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13<br />
How does the Zika virus work?<br />
As <strong>of</strong> May 2015, there has been a large Zika epidemic in the Americas and the Pacific. Ever<br />
since then, there has been increased research <strong>of</strong> the Zika virus. Researches say that the Zika<br />
virus causes microcephaly to the unborn child. Jae Jung from the University <strong>of</strong> Southern<br />
California reported in Cell Stem Cell that 2 <strong>of</strong> the 10 proteins that are produced by the Zika<br />
virus cause microcephaly. These two proteins, NS4A and NS4B, prevent the phosphorylation<br />
<strong>of</strong> two amino acids in the Akt protein by mTOR. This leads to inhibition <strong>of</strong> the signalling<br />
pathway <strong>of</strong> Akt-mTOR. Akt without phosphorylation is inactive, meaning it cannot activate<br />
the proteins normally regulating the cell’s autophagy, thus, random autophagy occurs. This<br />
means infected cells digest their own organelles without any form <strong>of</strong> control. The energy and<br />
nutrients that come free in this digestive process are used by the virus. The signalling pathway<br />
<strong>of</strong> Akt-mTOR is very important for the growth <strong>of</strong> neurons in the brain <strong>of</strong> the unborn baby. It<br />
is likely that the Zika virus’ inhibition <strong>of</strong> the signalling Akt-mTOR pathway leading to random<br />
autophagy destroy so much <strong>of</strong> the cell’s compartments that neurons die, disabling the brain’s<br />
growth. It would be reasonable to think that medicines are being developed inhibiting the<br />
production <strong>of</strong> NS4A and NS4B, but unfortunately there is no medicine yet.<br />
Source; C2W (2016). Wat zika met embryo’s doet. C2W life sciences 15, 09-09-2016, <strong>17</strong>.<br />
Jung, J.U. et al. (2016). Zika Virus NS4A and NS4B Proteins Deregulate Akt-mTOR Signaling in Human Fetal Neural Stem Cells to<br />
Inhibit Neurogenesis and Induce Autophagy. Cell Stem Cell, 11-08-2016.<br />
Figure 2. Monocercomonas sp.<br />
Eukaryotes without mitochondria<br />
Most people learn at school – or in college – that all<br />
eukaryotes have mitochondria. But that ground rule <strong>of</strong> cell<br />
biology has recently been proven wrong. Czech researchers<br />
discovered a single-cell organism in the guts <strong>of</strong> a chinchilla<br />
that does not contain mitochondria. This organism, part<br />
<strong>of</strong> the genus Monocercomonoides, is an oxymonad, living<br />
a parasite life. It was already known that oxymonads have<br />
unusual mitochondria, since they do not need mitochondria<br />
for their energy supply, as they are anaerobe organisms and<br />
mitochondria use oxygen. When the researchers sequenced<br />
the DNA <strong>of</strong> the Monocercomonas sp. they were unable to<br />
find any sign <strong>of</strong> typical mitochondrial DNA or mitochondrial<br />
proteins. It is likely that other proteins take over the functions<br />
<strong>of</strong> the mitochondria, because these single-cell organisms have<br />
copied DNA from bacteria that do not contain mitochondria<br />
either. According to the researchers, the most logical explanation <strong>of</strong> this phenomenon is<br />
that all mitochondria are evolved out <strong>of</strong> the eukaryote’s genome: there is simply no need for<br />
them, so it is more efficient to dispose <strong>of</strong> them completely. Another explanation is that the<br />
mitochondrial proteins are so well evolved that they cannot be recognised. However, the Czech<br />
researchers think that this is extremely unlikely, as mitochondrial proteins normally do not<br />
evolve at such speeds.<br />
Science<br />
Source; C2W (2016). Kijk mama, zonder mitochondriën. C2W life sciences 11, 06-<strong>17</strong>-2016, 7.<br />
Job Deen