Zika Virus: From Obscurity to Potentially Devastating International Threat

Le résumé fourni par la source

In the fall of 2015, an epidemic of microcephaly in newborn infants was reported in Brazil. Zika virus (ZIKV),5 a previously obscure arthropod-borne flavivirus in Africa transmitted by the Aedes aegypti mosquito, was identified as the suspected etiology. As pictures of severely affected infants began to appear in the news, the virus spread to additional countries in the Western hemisphere, and alarm grew. Travel alerts were issued and in some areas women were advised to defer pregnancy. Within a few months, the link of ZIKV infection to microcephaly was confirmed, and new information began and continues to emerge at a rapid pace. ZIKV is unique for an arbovirus, not only for its devastating outcomes in the fetus, but also for its potential for sexual transmission. Furthermore, it has become apparent that obtaining a rapid and accurate ZIKV diagnosis can be challenging. The public health, medical, and research communities are working with great focus and urgency to better understand transmission, pathogenesis, and outcome, to accurately diagnose, and to ultimately prevent human infections. Three experts currently involved in the response to ZIKV have taken the time to share their knowledge and their insights on what we have learned to date, even as the epidemic continues to unfold. ZIKV was first discovered in primates in the Zika Forest of Uganda in 1947. What changed to facilitate the recent explosive spread in humans? Laura Kramer: Intercontinental air travel, globalization, and urbanization facilitate spread of viruses and vectors to distant places. Furthermore, global warming and climate change are redefining the geographical distributions of mosquito vectors. In 2007, ZIKV spread from Africa and Southeast Asia to cause the first large outbreak in humans on the Pacific island of Yap, in the Federated States of Micronesia. Before this event, no outbreaks and only 14 cases of Zika disease in humans had been documented worldwide. Although wind-blown mosquitoes can travel distances of several hundred kilometers over open ocean, introduction of ZIKV by travel or trade from Southeast Asia, involving an infected person or mosquito, is considered the most likely source of the 2007 Yap outbreak. Lack of population immunity likely contributed. Nonetheless, previous outbreaks of infection may have been missed due to the clinical similarities of mild illness associated with ZIKV, dengue virus (DENV), and chikungunya virus (CHIKV) infections, and the frequent cocirculation of all 3 arboviruses. After Yap Island, ZIKV spread to French Polynesia in 2013, and then to other Pacific Islands in 2013–2014. ZIKV may have been introduced into Brazil in 2013 during the Confederations Cup Soccer Tournament or 2014 during the Va'a canoe race. During both events, teams from French Polynesia and other Zika-endemic Pacific island countries competed. Alternatively, Zika may have been introduced during the 2014 World Cup Soccer Match. Nikolaos Vasilakis: We really do not know the underlying reasons for the observed global spread of ZIKV. However, there are a number of hypotheses that research groups are currently exploring. These include: (i) ZIKV underwent adaptive evolution to enhance infectivity of urban Aedes species vectors (such as, Aedes aegypti or A. albopictus), as recently occurred with CHIKV; (ii) ZIKV underwent adaptive evolution in the human host, leading to higher levels of viremia which would enhance both transmission by the biting mosquitoes and the risk of transplacental fetal transmission; (iii) ZIKV circulation in Asia or Africa resulted in relatively stable levels of human herd immunity that limited the potential for recognized outbreaks; and lastly (iv) the introduction of ZIKV into naïve populations in the South Pacific was stochastic and allowed for sufficient levels of amplification to facilitate the introduction into Brazil fueled by increased global travel, expansion of tropical cities, and susceptible Aedes mosquito populations. DENV and CHIKV viruses are transmitted by the same A. aegypti mosquito vector as ZIKV and so far have had minimal transmission in the continental US. Are there reasons to think Zika will be different? Albert Ko: Our best guess is that ZIKV will behave similarly to the other Aedes-transmitted viruses, where the risk of focal autochthonous transmission occurs in regions such as the Texas–Mexico border and southern parts of Florida. However, there are some important caveats. We do not have a clear understanding of the vectorial capacity, the rate of new ZIKV infections that an Aedes mosquito can generate after biting an infected individual, especially for A. albopictus, which has a wider distribution within the continental US. Moreover, introduction of the virus at the right place and time, such as during our summer months, may potentially produce a larger impact than what is predicted. Nikolaos Vasilakis: In the context of continental US, socioeconomic factors would play an important role in limiting the extent and breadth of mosquito transmission. For example, the extensive use of window and door screens and air conditioning, piped water infrastructure, and good drainage significantly reduces available breeding and resting habitats for these mosquitoes. To maintain the likelihood of minimal transmission, vector control and surveillance programs at the federal, state, and community level must continue to enjoy sustainable long-term financial and logistical support. Laura Kramer: Since 1980, locally acquired US cases of DENV have been confirmed along the Texas–Mexico border, associated with large outbreaks in neighboring Mexican cities. Limited mosquito-transmitted DENV was detected in Key West, Florida, in 2009 and 2010, with single isolated reported cases in other Florida counties in 2010 and 2011, demonstrating the potential in this state. In 2014, 12 locally transmitted CHIKV cases were reported from Florida, and in 2016, one local CHIKV case in Texas. All other CHIKV cases have occurred in travelers returning from affected areas. It is unlikely ZIKV transmission by A. aegypti and A. albopictus will be different from DENV and CHIKV in the US. Most likely, there will be focal flare-ups of infection, which may go unnoticed since 80% of ZIKV cases are asymptomatic. But once introduced, there may be ZIKV sexual transmission between partners without mosquitoes being involved. Recently, probable ZIKV transmission by oral sex has also been reported. Of all arboviruses, sexual transmission is unique to ZIKV and may be contributing to current outbreaks. Clearly, the greatest concern for ZIKV is infection in pregnant women. What have we learned so far regarding risk factors for congenital infection and the spectrum of disease in the infant? Albert Ko: The CDC and the WHO have concluded that ZIKV causes congenital birth defects, including microcephaly. However, we are still uncertain about how large the risk actually is. A small prospective study from Brazil identified severe fetal outcomes among 29% of women who acquired symptomatic ZIKV infection during pregnancy. In contrast, a retrospective study of microcephaly after the outbreak in French Polynesia estimated that microcephaly occurred in roughly 1% of the newborns of women infected during pregnancy. Furthermore, important questions remain unanswered with respect to which period and what type of exposure, symptomatic vs asymptomatic infection, during gestation impart the greatest risk to the fetus. Microcephaly is usually a severe “tip-of-the-iceberg” manifestation for most congenital infections. Case reports have identified central nervous system and ophthalmological lesions in newborn infants who were exposed to ZIKV during gestation but did not develop microcephaly. Yet at present, we do not know the disease burden attributable to congenital ZIKV infection that may be uncovered once infants without microcephaly are systematically investigated. Nikolaos Vasilakis: We have lea

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