Researchers have discovered a ‘vampire virus’—a virus that latches onto the neck of another virus. The virus is known as a phage, or a virus that latches onto bacterium.
The vampire virus, nicknamed MiniFlayer, has developed a never-before-seen evolutionary appendage connecting to another virus's neck.
Researchers believe this discovery could lead to the development of new antiviral strategies
For the first time, researchers at the University of Maryland have discovered what’s been dubbed a novel “vampire virus,” or a virus that latches onto another virus’ neck.
The vampire virus was found by undergraduate students at the University of Maryland looking for phages (or viruses that latch onto bacterium) within soil samples from St. Louis, MO, and Poolesville, MD. They discovered the vampire virus—or satellite phage, nicknamed ‘MiniFlayer’—in the soil bacterium Streptomyces scabiei. MiniFlayer was found to be working with a helper virus, MindFlayer—a bacterium that infects Streptomyces.
Ivan Erill, a professor in the Department of Biological Sciences at the University of Maryland Baltimore County, recently described the discovery of this “vampire virus” in Scientific American, writing, “When a virus enters a cell, it can either go dormant or start replicating right away…Sometimes a virus enters a cell only to find that its new temporary dwelling is already home to another dormant virus.”
What happens then is one of two things, he says: They’ll either battle for control of the cell or, in this case, the virus already living in the cell attacks the virus that’s trying to move in.
MiniFlayer didn’t just wait dormantly, however. It evolved a small appendage with which to attack the incoming virus. “MiniFlayer tail fibers absorb specifically to neck proteins of MindFlayer, which were not observed to be attached to any other location on the helper,” researchers write in Nature. And according to those findings, “No satellite viruses infecting bacterial hosts have been reported to date, but several families of satellite nucleic acids have been described and are commonly referred to as phage satellites.”
But why would MiniFlayer do this? Kirsten Hokeness, PhD, an immunologist and virologist, and director of Bryant University’s School of Health and Behavioral Sciences, explains that when a virus becomes replication-defective, it has to find a creative way to replicate.
“These ‘satellite’ viruses create a unique relationship with a ‘helper’ virus that will aid in replication,” Hokeness says. “Most times these satellites will hide in host cells and wait for another virus to infect the host and then solicit help from them.”
The ‘vampire virus’ can’t hide in the host cell and wait for help like some of its counterparts. “So as evolution goes, the virus had to figure out how to keep infecting, so it latched directly onto a helper virus so they can infect and replicate together,” Hokeness continues. Some of this isn’t entirely groundbreaking. Researchers have long known of virus-attacking viruses (viral satellites). For example, “In humans, the hepatitis D virus uses the hepatitis B virus as a helper to replicate—causing hepatitis,” Hokeness says.
What does this discovery mean for clinicians?
Researchers are already working with phages, Erill notes. He points to research published in Pulmonary Therapy, which found that “Mycobacteriophages—viruses that infect Mycobacterium hosts—show promise as therapeutic agents for non-tuberculous mycobacterium infections and have been used in 20 compassionate use cases.” However, MiniFlayer’s never-seen-before ability to selectively attach itself to another virus is something that researchers hope could be used to develop drug delivery treatments or to target selectively viruses. He hopes this is in a not-so-distant future.
Thus far, the research is basic and preliminary, though Erill tells MDLinx. “The implications down the line, and especially in a clinical setting, are hard to anticipate,” he says. “I believe that satellite-helper systems, where two viruses are deadlocked in an evolutionary arms race to best each other, pose a very interesting opportunity to discover new antiviral strategies.”
How might this work? “If the two entities fighting are viruses, their biological warfare must necessarily center on deploying mechanisms to interfere with the other virus' ability to replicate, which is pretty much the definition of an antiviral system or compound,” Erill explains. Hokeness also shares these hopes for new treatments. “The more we know, the better we are armed in combating current and future infections…What we have seen is that this symbiotic relationship in bacterial viruses can help to drive antibacterial resistance. Therefore, limiting these interactions may prove beneficial for averting the spread of resistance genes,” she says.