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IBM Designs Macromolecule 'Like Honey' To Prevent Viral Infections, Like Zika And Ebola, From Spreading
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The Zika virus, Ebola, and dengue fever often elude vaccines with their shape-shifting abilities. Strains of these viral infections rapidly mutate, so they're not only resistant to treatment but also difficult to prevent from spreading in the first place. But team of researchers from IBM and the Institute of Bioengineering and Nanotechnology in Singapore may have figured out how to finally make some headway toward finding a cure. Their study, published in the journal Macromolecules, reveals it's possible to treat viruses in a unique, alternative way – from the outside in.
"Viral diseases continue to be one of the leading causes of morbidity and mortality," said the study’s lead author Dr. Yi Yan Yang, a group leader at IBN. "We have created an anti-viral macromolecule that can tackle viruses by blocking the virus from infecting the cells, regardless of mutations. It is not toxic to healthy cells and is safe for use. This promising research advance represents years of hard work and collaboration with a global community of researchers."
published - May 15, 2016 02:53 PM By
see more at: http://www.medicaldaily.com/ibm-molecule-viral-infection-zika-virus-ebola-outbreak-386228
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IBM Designs Macromolecule to Prevent Spread of Viral Infections
CLICK HERE - STUDY - Cooperative Orthogonal Macromolecular Assemblies with Broad Spectrum Antiviral Activity, High Selectivity, and Resistance Mitigation
Macromolecules - pubs.acs.org
Macromolecules, 2016, 49 (7), pp 2618–2629
DOI: 10.1021/acs.macromol.6b00091
Publication Date (Web): March 17, 2016
Abstract
Treatment of viral infections continues to be elusive owing to the variance in virus structure (RNA, DNA, and enveloped and nonenveloped viruses) together with their ability to rapidly mutate and garner resistance. Here we report a general strategy to prevent viral infection using multifunctional macromolecules that were designed to have mannose moieties that compete with viruses for immune cells, and basic amine groups that block viral entry through electrostatic interactions and prevent viral replication by neutralizing the endosomal pH. We showed that cells treated with the antiviral polymers inhibited TIM receptors from trafficking virus, likely from electrostatic and hydrogen-bonding interactions, with EC50 values ranging from 2.6 to 6.8 mg/L, depending on the type of TIM receptors. Molecular docking computations revealed an unexpected, and general, specific hydrogen-bonding interactions with viral surface proteins, and virus and cell binding assay demonstrated a significant reduction in infection after incubating virus or cells with the antiviral polymers. Moreover, the mannose-functionalized macromolecules effectively prevented the virus from infecting the immune cells. Representative viruses from each category including dengue, influenza, Chikungunya, Enterovirus 71, Ebola, Marburg, and herpes simplex were surveyed, and viral infection was effectively prevented at polymer concentrations as low as 0.2 mg/L with very high selectivity (>5000) over mammalian cells. The generality of these cooperative orthogonal interactions (electrostatic and hydrogen-bonding) provides broad-spectrum antiviral activity. As the antiviral mechanism is based on nonspecific supramolecular interactions between the amino acid residues and mannose/cationic moieties of the macromolecule, the ability to form the virus–polymer and polymer−cell assemblies can occur regardless of viral mutation, preventing drug resistance development.