A hot topic recently that has been hitting the news or social media is the recent emergence of the Zika virus. Most of us have heard of this virus causing a huge public emergency recently, beginning around May 2015, in Brazil. The Zika virus has been reported to be carried by some mosquitos and through their bites, the virus can be transferred to humans. Reports say that due to the Zika virus, if a pregnant woman is bitten there is a higher chance of birth defects such as microcephaly (improper formation of a baby’s head), which has been implicated to result in brain problems, developmental delay, and many others. Due to all these different birth defects caused by the Zika virus, the WHO has declared this a public health emergency.
Scientists all over the world are trying to figure out how the Zika virus infects fetuses to cause the birth defects. There are many ways by which the Zika virus could potentially infect the fetuses of pregnant women. There is speculation that Zika Virus infection may happen through infected sperm, transport via immune cells, through the placenta, and many others, but the mechanism on how each may occur is yet to be understood. The placenta plays an important role for the health and well being of the fetus, as it provides nutrition and protection via infection (Women’s antibodies: defence mechanism against harmful pathogens). It can be seen as to why the placenta would be the first place to which scientists may study for the virus, as it may be the first line of entry towards to cause infection. This is exactly what the Conye group (Bayer et al., 2016) from Pittsburgh is studying: does the infection of the Zika virus happen through the placenta of pregnant women?
Figure 1. The hindrance of Zika Virus entry via syncytiotrophoblast cells. Focusing on on image C, through constant release of IFN via syncytiotrophoblast, it signals itself (autocrine signaling) as well as other neighbouring cells (paracrine signaling) to turn on Interferon stimulate genes for a defense mechanism that hinders the entry of the Zika virus into the placenta of the fetus.
Image:(Bayer, A. et al. 2016)
The Conye group has discovered that the human body does have some type of mechanism to hinder the entry of the Zika virus to the fetus. They discovered that a layer of cells called syncytiotrophoblasts (cells that line the placenta) resist the infection of the Zika virus. They also uncovered that the syncytiotrophoblasts cells were constantly releasing signalling molecules, called interferons (IFN) that protect itself as well as other types of non-placental tissues to hinder virus infection. IFN molecules play an important role for signalling to other cells to turn on defence mechanisms like interferon stimulated genes (ISG), which act to turn on cellular mechanisms like increased protein content to hinder virus entry, limit viral replication, increase cell death (to stop spread of the virus), an many others.
With this research from the Coyne group, it has uncovered that the body does have a mechanism to help stop, or at least slow, the infection of the Zika virus to the fetus. The big problem now is pinpointing which mechanism of entry is causing birth defects. Nevertheless, this research gives powerful insight on the how the body is able to fend off viruses like the Zika. This also brings up important research questions such as how are the cells hindering the entry of the virus into cells, what proteins are involved, if the ISG is being turned on by IFNs and what is that doing to prevent virus infection.
Photo Credit: Bayer, A. et al. Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection. Cell Host Microbe (2016). doi:10.1016/j.chom.2016.03.008
Article title: Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection.
Source: Bayer, A. et al. Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection. Cell Host Microbe (2016). doi:10.1016/j.chom.2016.03.008