This article is more than 5 years old. Information may no longer be current.
Q&A: Zika mutation could explain epidemic severity
A recent paper published in Nature found that a spontaneous mutation that developed in the protein of the Zika virus promotes virus infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent epidemics. These results could shed some new light on how Zika virus rapidly and explosively spread in the Americas, and provide clinicians with new information on mosquito-borne viruses that they can use to improve prevention efforts for future outbreaks and combat infectious disease.
To explain the findings as well as discuss the latest information on Zika and other flavivirus, Infectious Disease News spoke with senior author Pei-Yong Shi, MD, I.H. Kempner professor of human genetics in the department of biochemistry and molecular biology at the University of Texas Medical Branch, and Nikos Vasilakis, PhD, professor in the department of pathology and member of the Center for Biodefense and Emerging Infectious Diseases.
Your recent paper in Nature explains how a spontaneous mutation caused Zika virus to become more infectious, which could have facilitated transmission during the recent epidemic in the Americas. Why has the virulence of Zika virus increased (ie, its ability to cause congenital Zika syndrome and Guillain-Barré syndrome)?
Shi: Our recent Nature paper has provided one possible explanation for why Zika virus has become explosive in epidemics. We showed that one mutation in the virus can enhance its ability to infect mosquitoes, which might lead to higher transmission in humans. However, the same mutation does not necessarily account for the increased diseases in human such as congenital Zika syndrome. We are currently investigating if other mutations in the epidemic strains of Zika virus are responsible for the enhanced diseases in humans.
Brazil is experiencing much higher rates of Zika-related birth defects compared with other countries affected by the epidemic. Why is that?
Vasilakis: We really do not know the answer to that. Several hypotheses have been suggested, like previous exposure to a related flavivirus (eg, dengue or yellow fever); environmental factors (eg, exposure to pesticides); the role of the host genome and so on. The first hypothesis is controversial and suggests that previous exposure to a related flavivirus primes the immune system to exacerbate the disease of the subsequent infection (eg, Zika). Although this may be the case with sequential infectious to various dengue serotypes, recent evidence in a human cohort from Brazil or in nonhuman primates suggest that this may not be the case. The second hypothesis is equally controversial, and to date, there are no data to support such claim. It will take a while through controlled human cohorts to decipher the reason for such observation, and in reality, we may never know as the Zika outbreak has subsided in the region.
Health officials in Puerto Rico recently announced that the Zika outbreak had ended there . What are the implications of their announcement?
Vasilakis: Arbovirus outbreaks in an immunological naive population follows a classic bell curve (introduction, expansion, dying out). What this tells you is that herd immunity was achieved, which is the main driver for outbreak cessation (along with vector control measures, vaccination drives and so on). However, that is no reason to lay back and rest. Surveillance and vector control programs should continue to be in place to be able to monitor circulation. As we know from previous outbreaks (eg, West Nile, chikungunya and others), outbreaks can pop up any time because herd immunity wanes and vector control programs are rolled back or eliminated.
Zika has dominated the headlines for some time. What are other vector-borne diseases that clinicians should be more aware of and why?
Vasilakis: Certainly chikungunya, dengue and yellow fever pose a threat because they are constantly re-emerging. All these diseases, and certainly the latter two, have a rich history of being a scourge here in the continental U.S. Although they were eradicated in the past 100 years (in the U.S.), dengue reappeared in the U.S. 10 years ago, and yellow fever is currently raging in Africa and South America. It is a matter of time when these diseases may re-establish sustained autochthonous transmission cycles here, an event that will be disastrous for public health. For chikungunya virus, there is no licensed vaccine; for dengue, there is a licensed vaccine, but its efficacy is not optimal; and for yellow fever virus, there is a global shortage of the vaccine, and it may take years to establish adequate stockpiles.
References:
Liu Y, et al. Nature. 2017;doi:10.1038/nature22365.
Pantoja P, et al. Nat Commun. 2017;doi:10.1038/ncomms15674.
Terzian ACB, et al. Clin Infect Dis. 2017;doi:10.1093/cid/cix558.
Disclosures: Vasilakis is a consultant for Newlink/Bioprotection Systems. Shi reports no relevant financial disclosures.