Rider says he hopes to license the technology for trials in larger animals and for eventual human clinical trials. Massachusetts Institute of Technology. Search MIT. Search websites, locations, and people. Enter keywords to search for news articles: Submit. Browse By. New drug could cure nearly any viral infection. Publication Date :. Press Inquiries. Press Contact : Marta Buczek.
Email: mbuczek mit. Phone: Fax: In this set of four photos, dengue hemorrhagic fever virus kills untreated monkey cells lower left , whereas DRACO has no toxicity in uninfected cells upper right and cures an infected cell population lower right. Switching off problematic genes with RNA interference promises treatments for a huge range of disease - if investigators can get it to where it's needed. Lisa Melton reports. It all started with a petunia. The technology is RNA interference, and enthusiasts predict it could soon be used to treat every ailment - from cancer and pandemic flu to type 2 diabetes and heart disease - by shutting down rogue genes.
RNAi has gone from discovery into clinical trials with astonishing speed. Large pharmaceutical companies are signing billion-dollar deals to access gene silencing know-how - hedging their bets on its clinical potential. The stakes are high, but the rewards could be colossal. There is a catch, however, and that is delivery. Getting RNAi therapies into specific parts of the body and across the cell membrane is the main challenge.
Given that the hurdle is considerable, is the hype over RNAi therapeutics warranted? We should be looking at RNAi in a different way. Fortunes are likely to be made from whoever resolves these issues, so no one is about to give up on medical applications. In fact, quite the contrary. The first generation therapies for age-related blindness, cancer, and respiratory syncytial virus are already being cautiously tested on humans. Clinical interest is such that it is easy to forget that RNAi is a natural process that operates in mammals as well as in lower organisms and plants.
The mechanism probably evolved as a way to fight off pathogenic viruses. Many viruses have their genetic material made from RNA. So when they infect a cell, the RNAi pathway strikes back, shutting off key viral genes and aborting the infection. The first clues of gene silencing were spotted in petunias in Dutch researchers were trying to produce more vibrantly coloured purple flowers by inserting extra RNA into normal plants.
Instead, they lost pigmentation and turned white. Scientists were intrigued, though exactly what triggered these effects was not clear at the time. A few years later, scientists discovered that the silencing mechanism is triggered by double-stranded RNA molecules, just 20 to 30 base pairs long, known as small interfering RNAs or siRNAs.
These short strands target matching pieces of messenger RNA mRNA that contain the information necessary to manufacture a particular protein.
Adding a few of these siRNAs to a cell disrupts that message. With no message there is no protein and the target gene shuts down.
They began exploiting RNAi to discover the function of thousands of genes. This tool became so useful that in the Nobel prize for physiology and medicine was shared by US scientists Andrew Fire of Stanford University and Craig Mello of the University of Massachusetts, barely eight years after their discovery of the phenomenon in worms. It soon became obvious to biomedical scientists that, at least in theory, short snippets of RNA could be used to treat every disease imaginable.
Ahead of the game is Alnylam Pharmaceuticals, of Cambridge Massachusetts. The company is entering Phase II studies with a treatment for respiratory syncytial virus, a childhood lung infection for which there is no treatment. If the strategy works, it could lead to a slew of anti-viral therapies. But the virus mutates and evolves resistance so rapidly that fighting it will take more than a single RNA target.
Plasma won't teach the body how to fend off the virus, and one injection won't last forever—but it could be a good way to prepare health workers before they head to a hot spot. Flood the zone with decoys—synthetic molecules that look like ACE2 and trick the virus into binding with them instead, protecting lung cells from damage. Invent drugs that hinder ACE2 from binding with the virus. In theory, these compounds would work on both SARS and Covid, stopping the viruses from sticking to cells.
But ACE2 plays a number of other roles throughout the body; it helps regulate blood pressure, kidney function, and even fertility. Messing with it could have dangerous consequences. All viruses wear heavy-duty protein coats to protect their precious genetic material from the elements. The new coronavirus sports an extra outer layer of fatty molecules. That's great news for humans, because it's easy to tear open with soap or alcohol-based disinfectants.
Soap works best, and you don't need to bother with the antibacterial stuff. Without its fatty layer, the virus dies. Wipe it away or wash it down the drain. By Meghan Herbst. A virus's sole purpose in life is to hijack the machinery of its host cell and force it to make viral copies. By changing how that machinery operates, it's possible to stymie the virus's attempts.
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