Scientists Discover How Antiviral Gene Works

It's been known for years that humans and other mammals possess an antiviral gene called RSAD2 that prevents a remarkable range of viruses from multiplying.

Scientists Discover How Antiviral Gene Works. Image credit: Nogas1974/Wikimedia Commons (CC BY-SA 4.0)

Now, researchers at Albert Einstein College of Medicine, part of Montefiore, have discovered the secret to the gene's success: The enzyme it codes for generates a compound that stops viruses from replicating. The newly discovered compound offers a novel approach for attacking many disease-causing viruses.

The compound, called ddhCTP, disrupts the replication machinery of Zika virus. The next step is to test the compound against a broad array of viruses.

Mammalian cells that become infected by viruses and other pathogens release signaling proteins called interferons. The interferons in turn trigger the expression of hundreds of genes -- one of which is RSAD2, the gene that codes for the enzyme viperin (short for "virus inhibitory protein, endoplasmic reticulum-associated, interferon-inducible").

Studies have shown that viperin's expression inhibits a broad spectrum of disease-causing viruses, including hepatitis C, rabies and HIV-1.

Researchers had proposed several theories for how viperin exerts its anti-viral effects, but precisely how it acted was a mystery. The current study reveals that viperin catalyzes the conversion of a nucleotide called CTP (cytidine triphosphate) into a structurally similar compound, or analog: the nucleotide ddhCTP -- a previously undescribed molecule that sabotages viral replication.

Many viruses use CTP as a building block to synthesize the new strands of genetic material they need to replicate.

The conversion of CTP to its analog, ddhCTP, throws a monkey wrench into virus' ability to copy its genome. The analogue's structure differs only slightly from CTP's -- but the difference is sufficient to bring viral replication to a halt.

ddhCTP may be able to inhibit all flaviviruses, a class of viruses that includes Zika as well as dengue, West Nile, yellow fever, Japanese encephalitis and hepatitis C

ddhCTP appears to be "a completely novel drug scaffold" for designing antiviral drugs. Those drugs would be based on a naturally occurring molecule, so they could have few off-target effects -- a common problem with manmade nucleotide analogs, which can be effective but also quite toxic. (Tasnim News Agency)

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