NEW HAVEN--Yale has been conducting research on the Zika virus, and has discovered some key information about how Zika infects us and causes damage.
According to the most recent study, the infection caused by Zika diverts a protein that is necessary for brain cell production for a developing a human fetus. It also kills brain stem cells. Those effects cause the birth defect microcephaly.
The most important part of the discovery is that it could direct researchers towards a cure or prevention method. The findings indicate that Zika could be susceptible to pre-existing anti-viral drugs, like FDA-approved Sofosbuvir, which may be able to stop the infection from disrupting the fetus' developing nervous system. More research needs to be done, but it's a promising lead.
Mark Onorati, co-first author on the research, said, "We hope these findings can lead to therapies that might minimize the damage caused by this virus" while more therapeutic solutions are found.
Microcephaly causes babies to be born with abnormally small brains.
Specifrically, the study found that the diverted proteins are being moved from their job of cell division (or creating more brain cells) to helping the mitochondria, or cell's energy system. Because of the lack of protein in the cell division area, cells die instead of being formed; that's what causes microcephaly.
A study from Yale released last week was one of the first to expand research on how the virus crosses the maternal-fetal barrier that normally protects the fetus. They discovered that certain cell types found in the placenta tissue were susceptible to Zika, meaning Zika could grow within the placenta, where the child is.
Some of the cells in that barrier are believed to travel around the placenta, which could explain the method by which the Zika virus infection moves to the fetus' brain.
