a specially designed rna enzyme to inhibit strains of the herpes simplex virus. the enzyme disables a gene responsible for producing a protein involved in the maturation and release of viral particles in an infected cell. the technique appears to be effective in experiments with mice and rabbits, but further research is required before it can be attempted in people infected with herpes. in 2016, researchers showed that the genome editing technology known as crispr/cas can be used to limit viral replication in multiple strains of herpesviruses, in some cases even eliminating the infection altogether. the researchers tested three different strains of herpesviruses: epstein-barr virus, the cause of mononucleosis and some cancers; herpes simplex viruses (hsv-1) and (hsv-2), which cause cold sores and genital herpes respectively; and human cytomegalovirus, which causes congenital herpes. the results indicated that crispr can be used to eliminate replication in all three strains of the virus, but that the technology was so far only successful in actually eradicating epstein-barr virus. the authors think this may be because the epstein-barr virus genome is located in dividing cells that are easily accessible to crispr. comparatively, the hsv-1 genome targeted by crispr is located in closed-off, non-replicating neurons, which makes reaching the genome much more challenging. another possibility to eradicate the hsv-1 variant is being pursued by a team at duke university. by figuring out how to switch all copies of the virus in the host from latency to their active stage at the same time, rather than the way the virus copies normally stagger their activity stage, leaving some dormant somewhere at all times, it is thought that immune system could kill the entire infected cell population, since they can no longer hide in the nerve cells. this is a potentially risky approach especially for patients with widespread infections as there is the possibility of significant tissue damage from the immune response. one class of drugs called antagomir could trigger reactivation. these are chemically engineered oligonucleotides or short segments of rna, that can be made to mirror their target genetic material, namely herpes micrornas. they could be engineered to attach and thus 'silence' the microrna, thus rendering the virus incapable of keeping latent in their host. professor cullen believes a drug could be developed to block the microrna whose job it is to suppress hsv-1 into latency. herpes has been used in research with hela cells to determine its ability to assist in the treatment of malignant tumors. a study conducted using suicide gene transfer by a cytotoxic approach examined a way to eradicate malignant tumors. gene therapy is based on the cytotoxic genes that directly or indirectly kill tumor cells regardless of its gene expression. in this case the study uses the transfer of the herpes simplex virus type i thymidine kinase (hsvtk) as the cytotoxic gene. hela cells were used in these studies because they have very little ability to communicate through gap junctions. the hela cells involved were grown in a monolayer culture and then infected with the hsv virus. the hsv mrna was chosen because it is known to share characteristics with normal eukaryotic mrna. the hsvtk expression results in the phosphorylation of drug nucleoside analogues; in this case the drug ganciclovir, an antiviral medication used to treat and prevent cytomegaloviruses, converts it into the nucleoside analogue triphosphates. once granciclovir is phosphorylated through hsv-tk it is then incorporating dna strands when the cancer cells are multiplying. the nucleotide from the ganciclovir is what inhibits the dna polymerization and the replication process. this causes the cell to die via apoptosis. apoptosis is regulated with the help of mirnas, which are small non-coding rnas that negatively regulate gene expression. these mirnas play a critical role in developing the timing, differentiation and death of cells. the mirnas effect on apoptosis has affected cancer development by the regulation of cell proliferation, as well as cell transformation. avoidance of apoptosis is critical for the success of malignant tumors, and one way for mirnas to possibly influence cancer development is to regulate apoptosis. in order to support this claim, hela cells were used for the experiment discussed. the cytotoxic drug used, ganciclovir, is capable of destroying via apoptosis transduced cells and non-transduced cells from the cellular gap junction. this technique is known as the "bystander effect," which has suggested to scientists that the effect of some therapeutic agents may be enhanced by diffusion through gap junctional intercellular communication (gjic) or cell coupling. gjic is an important function in the maintaining of tissue homeostasis and it is a critical factor in balance of cells dying and surviving. when hela cells were transfected with the hsv-tk gene, and were then put in a culture with nontransfected cells, only the hsv-tk transfected hela cells were killed by the granciclovir, leaving the nonviral cells unharmed. the hela cells were transfected with the encoding for the gap junction protein connexin 43 (cx43) to provide a channel that permits ions and other molecules to move between neighboring cells. both hela cells with the hsv-tk and without the hsv-tk were destroyed. this result has led to the evidence needed to state that the bystander effect in the hsv-tk gene therapy is possibly due to the cx-mediated gjic. other research amino acids (arginine, lysine) - cold sores research from 1964 into amino acid requirements of herpes simplex virus in human cells indicated that "...the lack of arginine or histidine, and possibly the presence of lysine, would interfere markedly with virus synthesis", but concludes that "no ready explanation is available for any of these observations". further medical evidence indicates that "absorbing more arginine may indirectly cause cold sores by disrupting the body's balance of arginine and another amino acid called lysine." further reviews conclude that "lysine's efficacy for herpes labialis may lie more in prevention than treatment." and that "the use of lysine for decreasing the severity or duration of outbreaks" is not supported, while further research is needed. essential oils hsv is found to be susceptible to many essential oils and their constituents, however there is concern with the cutaneous use of essential oils is the degree of skin and mucous membrane irritation.