing technology can suppress virus replication and, in some cases, lead to elimination of the virus.
The CRISPR/Cas9 system targets specific DNA sequences and induces clean cuts across both strands of the DNA. In mammalian cells, such cuts are flagged and quickly repaired by an emergency repair system called NHEJ (for non-homologous end-joining). NHEJ is efficient but not very accurate and often results in insertion or deletion of a few DNA bases at the repair site. Because DNA is read in codons of three bases at a time, such small changes in critical positions often destroy the function of the respective gene and its protein product.
Robert Jan Lebbink, from the University Medical Center in Utrecht, The Netherlands, and colleagues reasoned that CRISPR/Cas9 could target and mutate latent herpesvirus DNA in infected human cells and so potentially prevent herpesvirus-associated diseases. To test this, the researchers devised specific guide (g)RNAs–sequences that are complementary to vital parts of the viral genome and function as ‘molecular addresses’. These gRNAs, combined with the ‘molecular scissors’ part of the CRISPR/Cas9 system, should induce specific cuts and subsequent mutations in the herpesvirus DNA, and so cripple the viruses.
In their systematic approach, the researchers looked at three different members of the herpesvirus group: herpes simplex virus type 1 (HSV-1) causing cold sores and herpes keratitis; human cytomegalovirus (HCMV), the most common viral cause of birth defects (when the virus is transmitted from mother to fetus); and Epstein-Barr virus (EBV) causing infectious mononucleosis and multiple types of cancer.
Working with lymphoma cells latently infected with EBV, the researchers showed that introduction of gRNAs that target specific EBV DNA sequences can introduce mutations at the targeted sites. Such mutations can eliminate essential functions of the virus as well as destabilize the viral DNA molecules. Consistent with this, the researchers report that by using two different gRNAs targeting an essential EBV gene, they can induce loss of over 95% of EBV genomes from the host cells.
During latent infection, HCMV genomes exist as circular DNA molecules in the nucleus of host cells. Upon virus reactivation, HCMV replication proceeds slowly. With appropriate gRNAs, the researchers found that CRISPR/Cas9 editing can efficiently impair HCMV replication. However, they also observed emergence of escape variants that bypass CRISPR/Cas9 editing, suggesting that simultaneous editing at multiple critical sites in the HCMV genome is necessary to avoid the development of resistant genomes.
Compared to HCMV, HSV-1 multiplies much faster. When the researchers tested various gRNAs targeting different essential HSV-1 genes in conjunction with CRISPR/Cas9, they found that many of them were able to reduce virus replication. When they combined two of those gRNAs, thereby simultaneously targeting two essential genes, they were able to completely suppress HSV-1 replication. On the other hand, they were unable to induce editing during the latent phase, i.e. when the viral DNA was not actively multiplying.
“We observed highly efficient and specific clearance of EBV from latently infected tumor cells and impairment of HSV-1 and HCMV replication in human cells,” the researchers summarize. They go on to say, “although CRISPR/Cas9 was inefficient at directing genome engineering of quiescent HSV-1, virus replication upon reactivation of quiescent HSV-1 was efficiently abrogated using anti-HSV-1 gRNAs.” Their results, they hope, “may allow the design of effective therapeutic strategies to target human herpesviruses during both latent and productive infections.”
The study is a good news for everyone with herpes simplex because this means the cure is almost achievable. Maybe the cure will not be available for the coming years but knowing that there is a progress is truly a relief for people with herpes infection.
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