Mechanisms of Zika Virus Infection and Neuropathogenesis and Flavivirus infection requires specific host genes
The researchers identified 9 genes that… are associated with the cell’s endoplasmic reticulum, where viral translation, replication, and assembly of viral particles takes place. Six of the genes also reduced infection of Zika, dengue, Japanese encephalitis, and yellow fever viruses when removed from human cells. Most showed similar effects when absent from insect cells tested for West Nile and dengue virus infections.
My comment: They linked virus-driven theft of quantized energy to a single amino acid substitution in the virus but do not appear to know that virus-driven energy theft is linked to all pathology by the conserved molecular mechanisms of biophysically constrained energy-dependent RNA-mediated protein folding chemistry in all living genera.
See: Structure of the thermally stable Zika virus
Excerpt: The Ala340 insertion in the C strand of DIII allows the CD-loop to stretch further towards the five-fold vertex compared to DENV2 (Fig. 3a). Gln350 of the CD-loop from one DIII could potentially form a hydrogen bond with Thr351 from another CD-loop in the neighbouring DIII, and thus may create a hydrogen bond network between the five DIIIs (Fig. 3a and Extended Data Fig. 6). In comparison, in DENV2, there is a lack of interaction between the DIIIs in this region (Fig. 3a). The possible hydrogen bond network around the five-fold vertex of ZIKV could be responsible for the rotation of the E protein molecule
Reported as: Cracking the Zika Mystery
…the Zika virus is more thermally stable than the dengue virus, and is also structurally stable even when incubated at 40 degrees Celsius, mimicking the body temperature of extremely feverish patients after virus infection.
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