Zika Virus: Expert Discussion by Scott Weaver, PhD

Zika Virus: Expert Discussion by Scott Weaver, PhD

May 17, 2016 Karie Youngdahl

Scott C. Weaver, PhD, at The College of Physicians of Philadelphia
Scott C. Weaver, PhD, at The College of Physicians of Philadelphia

We know so little about Zika virus that we can’t even spell it correctly. Scott C. Weaver, MS, PhD, visiting Philadelphia from the University of Texas Medical Branch at Galveston, noted that the forest where Zika virus was discovered in the 1940s is actually spelled Ziika

Weaver brought years of research experience to his talk Monday, May 16, at The College of Physicians of Philadelphia. He is an arbovirus specialist and has worked extensively on Chikungunya virus, and, even before the current Western Hemisphere Zika virus epidemic, on Zika virus itself.

Given that human cases of Zika virus disease were not known until the 1950s and that 80% of Zika cases present with no symptoms, it’s not surprising that we don’t know more about the virus and how it works. Before 2007, only 14 human cases had been diagnosed.

Weaver traced the spread of Zika virus across the globe, showing a CDC map representing incidence of Zika virus antibodies and infection in local populations throughout many African and Asian countries. The virus almost certainly originated in Africa at least a millennium ago; about 50-100 years ago it spread to Asia. In 2007 the virus jumped to Yap Island from Asia, with a population of about 7,000 people, most of whom became infected. Then, in 2013, it moved to French Polynesia, with more than 100,000 people to potentially infect. French Polynesians then started to transport the virus around the world, probably to Brazil in late 2013. With this move to South America, hundreds of millions of people are now susceptible to infection. 

Now, 38 countries in the West have documented local Zika virus transmission. Brazil has had an estimated 1.5 million cases. In the United States, 472 imported cases have been documented, 44 of them in pregnant women. Zika virus is the first mosquito-borne virus shown to be transmitted sexually, and about 10 cases of sexual transmission have occurred in the United States.

Though the harmful effects of Zika virus infection on the fetus have been known only since the disease began to be observed in Brazil in 2015, Weaver is of the mind that the virus has not changed to become more neurotropic. Rather, he thinks that the crucial difference between Zika in Brazil versus French Polynesia or Yap Island is that it finally infected enough people so that rare complications could be detected.

Weaver outlined some interesting and worrying characteristics of Zika virus infection in pregnant women. Despite one study showing that harm to the fetus was rare and that the risk window was mainly in the first trimester of pregnancy, another, larger study demonstrated that damage to the fetus is possible even through late pregnancy, and that the rate of complications is higher than previously thought. What’s more, pregnant women infected with Zika virus have a prolonged viremic period as compared with non-pregnant individuals. They are, therefore, potentially capable of transmitting the disease to mosquitoes for a longer time than other individuals. It’s even possible that this characteristic of infection has fueled the current Western epidemic.

Weaver thinks that the spread of Chikungunya virus is the best model for what’s going to happen with Zika virus in the United States. Chikungunya cases were reported in the Western Hemisphere a few years before reported Zika cases in 2013, and in 2014, 2,811 imported cases of Chikungunya virus disease were reported in the United States. Twelve locally acquired cases were reported in Florida beginning in May of that year. However, U.S. transmission has since ceased, probably because of effective mosquito control measures. Weaver thinks that we may soon be getting to the point where we have enough imported U.S. Zika cases that local transmission might be possible. 

Transmission is most likely to occur, Weaver suggested, in low-income areas where people are at risk from daytime-biting mosquitoes and where there are likely to be viremic travelers returning from Zika-endemic areas. South Texas, which has an abundant population of Aedes aegypti mosquitoes that can spread Zika, is a likely candidate.

The Rio Olympics approach, but Weaver isn’t especially worried about a huge outbreak stemming from that event. He is certainly not concerned enough to advocate cancelling the Olympics, as Amir Attaran recently advocated in the Harvard Public Health Review. So many people have already been infected in Brazil that there may not be enough immunologically naive people to fuel widespread disease.

In the short term, Weaver says that our most effective preventive measure could simply be educating people about avoiding Zika virus infection and preventing Zika virus transmission in the United States. In particular, he thinks pregnant women shouldn’t travel to endemic areas. Moreover, travelers returning from a Zika endemic area should protect themselves from mosquito bites on their return so as to prevent local mosquitoes from acquiring the virus (Weaver notes that even individuals with no apparent illness should consider this measure, as about 80% of Zika virus disease cases are asymptomatic).

In the long term, Weaver thinks we will have a vaccine to prevent Zika virus disease as well as monoclonal antibodies to treat individuals at high risk of harmful side effects. A recombinant or DNA vaccine may be the first vaccine tested and used (see my blog post on this), but ultimately, as with yellow fever vaccine, a live, attenuated vaccine given to young children may be the most effective route to suppressing Zika epidemics.

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