About five months have passed since the Brazilian government first announced the now well-known Zika outbreak. In that time, the virus has spread across many parts of the Americas and now threatens many areas of the United States.
As the virus spreads, researchers across the globe are working tirelessly to learn more about the virus and to discover therapeutics and possibly a vaccine. Unfortunately, the pace of laboratory work is intrinsically slow and results may take years to develop.
In this world, five months is akin to a blink of an eye. It's a difficult reality to grasp for those worried about how this virus could affect their lives. With this in mind, the introduction of a therapeutic, even at the most preliminary level, might be considered an impossible challenge.
Yet, last week an experimental therapeutic option for Zika was unveiled at the conference of the International Society for Neglected Tropical Diseases Co-Infection in London, England. The treatment, known simply as ICI406, may one day offer possible relief to help those suffering from the infection. The results also suggest this chemical may also help to reduce the chances for secondary conditions such as microcephaly and Guillain-Barré syndrome (GBS).
I reached out to man behind ICI406, Dr. Neil Bodie. He's a research colleague who has devoted the last decade to stop viruses like Zika. His work, in collaboration with researchers from Middle Tennessee State University, led to the rapid confirmation of the therapeutic in the lab. But as Bodie points out, they were given some help along the way thanks to the nature of the virus.
"We had no idea Zika could cause a multinational outbreak."
"Zika virus is a member of the Flavivirus family. This means it's similar in many ways to dengue virus, which I have been studying for close to 10 years," says Bodie. "When Zika first appeared, I had hoped our decade-long experience in understanding dengue would translate to a new therapeutic for Zika. We looked at what Zika does that dengue doesn't -- the most obvious is that Zika crosses natural barriers to infection like the placenta, while dengue generally doesn't. Also, being a neurotropic virus, Zika causes GBS and other neurological complications."
Some genetic information regarding Zika had been published nearly a decade earlier but the data suggested Zika was a different branch of the evolutionary tree. A more in-depth analysis was performed a year later and revealed there may be enough similarity to investigate the use of dengue-based therapeutics.
However, this avenue wasn't explored until the outbreak began. As Bodie points out, there was apparently no need. "We had seen outbreaks in Asia but they were relatively small and seemed to fizzle out. We had no idea Zika could cause a multinational outbreak," he says. "Now that we know we have focused our attention and work to this virus."
While Bodie initially focused on the differences between Zika and dengue, the therapeutic is a trait shared by dengue and Zika. They have the ability to mimic a part of the human immune system called the antibody fragment crystallizable gamma receptor, better known by its abbreviation, FcγR. This protein is responsible for recognizing antibodies and then engulfing whatever might be attached for destruction. It's incredibly useful in fighting infections as it helps to isolate and remove the threatening invader.
But if a similar form of FcγR is present on a virus, such as dengue and Zika, they can take advantage of the immune system to worsen the infection. It's called antibody dependent enhancement (ADE) and can quickly worsen the prospects for the individual.
The viruses can gain access to more cells, including those known to cross certain boundaries such as the blood-brain barrier and the maternal-fetal barrier. This increases the chances for wider spread in the body and secondary complications such as microcephaly and GBS. For Bodie, this represented the key to developing a therapeutic.
"We have a therapeutic that works in the lab and hopefully will be available sooner than later. But we need to go on the offensive."
"My colleagues and I theorized a therapeutic that blocks FcγR would inevitably reduce the extent of infection. It took time but we eventually found ICI406 and it did exactly what we needed," he says. "We were able to stop the effects of dengue and ADE in laboratory cell cultures. All that was needed was to repeat the process using Zika."
When they did, the results, although expected, were still welcoming. The compound was able to bind to the viral FcγR and block the formation of ADE by up to 90 per cent. For Bodie, this meant they could potentially prevent the onset of secondary symptoms and possibly reduce the extent of infection.
"We have the ability to block the first step in a rather vicious cascade. With further testing and finally in human clinical trials, we may be able to develop a therapeutic to prevent severe secondary effects," he says.
While Bodie and his team could rest on ICI406, they know Zika is evolving. It's why they are continuing to work on learning more about the virus to stay ahead of the curve. To this end, they are looking to the government as well as the public for help.
One particular avenue is already out on the crowdfunding site, experiment.com. Bodie is hoping to take a closer look at NS1, another protein known to be involved in infection. He hopes to identify any mutations that could open the door to improved therapeutics.
"The virus is continually evolving but we would prefer not to play catch up. We have a therapeutic that works in the lab and hopefully will be available sooner than later. But we need to go on the offensive," he says. "With this type of investigative research sponsored by the public we can work to put Zika behind us so that it doesn't take us by surprise again."
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