Dr. Aaron Brault, PhD: Sexual Transmission of Zika Through Animal Models

OCTOBER 30, 2017
Jenna Payesko
Dr. Aaron Brault, PhD, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, sat down with MD Magazine to discuss what animal models tell us about sexual transmission of Zika virus and its future.

Can you speak to the current state of Zika?
So compared to 2016, we've seen a pretty dramatic drop in activity of Zika between 2016–2017. Although there are continued cases, the numbers have dropped pretty dramatically. I would anticipate that Zika virus will be maintained in the Western Hemisphere, much like the way we've seen with other recently introduced viruses such as West Nile Virus introduced in 1999, where we see ebbs and flows in terms of the severity of transmission and the intensity of transmission from 1 season to the next. There are a lot of ecological factors that play into whether or not we see transmission and I would assume that Zika will probably be 1 more component in that multitude of viruses that we're seeing that can pop up in different geographic areas and it becomes very difficult to predict where those incidents will actually happen from 1 year to the next.

Do you consider Zika a sexually transmitted infection?

I’d classify Zika as a sexually transmissible infection, but not a sexually transmitted disease. So an STD being, the criteria of which requires sexual transmission to complete the full cycle of the transmission. I think we’ve identified considerable levels of sexual transmission between men and women, but there’s no evidence to suggest that we can see efficient reciprocal transmission from a woman to a man without the involvement of a mosquito to perpetuate transmission. 

Can you speak to the genetic mutation of the virus that causes microcephaly?

There’s a recent paper in Science that has identified mutation in the pre-membrane protein that was genetically identified around the time of the French Polynesian outbreak which is also a time when retrospect of studies have identified microcephaly cases, and then of course as the virus moved into the Western Hemisphere that mutations persisted. In terms of its role in microcephaly, they've demonstrated that in an immune confident mouse model they had a higher incidence of brain involvement and other mediating factors that could result in microcephaly in variance in viral mutants that contain that mutation and a lower level in viruses that didn't have the mutation. Although the data did indicate as well that they're probably other viral genetic factors that are involved in that phenomena, given that the variance that didn't have that mutation, they developed a level of neurological involvement that's consistent with microcephaly. So it's probably the dominant factor in the mouse model and it'll be really intriguing to see if that correlates with what we see going into the future with other potential outbreaks where microcephaly has been associated, because this mutation hasn't been found in African age viruses for a potential multitude of reasons we haven't seen microcephaly, but it might be interesting to see if this mutation emerges again and could be associated with microcephaly with a different lineage or a different genotype of Zika. Then you really question what kind of evolutionary advantage this provides the virus so that the mutation be maintained in the population because in terms of developing microcephaly in a neonate and right now, it's not really obvious how that would perpetuate unless this is just an offshoot, a pathological hangover if you will, for what can happen because that mutation is somehow associated with increased deficiency of transmission of the virus in its normal transmission route.

What do you see as the future for Zika?

Well we've been working with animal models and trying to compare and contrast that to what's going on with humans and 1 of the things that we're really trying to take into the future is what the animal modeling work will actually allow us to infer in human samples. And so, we're working on a number of facets of that in terms of developing longer term persistence models, developing models where we can see ornate persistence in the mice and we can immunosuppress the mice to see if we can get recrudescent infections which is of course another concern that we have. You think of Ebola and its sexual transmission potential, you have men that are RNA positive for an excess of 500 days, and we've seen an excess of 300 days for Zika and under certain conditions if people are immunosuppressed because they go on steroid treatments for a myriad of medical conditions, is it possible we can see recrudescence of infection of sexual transmission long after a man was actually initially infected? Those are big questions that we need to address.

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