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Creating effective vaccines against dengue virus and Zika involves the E protein that covers the surface of each viral particle, strong antibodies against E protein could be a strong vaccine against the virus, the 180 E proteins come in pairs,making it difficult to produce. UNC School of Medicine researchers have delineated the details of one major barrier to a promising vaccine.
Previous studies have shown that humans create strong antibodies to the E protein on the virus surface, suggesting that a soluble version of the E protein-called sRecE) could make a good vaccine. UNC researchers led by Brian Kuhlman, PhD, professor of biochemistry and biophysics, and Aravinda de Silva, PhD, professor of microbiology and immunology, have shown that body temperature reduces the pairing propensity of sRecE and its ability to be recognized by these strong antibodies.
Stabilizing the pairing propensity of sRecE may lead to production of an effective vaccine. Dengue infection can lead to life-threatening hemorrhagic disease, Zika outbreak has linked Zika infection to serious neurological disorders, like microcephaly in infants and Guillain-Barré Syndrome in adults. The surface of dengue and Zika viral particles are structurally similar-both viruses are coated with a single protein – called the envelope (E) protein. Each virus contains 180 copies of the E protein on the surface, in pairs of two, known as homodimers.
A soluble version of the E protein, called sRecE, can form the same homodimer structure observed by E proteins on the surface of the virus. Dengue- and Zika-infected patients develop neutralizing and protective antibodies that target specific regions on the E protein called epitopes. Colder temperatures help to keep proteins in their native or active structure, because of this, they tested how sRecE from three dengue serotypes and in Zika can form homodimers, as seen on the surface of the virus, in buffer at room temperature.
The UNC researchers discovered that dengue and Zika sRecE do form homodimers at room temperature, but when the experiment was performed at physiological temperature [98?F], all sRecE’s – including dengue serotype 2 (DENV2) and Zika sRecE homodimers fell apart and became monomers. This showed that the physiological temperature-induced E protein changes observed on the virus surface also occur in the sRecE.
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