When Congress returns from its August recess, it will confront the growing consequences of its inaction on Zika: Since it adjourned in July, more than three dozen cases of locally acquired Zika infection have been reported in Florida. (That brings the total number of confirmed cases in the United States and its territories to nearly 17,000, with most cases in Puerto Rico). The federal government has yet to dedicate any new funds to fighting the virus—no money for prevention, no money for research, no money toward international relief. As of now, the Centers for Disease Control and Prevention has spent $200 million of the $222 million it had borrowed from other programs to respond to Zika. In the context of ongoing debates about the amount and source of new funding, one proposal that the House of Representatives’ Committee on Appropriations will consider would offset the costs of an emergency Zika appropriations bill by cutting $107 million previously dedicated to rebuilding health systems across West Africa in the wake of the recent Ebola epidemic.
This is a shortsighted move that would likely increase the risks of a recurrent Ebola outbreak and imperil the lives of women and children in the region with the world’s highest maternal and child mortality rates. For that reason alone, this is not the path we should pursue.
But there is another reason to reconsider—one that has been overlooked to date: A growing body of evidence suggests the Zika virus is widespread in West Africa, and it may be responsible for an undetected epidemic of microcephaly there.
Until recently, it was widely believed that infection with African strains of Zika never resulted in microcephaly or other serious complications, including stillbirths, vision and hearing problems in newborns, and Guillain-Barré syndrome—a transient paralysis often requiring intensive care—in adults.
Some public health experts argued that given funding shortfalls, no detailed investigations were warranted in Africa because microcephaly had not been reported in association with Zika infection there. That must be because 3.5 percent of the virus’s protein building blocks had changed during evolution from the first strain discovered in Africa to the strain now spreading in Latin America, they suggested, inferring that these changes could have led to greater virulence. But such a conclusion would be premature, as the functional significance of those genetic changes has yet to be specifically investigated.
The relationship between the disease and microcephaly has been established in a host of studies published since May in leading scientific journals including Science, Nature, and Cell. Using human brain stem cells and live mice, investigators across Brazil and the United States have repeatedly demonstrated that the Zika virus can infect and kill large proportions of these cells, sharply decreasing the growth rates of important early brain structures. This research helped international health authorities to confirm that Zika infection during early pregnancy is causally linked to microcephaly and other serious birth defects.
But they overlooked one critical fact: Seven of these studies used a strain known as MR-766. Named for the captive rhesus monkey (No. 766) from which it was first isolated in Uganda’s Zika Forest in 1947, MR-766 is endemic in Africa. The hope that the strains of Zika found in Africa might not cause microcephaly now seems quite unlikely.
How did we get to this point without realizing it? A Brazilian law adopted in May 2015, it turns out, had precluded the sharing of human genetic materials—including blood specimens containing Zika—collected in Brazil with international investigators. Before the law was amended in February, laboratory teams around the globe were therefore forced to work instead with older Zika samples; the most widely available of these was MR-766. None of these teams had explicitly set out to challenge the assumption that African strains could not cause microcephaly, yet taken together, their data reveal that there are likely few major differences between the infectious properties of MR-766 and the Zika strain circulating in Latin America.
We know Zika is widespread across most of Africa: Published studies have reported the presence of antibodies against the virus in 25 of the continent’s 54 countries, including Liberia, Sierra Leone, Nigeria, Senegal, and Mali (where Ebola cases were recorded in 2014 and 2015). Not all of these results are definitive—some of these antibodies could be responding to closely related viruses like dengue and chikungunya, and older tests cannot perfectly distinguish between them. But scientists have specifically isolated the Zika virus from blood samples and mosquitoes in 21 separate studies across the African continent, which is home to 20 species of mosquito capable of carrying Zika.
As a recent genetic sequencing study demonstrated, the world’s first documented cases of Zika in an urban setting occurred not in Rio de Janeiro or in Miami, but in Libreville, the capital of the West African nation of Gabon. What’s more, a study published in 1982 reported a suspected case of mother-to-child transmission of Zika in that country’s rural southeast.
So if African strains of Zika were able to cause microcephaly, why haven’t we heard about it before? Part of the problem is that high infant mortality and weak or absent laboratory systems are the norm in the settings where the virus circulates across the region. Zika is particularly challenging to track because it causes no immediate symptoms in 60–80 percent of those infected. Even in places with more complete health data available, such as French Polynesia, where more than 30,000 people were infected with Zika in 2013, the challenges of detecting rare and unexpected anomalies are clear: Microcephaly was not identified as a possible outcome of infection during pregnancy until much later reviews were performed in 2016 (and might never have been if not for the recent surge in interest in that outbreak).
While no systematic studies of Zika’s effects in Africa have been conducted yet, concerning circumstantial evidence from West Africa warrants careful follow-up. In Guinea-Bissau, a coastal nation between Senegal and Guinea, a 1967 survey found that 1 out of every 9 adolescents across the country had antibodies to Zika. Just Thursday, Guinea-Bissau’s Ministry of Health reported multiple clusters of confirmed Zika cases in the region caused by a West African strain. Five cases of microcephaly in the same areas were also reported, though the results of genetic tests to determine whether these infants were infected with the same strain are still pending.
Two thousand miles away in western Nigeria, nine antibody studies published over the course of three decades have demonstrated extensive human exposure to the Zika virus. Isolation of the virus had been possible in each of the five studies that has attempted it there. As it happens, the only published cohort study of microcephaly among newborns in an African setting was conducted at a maternity hospital in western Nigeria. Of 3,196 full-term, single-birth infants studied, 340 (10.6 percent) were found to be microcephalic by World Health Organization criteria. That’s much higher than anywhere else: A 2016 study in Pernambuco, Brazil’s most-affected state, reported that 0.4 percent of babies were born with microcephaly. These estimates are subject to different biases and are not directly comparable, but the 25-fold difference is striking.
Unfortunately, the world seems to need repeated reminders that the absence of diagnostic capability is not the same as the absence of disease. As the Zika virus’s co-discoverers wrote from Uganda in 1952, “the absence of the recognition of a disease in humans caused by Zika virus does not necessarily mean that the disease is either rare or unimportant.”
After all, it was through these same diagnostic deserts that Ebola smoldered unnoticed for years before exploding across West Africa—where it killed more than 11,000 people—and eventually making its way to the United States. Despite clear warnings from scientists that the virus was circulating in Liberia, Sierra Leone, and Guinea as far back as 1982, nothing was done to combat the risk of an outbreak until the recent epidemic that shook the world.
All of this serves to remind us of something Paul Farmer observed of so-called emerging infectious diseases like Zika 20 years ago: “One place for diseases to hide is among poor people, especially when the poor are socially and medically segregated from those whose deaths might be considered more important.”
Congressional action to mitigate the danger that Zika poses is long overdue. But financing our efforts at home by taking resources from West Africa’s beleaguered health systems would be both shortsighted and unjust. The costs of inaction in either setting are too high to allow such a choice. Efforts to define and then address the consequences of Zika in Africa are a moral and scientific imperative, and in fact likely deserve new funding of their own.
The Zika virus reminds us that microbes and their vectors have little respect for the walls we erect between ourselves. Success against this latest pandemic must mean sustained investments that equip health systems to detect, report, and offer equitable protection against such threats where the risk is greatest—not only where it is most visible.