There's new information on Zika -- and scientists at the University of Texas Medical Branch at Galveston are key reasons why.
Although the Zika virus was discovered nearly 70 years ago, scientists do not yet fully understand how the virus causes infection once it enters the host.
A research team from the U.S., Germany and Singapore, led by UTMB-Galveston, has uncovered evidence that parts of the Zika virus closely resemble parts of the host’s own immune system. In turn, they say, that may trigger the host’s body to mount a defense against both the Zika virus as well as its own complement system, which is important for fetal development as well as for the immune system. This mistaken identity may contribute to the birth defects and adult neurological disorders seen in people who have been infected with Zika.
In healthy people, a Zika virus infection usually results in mild or symptom-free infections, the risk of a disorder in which your body’s immune system attacks your nerves called Guillain-Barre syndrome and microcephaly in a developing fetus is an alarming consequence that has created a worldwide health threat.
The researchers from the multinational team sought out to determine whether there were Zika proteins that “mimic” the host proteins and if the immune response could be aimed against both. Different proteins serve different roles within the body and understanding what the proteins targeted by the immune system or the virus do could explain why Zika infection can result in neurological complications.
These findings are detailed in Scientific Reports.
Slobodan Paessler, UTMB professor in the department of pathology, says that as potential Zika vaccines enter clinical trials, it’s important to ensure that these vaccines do not induce antibodies that may lead to an autoimmune response.
Other authors include UTMB’s Takaaki Koma, Shannan Rossi, Pei-Yong Shi, David Beasley, Nayalya Bukreyeva, Jeanon Smith, Steven Hallam and Cheng Huang.