Key takeaways
- Scientists at CSIR-CCMB in Hyderabad, India, have identified a protein called DZIP3 that does two jobs at once: it detects viral genetic material inside cells and switches on the cell’s immune defences.
- The discovery, published in The EMBO Journal, could point toward broad-spectrum antiviral drugs — medicines that work against many viruses rather than just one.
- In lab tests, the DZIP3 pathway restricted four dangerous viruses: SARS-CoV-2, chikungunya, influenza A and Japanese encephalitis.
When a virus slips into one of your cells, a race starts. The intruder rushes to copy itself thousands of times; the cell scrambles to notice the break-in and sound the alarm before it is overwhelmed. This week, researchers in India reported finding one of the alarm’s most versatile tripwires.
The protein is called DZIP3, and a team led by Dr Santosh Chauhan — a senior principal scientist at the CSIR-Centre for Cellular and Molecular Biology (CCMB) in Hyderabad — has shown that it performs a rare double duty. Most cellular proteins either detect a virus or fight it. DZIP3 does both: it recognises viral RNA floating inside the cell, then directly triggers the immune response that holds the virus back.
“About seven years ago, we hypothesised that a specialised group of human proteins could perform two functions — detect viral genetic material and activate key cellular proteins to trigger an immune response,” Chauhan told The New Indian Express. The new study, published in The EMBO Journal, confirms the hunch.
How the alarm works
Here is the sequence the team pieced together. When DZIP3 encounters viral RNA, it changes shape — effectively switching itself on. Once activated, it drifts toward the mitochondria, the cell’s energy factories, where the heavy machinery of innate immunity is parked. There it joins two well-known immune proteins, RIG-I and MAVS, and uses a built-in enzymatic tool (an E3 ubiquitin ligase, in the jargon) to tag RIG-I with a molecular marker. That tag keeps the alarm ringing longer and louder.
The payoff is a surge of type I interferons — signalling molecules that warn neighbouring cells and block viruses from multiplying. The researchers demonstrated that this pathway restricted four very different viruses in laboratory experiments: SARS-CoV-2 (the cause of COVID-19), chikungunya, influenza A and Japanese encephalitis.
DZIP3 is not a newcomer to science. It was first spotted more than two decades ago, in 2003, because it interacted with RNA from the hepatitis B virus — but nobody knew it had this immune role. As the paper’s authors put it, it is “a rare example of a dual-function effector, both a viral dsRNA detector and an executor of antiviral immunity.”
Why this matters beyond the lab
Most antivirals are bespoke: one drug, one virus, years of development. A protein that sits at a choke point of the cell’s general antiviral response is a different kind of prize. Chauhan’s team is already developing small-molecule drug candidates designed to boost DZIP3’s activity — in effect, turning up the volume on the body’s own alarm.
“Targeting DZIP3 with small molecules could lead to broad-spectrum antiviral therapies against emerging viral threats,” Chauhan said. That word — emerging — is doing heavy lifting. The next pandemic virus will almost certainly be one nobody has a drug for yet. A therapy that strengthens a universal early-warning system could buy the time that vaccines and targeted drugs need.
There are caveats, and the honest ones matter. Everything so far comes from cell experiments; animal and human studies are still ahead. And the interferon system is powerful precisely because it is blunt — drugs that amplify it will need to avoid triggering the kind of runaway inflammation that makes some viral infections deadly. But as a piece of basic biology, this is the real thing: a new gear in the oldest defence system humans have.
The paper, “DZIP3 is a viral RNA co-sensor for RIG-I that promotes type-I interferon responses,” appeared in The EMBO Journal. For background on how the immune system’s other defences work, see our explainer on how mRNA vaccines work.
