Researchers report that the same driving force that makes Zika so detrimental to unborn babies gives it promise as a cancer treatment.
Zika virus, feared for its severe effects on pregnant women and unborn babies, may hold potential as a cancer treatment for neuroblastoma, according to early findings published in PLOS One. Researchers in Florida are reporting that the same driving force that makes Zika so detrimental to unborn babies gives it promise as a cancer treatment. They have discovered that it appears to attack developing nerve cells, which are the same type of cells that neuroblastoma is derived from.
“Our team found that Zika virus killed nearly all neuroblastoma cells. We were surprised by how effective the virus was against these cancer cells, and we were surprised that there was one line that was not killed, which lacked the CD24 protein. This showed that CD24 plays a very significant role in susceptibility to Zika virus,” said study author Kenneth Alexander, MD, PhD, chief of the division of infectious diseases at Nemours Children’s Hospital in Orlando.
Alexander and colleagues noted that neuroblastoma is the second most common childhood tumor, and survival rates are poor even with intensive therapy. Zika virus is a mosquito-borne pathogen and is unique among flaviviruses because of its association with congenital defects.
Researchers at Nemours Children’s Hospital along with investigators at the University of Central Florida College of Medicine examined the impact of the Zika virus on neuroblastoma cells by infecting different types of cultured neuroblastoma cells with Zika. They found that most neuroblastoma cells were killed after just 10 days. However, one specific neuroblastoma cell line (SK-N-AS) showed resistance to Zika infection.
Upon closer examination, the researchers found that this cell line had poorly expressed levels of the membrane protein CD24 when compared with the other neuroblastoma cell lines. They also determined that CD24 on neuroblastoma cells was required for Zika viral infection.
“We are most interested in the fact that CD24 is an important determinant of viral cytotoxicity,” Alexander told Cancer Network. “We hypothesize that other tumors are susceptible to CD24 to Zika virus–mediated lysis.”
He noted that different labs working side by side on this project have demonstrated the power of collaboration among basic science, clinical medicine, and clinical surgery. “We are years away from any potential clinical implication, but we need more clinicians bringing their experience and expertise to the lab to further our understanding of diseases and open the door for new treatments,” said Alexander.
Milan Chheda, MD, assistant professor at Washington University and Siteman Cancer Center, said this current study nicely demonstrates that the CD24 protein is one component of the door that Zika uses to enter and kill neuroblastoma cells. “This is an interesting observation, which will help our understanding of Zika virus as a potential cancer therapy. I am sure there will be interest in building on these findings over the next several years and testing their applicability to disease in patients,” Chheda told Cancer Network.