Animal viruses have a secret ally to infect human cells

Viruses, those tiny invaders wriggling their way into host cells are a marvel of biological survival. Among them, arteriviruses, found in a variety of animals across the globe, have evoked great interest.

These viruses have remained largely elusive to the human immune system. A recent study has unveiled an intriguing mechanism by which arteriviruses sneak into host cells and initiate an infection.

Friendly protein turned foe

In the center of this microscopic drama is a protein found in mammals – an unsuspecting gatekeeper that unwittingly opens the door to arteriviruses.

The research team also discovered a monoclonal antibody – an immune system ally – that binds to this protein, effectively shielding the cells from viral infection.

Arterivirus infections

Why should we concern ourselves with arteriviruses? These are viruses that we do not have immunity against.

“It’s important to consider that since we have no known arteriviruses infecting people that we’re essentially immunologically naïve, so we can’t rely on preexisting immunity to help us,” said co-lead author Cody Warren, assistant professor of veterinary biosciences at The Ohio State University (OSU).

To understand the gravity of the situation, we must consider the potential implications. Arteriviruses are found in various mammals like non-human primates, possums, pigs, and horses. They are often present without causing noticeable disease.

But, when they switch hosts, the viruses can cause serious health problems such as pneumonia, hemorrhagic fever, or encephalitis.

Journey of a virus in a cell

In the realm of viruses, breaking and entering is a step-by-step process. For arteriviruses, the first stop is the FcRn receptor, a protein complex formed by the coming together of two genes – FCGRT and B2M. This receptor otherwise plays a benign role, carrying antibodies across the placenta to a fetus.

However, when a virus comes along, the FcRn receptor becomes a conduit for infection. It is responsible for ushering in at least five different arteriviruses infecting monkeys, pigs, and horses.

When the researchers disrupted the FCGRT gene, the primary component of the FcRn complex, the cells became resistant to the infection. Better yet, pre-treating cells with monoclonal antibodies against FcRn protected them entirely.

Arteriviral infection of host cells

There’s a fascinating genetic subplot to this story. It turns out, the susceptibility of mammalian hosts to the arterivirus infection varies based on differences in their FcRn’s genetic sequence.

Essentially, the sequence variations of this receptor protein can either facilitate or impede cross-species infections.

The surface protein CD163, which has a history of playing a gatekeeper role for the simian hemorrhagic fever virus (an arterivirus), also came into the spotlight in this study.

Experiments demonstrated that CD163 interacts with FcRn and aids in arteriviral infection of host cells. By identifying these arterivirus infection steps, we have reached an important milestone.

“If we’re looking at virus biology, one of the most important things we can understand is entry mechanisms. Because if you can stop the ability of a virus to infect a cell through disrupting that initial virus-receptor contact, now you have a potential therapeutic strategy,” said Warren.

Getting prepared for the next pandemic

Unveiling the secrets of how arteriviruses infiltrate host cells leaves us better prepared to face any future viral threats that may emerge.

With an existing monoclonal antibody that can prevent viral infection in cells, we have a ray of hope in our pre-pandemic preparedness toolkit.

“If one of these viruses emerged in humans, I believe we’d be in big trouble. So that is the motivator for me,” said Adam Bailey, assistant professor of pathology and laboratory medicine at the University of Wisconsin-Madison and co-lead author of the study.

Significance of the study

Knowledge is indeed power. As we deepen our understanding of viruses infecting cells, we inch closer to better prevention methods and ideally, fewer global health crises.

“Understanding the nuances of species-specific FcRn utilization will be important in anticipating the spillover of arteriviruses into new hosts, as our data indicates that FcRn can function as a molecular barrier to cross-species arterivirus infection,” wrote the researchers.

The study is published in the journal Nature Communications.

—–

Like what you read? Subscribe to our newsletter for engaging articles, exclusive content, and the latest updates. 

Check us out on EarthSnap, a free app brought to you by Eric Ralls and Earth.com.

—–