Scientists have gained a better understanding of a potentially fatal tick-borne virus that emerged in China about a decade ago.
Researchers from the University of Southern California (USC) may have finally discovered the molecular mechanisms behind severe fever with thrombocytopenia syndrome (SFTS), a condition that has stumped researchers since 2009 when it was discovered to be caused by the Asian longhorned tick (Haemaphysalis longicornis).
“The ticks are already in the United States,” Jae Jung, the study’s senior author and chair of the Department of Molecular Microbiology and Immunology at the Keck School of Medicine of USC, said in a statement. “If they start spreading the virus, it will be a major problem.
“I started studying this virus five years ago because once it appeared in China, I knew it would eventually appear in the United States,” he added.
The researchers found that aged ferrets with the virus show similar symptoms to older humans infected by it, while young ferrets developed no clinical symptoms. This represents the first time researchers found an acceptable animal model to study the virus and develop possible drugs or vaccines to treat the hemorrhagic fever transmitted by the tick species.
H. longicornis is a tiny, parasitic arachnid that thrives in temperate conditions where it feeds on livestock. After feeding on the animal’s blood, the female tick drops off their host to produce 2,000 eggs at a time without even needing help from the male tick.
SFTS, which causes nausea, diarrhea and muscle pain, strikes by depleting blood platelets as it replicates to prevent clotting and cause hemorrhaging similar to the Ebola virus. SFTS infects thousands of people a year in China, 30 percent of which are killed by the virus.
The researchers also discovered that the virus targets TPL2, a gene that is involved in the body’s inflammatory response. SFTS directs the gene to switch off the body’s protective inflammatory response at the site of a tick bite to create a protected spot where the virus can copy itself and spread throughout the body.
After disabling TPL2 with an inhibitor in animals, the researchers found that the body’s healthy immune function kept the virus from replicating, resulting in a much milder infection. This suggests that the gene’s signaling pathway presents a potential therapy target.
“We’re very optimistic that these findings will help us get a vaccine up and running within several years,” Younho Choi, a post-doctoral researcher in the Jung lab and the study’s first author, said in a statement. “We’re already developing various vaccine candidates in mouse and ferret animal models.
“The idea behind the vaccine is to outsmart the virus by putting a roadblock, allowing the body’s immune system to keep doing its job,” he added.
Recently, health officials have expressed concern about the growing danger of tick-borne illnesses. Lyme disease, which accounts for the majority of cases, as well as other tick borne illnesses are on the rise in the U.S and has more than doubled in the last 13 years, according to the U.S. Centers for Disease Control and Prevention.
While the SFTS virus has spread to Japan and Korea since originating in China, it has not yet made it to the U.S. However, the Asian longhorned tick has been found in Arkansas, Connecticut, Maryland, New Jersey, New York, North Carolina, Pennsylvania, Virginia and West Virginia.
The study was published in Nature Microbiology.