Many efforts to fight viral diseases like Zika and Ebola focus on targeting the specific virus. But now, a new study reports progress toward a different solution – a universal antiviral that targets several diseases and relies on a mechanism that appears to be resistance-proof.

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The researchers tested their new approach on different types of virus, including the herpes simplex virus, and found it blocked them from entering the host cells.

A paper on the new approach, led by scientists at the Institute of Bioengineering and Nanotechnology in Singapore and the National University of Singapore, is published in the journal Macromolecules.

Viruses are tiny, microscopic organisms that can only replicate inside the cell of a host organism. About 100 times smaller than bacteria, viruses are thought to be the most abundant type of biological entity on our planet and can be found in virtually all of its ecosystems.

Some scientists argue that viruses are not life forms as such because they have no ability to metabolize – that is to break down nutrients into the compounds they need to replicate. Instead, they hijack mechanisms in the host cell.

Nevertheless, they have many of the attributes one normally associates with living entities – they have genes that pass on to new generations, they have a protein coating (instead of a cell membrane), they are capable of self-replication and they can mutate.

However, despite many disease viruses – such as the ones that cause dengue and Ebola – having been around for decades, there are still no treatments for them. The huge variety in their structure, together with their ability to rapidly mutate and garner resistance, present considerable challenges to drug developers.

The approach described in the new paper aims to act more broadly against several different types of virus. It uses a modified polymer to interact with the surfaces of the viruses and human cells.

Essentially the interactions – involving electrostatic activity and hydrogen-bonding with virus surface proteins and virus-trafficking receptors on the cell surfaces – prevent the virus from entering the host cell.

The team had already described these effects of the polymer – called polyethylenimine (PEI) – in previous studies. However, in those studies, the polymer went too far and also killed the mammalian host cells.

As such, in the new study, the team looked for ways to modify the polymer so it interfered with the ability of viruses to enter host cells, but without harming the host cells.

They found the answer was to modify the PEI with a type of sugar called mannose. Lab tests showed the “mannose-functionalized” PEI interacted with both viral and cell surfaces and stopped a range of viruses from entering human host cells. The researchers note in their paper:

Representative viruses from each category including dengue, influenza, Chikungunya, Enterovirus 71, Ebola, Marburg, and herpes simplex were surveyed, and viral infection was effectively prevented […]”

They also note that because of certain features of the antiviral mechanism – such as reliance on non-specific interactions – it “can occur regardless of viral mutation, preventing drug resistance development.”

The team also ran some preliminary safety tests on the modified PEI and found that after 2 weeks of testing in an animal model, it showed no toxic effects.

Meanwhile, Medical News Today recently learned that health officials in the US conclude that the Zika virus causes microcephaly and other severe brain defects in babies.