"At this point, there is no cure for the herpes virus infection. Once infected, you're infected for life," said Robert Jan Lebbink, co-author of the study and a molecular biologist at University Medical Center in Utrecht, Netherlands.
The virus develops a latent stage, in which it lies dormant in an infected cell without reproducing. Because our immune systems cannot recognize latent infections, we cannot clear them from our bodies.
Occasionally, though, these viruses will wake and reproduce, spreading the virus to other cells -- or other people. The new research, published in the journal PLOS Pathogens
, explores a new approach to stopping this sometimes deadly virus.
Herpes comes in more than a hundred strains, though only eight routinely infect humans. Herpes simplex virus type 1 causes cold sores, while herpes simplex type 2 is responsible for genital herpes. Human cytomegalovirus can cause birth defects if transmitted from mother to fetus. Epstein-Barr virus, another version, can cause mononucleosis or even cancer.
All told, herpes viruses may result in cold sores, corneal infections, shingles, genital sores, the "kissing disease"
Any of the drugs currently used to treat herpes addresses the symptoms but does not destroy the virus itself. This is why any sores or infections may return repeatedly throughout our lives.
CRISPR-Cas9 is gene-editing technology that is based on a natural system used by bacteria to protect themselves from viruses. Because CRISPR/Cas9 can target double-stranded DNA such as the herpes virus, Lebbink and his colleagues decided to put the two together in a death match.
"Can we design CRISPRs that specifically target the genome of these viruses in infected cells?" Lebbink asked. By cutting the viruses to pieces or mutating regions of their genomes, he figured, virus replication would be blocked, or better yet, the virus might be cleared from infected cells altogether.
More research needed
When attacked by a virus, bacteria produce two types of short RNA, one of which corresponds exactly to stretches of code within the virus' DNA. These two RNA then join with a protein called Cas9. The RNA with identical code spots the same stretch within the viral genome, and Cas9 snips it, effectively disabling the virus.
For his own study, Lebbink and his co-authors targeted just three types of herpes viruses: herpes simplex type 1, human cytomegalovirus and Epstein-Barr.
The experiments showed that CRISPR/Cas9 could severely block virus replication for herpes simplex and human cytomegalovirus. The results for Epstein-Barr were even more dramatic.
"Also, for [Epstein-Barr], a herpes virus that in some cases causes cancer, we were even able to remove the virus from infected tumor cells, essentially curing the cells from their invader," Lebbink said.
Though dramatic, all of these experiments were done on monkey and human cells in a mere petri dish; none was performed on live animals -- or live humans. So, while it appears the CRISPR/Cas9 system may be very effective in rooting out herpes, Lebbink explained that much more research is needed.
First, animals studies need to be done, and human tests would follow. Still, he is hopeful the science will profoundly influence health care.
"Scientists now have a very powerful tool to make specific edits at almost any site in the human genome, remove genes, introduce genes, alter cancer-causing genes, repair genetic defects, et cetera."