Abstract
In 2015 and 2016, Zika virus (ZIKV) swept through dengue virus (DENV) endemic areas of Latin America. These viruses are of the same family, share a vector and may interact competitively or synergistically through human immune responses. We examine dengue incidence from Brazil and Colombia before, during, and after the Zika epidemic. We find evidence that dengue incidence was atypically low in 2017 in both countries. We investigate whether subnational Zika incidence is associated with changes in dengue incidence and find mixed results. Using simulations with multiple assumptions of interactions between DENV and ZIKV, we find cross-protection suppresses incidence of dengue following Zika outbreaks and low periods of dengue incidence are followed by resurgence. Our simulations suggest correlations in DENV and ZIKV reproduction numbers could complicate associations between ZIKV incidence and post-ZIKV DENV incidence and that periods of low dengue incidence are followed by large increases in dengue incidence.
Highlights
In 2015 and 2016, Zika virus (ZIKV) swept through dengue virus (DENV) endemic areas of Latin America
We constructed time series of probable case counts for each state in Brazil (1999–2017)[25,33,34] and department in Colombia (2007–2017)[25,35,36]
In models incorporating year effects, we found that biweekly expected dengue incidence in 2015 was higher than that of corresponding biweeks in other years in both Brazil and Colombia
Summary
In 2015 and 2016, Zika virus (ZIKV) swept through dengue virus (DENV) endemic areas of Latin America These viruses are of the same family, share a vector and may interact competitively or synergistically through human immune responses. In 2015 and 2016, Zika virus (ZIKV) swept through many Latin American countries[1] where dengue virus (DENV) is endemic Following this epidemic, many locations appeared to experience abnormally low dengue incidence. DENV and ZIKV share a vector[2,3] and are both flaviviruses Evidence suggests these viruses may interact competitively or synergistically through human immune responses: via antibodies in the case of non-overlapping infections[4,5,6,7,8,9,10] or innate defenses during co-infections[11,12].
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