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Herd Immunity: Keeping Zika at Bay, For Now

Amesh A. Adalja, MD, FACP, FACEP, FIDSA, November 17, 2017

In 2015 it was discovered that the Zika virus was circulating in the Western Hemisphere. It was characterized by a high burden of infection and confirmation of the virus’s capacities to cause both a devastating congenital infection syndrome and Guillain-Barré syndrome, and to persist in semen for a long time. Since then, Zika infection rates appear to have ebbed, and a new study published in mBio reveals that Zika’s extraordinary trajectory in nations like Brazil may explain its diminished ability to cause new infections.1

 

Population Immunity

In this study, Netto and colleagues conducted serosurveys on 910 individuals from Salvador, Brazil, using ELISA and confirmatory PRNT assays. Several different subpopulations were studied in order to ascertain specific associations: women who gave birth during the outbreak, neonates born during the outbreak, more than 500 HIV-positive individuals (in order to compare serologies from prior pre-outbreak blood samples), and tuberculosis patients and university workers, to determine if socioeconomic status had any association.1

The most significant aspect of this study is the determination of temporal spread of the virus, evidenced via the stored blood samples from HIV-positive patients. Also, socioeconomic status, using tuberculosis as a surrogate for a lower status, tracked with higher Zika seroprevalence.1

Not surprisingly, women with microcephalic neonates were statistically more likely to be positive for Zika. In 2013, Zika seroprevalence was just 4.2%, but by 2016 it had climbed to 58.8%.1

Pooling all individuals sampled, seroprevalance was estimated to be approximately 63%, with similar prevalence rates in all age and gender cohorts studied. This level of herd immunity basically quenched the outbreak in Salvador. Interestingly, chikungunya--another Aedes-spread arbovirus that made a recent appearance in Brazil--maintained a low relative seroprevalence rate (7.4%) when compared to Zika.1

The authors also looked at cases of Zika-like rashes from Salvador that had been reported in surveillance programs from 2016 and determined a low rate of Zika PCR or serological positivity. This lack of new Zika cases in Salvador was attributed to the high level of population immunity that developed pre-2016. Applying modeling techniques to the data, an R0 of 2.1 was computed for the height of the outbreak in Salvador, which occurred in 2015. Subsequently, the R0 fell because population immunity delimited new infections.1

 

Potential Vulnerabilities Until Vaccine Is Available

While the study by Netto et al provides evidence of the ability of herd immunity in Salvador to keep the virus at bay, which provides a respite for many areas affected by Zika, it is not universal, and many areas of the world in which Aedes mosquitoes flourish remain at risk. Some vaccines that are being developed have progressed successfully through phase I and into phase II,2,3 but until they are fully developed with each year, as new individuals are born naïve to the virus, the susceptibility of populations will increase. Lastly, a mutation--which was likely responsible for the predilection for microcephaly4--could promote immune evasion.

 

References

  1. Netto EM, Moreiro-Seto A, Pedroso C, et al. High Zika virus seroprevalence in Salvador, northeastern Brazil limits the potential for further outbreaks. mBio 2017;8(6). http://mbio.asm.org/content/8/6/e01390-17.full. Accessed November 16, 2017.
  2. Tebas P, Roberts CC, Muthamani K, et al. Safety and immunogenicity of an anti-Zika virus DNA vaccine--prelimanry report. N Engl J Med 2017. http://www.nejm.org/doi/full/10.1056/NEJMoa1708120#t=article. Accessed November 16, 2017.
  3. National Institutes of Health. Phase 2 Zika vaccine trial begins in U.S., Central and South America [news release]. NIH website. March 31, 2017. https://www.nih.gov/news-events/news-releases/phase-2-zika-vaccine-trial-begins-us-central-south-america. Accessed November 16, 2017.
  4. Yuan L, Huang XY, Liu ZY, et al. A single mutation in the prM protein of Zika virus contributes to fetal microcephaly. Science 2017. http://science.sciencemag.org/content/early/2017/09/27/science.aam7120/tab-pdf. Accessed November 16, 2017.