Zika virus was first described in Uganda in 1947. Before last year, it had circulated in people in Africa, southeast Asia and in the Pacific Islands and only sporadically caused disease. The virus is transmitted by mosquitoes and typically causes mild, flu-like symptoms, when it causes symptoms at all. (Read More: http://www.cusabio.com/)However, in 2015 the virus began infecting unprecedented numbers of people in Brazil and then spread throughout the Americas. According to the U.S. Centers for Disease Control and Prevention, Zika virus infection during pregnancy can affect early brain development. The size of a newborn's head may be smaller than normal babies.
Recently, scientists have identified a mechanism about how Zika infection does harm to developing brain cells. The study, led by scientists at the University of California San Diego School of Medicine, opens a door to treat Zika infection in pregnant women, and its results are reported in the journal Cell Stem Cell.
The researchers first developed a 3D organoid model that are based on stem cells. The model can mimic the early developing human brain. The stem cells in this model are able to differentiate into different kinds of brain cells, which is similar to what happens in the development of the human brain.
With the help of the model, the researchers found that Zika virus activates a specific molecule called TLR3. TLR3 is known to help combat viral infection. It was found that hyper-activated TLR3 not only blocks the genes associated with stem cells differentiation into brain cells, but also switches on the genes that induce cell death. Furthermore, inhibiting TLR3 decreased the injury of brain cells. The team also discovered that the size of Zika-infected models was reduced by about 16 percent.
The innate immune system in our body is responsible for protecting against viruses. However, Zika virus has the ability to hijack this defensive mechanism to attack our body. The virus negatively affects the brain development through stimulating TLR3.
As the researchers noted, TLR3 inhibitors seemed to block this process. They found that the TLR3 inhibitor significantly tempered Zika virus' severe effects on brain cell health and organoid size, underscoring TLR3's role linking infection and brain damage. However, the treated organoids weren't perfect. As evidenced by their non-smooth outer surfaces, infected but treated organoids still encountered more cell death and disruption than uninfected organoids.