Acute Zika infection is often asymptomatic, though affected individuals commonly present with symptoms including rash, low-grade fever, arthralgias and conjunctivitis. The virus responsible, Zika virus (ZIKV), shares extensive homology with dengue virus (DENV), and throughout the Americas, a precipitous decrease in the number of dengue cases was observed followed widespread Zika epidemics. This suggests that ZIKV infection may induce cross-protective immune responses against DENV. In this prospective cohort study, researchers describe the introduction of ZIKV into the Pediatric Dengue Cohort Study (PDCS) (n=3,893), a long-standing pediatric dengue cohort established in 2004 in Managua, Nicaragua, to establish the incidence of symptomatic and inapparent ZIKV infections from January 1, 2016 to February 28, 2017. Researchers found that over the course of the study period, 560 symptomatic ZIKV infections and 1,356 total ZIKV infections (symptomatic and inapparent) were identified, for an overall incidence of 14.0 symptomatic infections (95% CI 12.9 to 15.2) and 36.5 total infections (95% CI 34.7 to 38.6) per 100 person-years. The incidence of symptomatic and total ZIKV infections was higher in females and older children. In examining the effect of prior DENV infection in 3,027 participants with documented DENV infection histories, 743 (24.5%) had experienced at least 1 prior DENV infection during cohort follow-up. Interestingly, prior DENV infection was inversely associated with the risk of symptomatic ZIKV infection in the total cohort population (IRR 0.63, 95% CI 0.48 to 0.81, p<0.005) as well as with the risk of symptomatic presentation (IRR 0.62, 95% CI 0.44 to 0.86) when adjusted for age, sex, and recent DENV infection. Recent DENV infection was significantly associated with decreased risk of symptomatic ZIKV infection when adjusted for age and sex (IRR 0.57, 95% CI 0.35 to 0.92), but not when adjusted for prior DENV infection (IRR 0.80, 95% CI 0.47 to 1.34). Prior or recent DENV infection did not affect the rate of total ZIKV infections. This study therefore shows that prior DENV infection may be protective against from symptomatic Zika infection. Further studies are needed in addressing possible immunological mechanisms of cross-protection between ZIKV and DENV.
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