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The views expressed in the contents above are those of our users and do not necessarily reflect the views of MailOnline. The Food and Drug Administration announced Tuesday that it has approved Imlygic for the treatment of melanoma lesions on the skin and lymph nodes. A modified form of herpes can kill cancer cells and stop tumors from growing, according to research published earlier this year in the Journal of Clinical Oncology.
Clearly, that’s a small price to pay compared to life-threatening skin cancer, but what happens if you already have herpes? However, he says, people should avoid oral anti-viral medicines when using Imlygic because the medicine will attack the virus and weaken or destroy it.
Melanoma is the most dangerous form of skin cancer, which is the most common form of cancer in the U.S. The European Union could see its first far-right president if Norbert Hofer wins the run-off round in Austria's election. More precisely, they say that 1 in 4 of the study participants responded well to the innovative treatment, and even more surprisingly, 16.3% remained in remission for 6 months after the initial experiments. By comparison, only 2.1% of the skin cancer patients included in a control group and treated with more conventional immunotherapy stayed in remission for such a long time.
Mind you, the researchers didn't use the herpes virus per se to treat these skin cancer patients. The modified herpes virus used in these experiments was engineered to target not healthy cells but cancerous ones. This triggered an immune response that further helped destroy tumors or at least shrink them to a considerable extent, say the specialists who tested the herpes-based drug.

Given their success in using the genetically engineered form of the herpes virus to treat melanoma, it should come as no surprise that the scientists behind this research project are now looking to make their innovative treatment available to skin cancer patients worldwide. True, they still have some hurdles to overcome but they are rather optimistic about the future.
Should all go well, the team expects that they will be granted permission to begin marketing their herpes-based skin cancer drug sometime in 2016, albeit only in the US and in Europe.
Heart failure drug shown to also inhibit Epstein Barr virus by targeting a pathway common to all herpes viruses.
At present, there is only one class of antiviral medicines against herpesviruses—a family of viruses that cause mononucleosis, herpes, and shingles, among other illnesses, which means options for treating these infections are limited.
Swaminathan's team uncovered spironolactone's antiviral properties in a screen to identify drugs that work through a mechanism that is different from that of existing anti-herpesvirus drugs.
Importantly, spironolactone's ability to block viral infection appears to be independent from its ability to treat heart failure. But because all herpesviruses depend on SM-like proteins to spread infection, the work also has broader implications.
According to the National Cancer Institute, about 74,000 Americans will be diagnosed with melanoma this year, and nearly 10,000 will die from it. Rather, they used a modified version made into a drug by the name of Talimogene Laherparepvec (T-VEC).
Having reached cancer cells, the virus would enter them and multiply until they popped open. Thus, they hope it will not be long until both the US Food and Drug Administration and the European Medicines Agency give their drug the green light.

If viruses become resistant to these frontline treatments, a growing problem particularly in clinical settings, there are no alternative drugs to serve as backup. They find that the drug's antiviral properties stem from its ability to block a key step in viral infection that is common to all herpesviruses. Currently available drugs block a middle step of the viral infection cycle by inhibiting virus' ability to replicate DNA. Previous studies showed that the drug treats heart failure through a different, metabolic mechanism. Spironolactone could be developed as a new medicine against EBV, a common and dangerous infection among transplant and other immunocompromised patients.
Spironolactone could be a template for a new class of drug directed against all herpesviruses.
Spironolactone's target is distinct from that of existing drugs, revealing that it could be developed into a new class of anti-herpesvirus drug. They found that like these drugs, spironolactone can block EBV replication in cells, but it does so by targeting the so-called SM protein, required for a late step in the infection cycle.
This study demonstrates that a drug similar to spironolactone shares its ability to treat heart failure but not its antiviral properties.

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