IBM Medical Anti virus breakthrough could enable new mode of vaccination against all viruses
As one of medicine’s largest challenges, viral infections often escape vaccines due to their natural ability to mutate rapidly and develop drug resistance easily. Many viruses, such as Zika, Ebola and dengue fever, have grown into major global health epidemics with great human and economic toll. IBM Research and Singapore’s Institute of Bioengineering, Nanotechnology (IBN) announced they have identified a new breakthrough macromolecule that could help prevent deadly virus infections with a unique triple-play mechanism that can also help prevent viral drug resistance.
The study exploits supramolecular chemistry – the study of large molecules designed with multiple features — to help combat viral infection. The research is believed to be a first of its kind in fighting viral diseases and IBM Watson, along with such experimental breakthroughs, could help further accelerate drug discovery.
A Unique Triple-Play Action that Helps Prevent Drug Resistance
The new macromolecule is composed of several specialized components to create a powerful triple-play action that helps fight viral infection and replication while inhibiting drug resistance.
Attraction – One specialized component of the macromolecule enables strong hydrogen bonds with electrostatic interactions to attract the proteins on the virus surface — disabling viral ability to infect healthy cells.
Prevention – Mannose (a type of sugar) components of the macromolecule bind directly to healthy immune cell receptors to help fight viral infection and allow the free flow of these naturally protective cells.
Neutralization – Another component of the macromolecule, known as basic amine groups, neutralize the pH inside the viral cell making it inhospitable for replication.
Additionally, the researchers aimed to design a very flexible macromolecule and surveyed a variety of representative viruses from various categories, including Ebola, dengue, Marburg, influenza, Chikungunya, Enterovirus 71 and herpes simplex. In early testing, scientists have seen no resistance. Also, by targeting both viral proteins and host−virus interactions, the antiviral macromolecule sidesteps the normal mutations that enable viruses to escape vaccines through the onset of resistance.