Zika virus (ZIKV) is an emerging arthropod-borne virus (arbovirus) belonging to the family Flaviviridae and genus Flavivirus. ZIKV was first isolated from a monkey in the Zika forest of Uganda in 1947 [ 1 x 1 Kirya, BG. A yellow fever epizootic in Zika Forest, Uganda, during 1972: Part 1: virus isolation and sentinel monkeys. Trans R Soc Trop Med Hyg. 1977; 71: 254–260 Abstract | Full Text PDF | PubMed | Scopus (23) | Google Scholar See all References 1 ].

Between October 2013 and April 2014, more than 30,000 cases of Zika virus (ZIKV) disease were estimated to have attended healthcare facilities in French Polynesia. ZIKV has also been reported in Africa and Asia, and in 2015 the virus spread to South America and the Caribbean. Infection with ZIKV has been associated with neurological complications including Guillain-Barré Syndrome (GBS) and microcephaly, which led the World Health Organization to declare a Public Health Emergency of International Concern in February 2015. To better understand the transmission dynamics of ZIKV, we used a mathematical model to examine the 2013–14 outbreak on the six major archipelagos of French Polynesia. Our median estimates for the basic reproduction number ranged from 2.6–4.8, with an estimated 11.5% (95% CI: 7.32–17.9%) of total infections reported. As a result, we estimated that 94% (95% CI: 91–97%) of the total population of the six archipelagos were infected during the outbreak. Based on the demography of French Polynesia, our results imply that if ZIKV infection provides complete protection against future infection, it would take 12–20 years before there are a sufficient number of susceptible individuals for ZIKV to re-emerge, which is on the same timescale as the circulation of dengue virus serotypes in the region. Our analysis suggests that ZIKV may exhibit similar dynamics to dengue virus in island populations, with transmission characterized by large, sporadic outbreaks with a high proportion of asymptomatic or unreported cases. Since the first reported major outbreak of Zika virus disease in Micronesia in 2007, the virus has caused outbreaks throughout the Pacific and South America. Transmitted by the Aedes genus of mosquitoes, the virus has been linked to possible neurological complications including Guillain-Barré Syndrome and microcephaly. To improve our understanding of the transmission dynamics of Zika virus in island populations, we analysed the 2013–14 outbreak on the six major archipelagos of French Polynesia. We found evidence that Zika virus infected the majority of the population, but only around 12% of total infections on the archipelagos were reported as cases. If infection with Zika virus generates lifelong immunity, we estimate that it would take at least 12–20 years before there are enough susceptible people for the virus to re-emerge. Our results suggest that Zika virus could exhibit similar dynamics to dengue virus in the Pacific, producing large but sporadic outbreaks in small island populations.

The successful development of several coronavirus disease 2019 (COVID-19) vaccines has substantially reduced morbidity and mortality in regions of the world where the vaccines have been deployed. However, in the wake of the emergence of viral variants that are able to evade vaccine-induced neutralizing antibodies, real-world vaccine efficacy has begun to show differences across the two approved mRNA platforms, BNT162b2 and mRNA-1273; these findings suggest that subtle variation in immune responses induced by the BNT162b2 and mRNA-1273 vaccines may confer differential protection. Given our emerging appreciation for the importance of additional antibody functions beyond neutralization, we profiled the postboost binding and functional capacity of humoral immune responses induced by the BNT162b2 and mRNA-1273 vaccines in a cohort of hospital staff. Both vaccines induced robust humoral immune responses to wild-type severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and to variants of concern. However, differences emerged across epitope-specific responses, with higher concentrations of receptor binding domain (RBD)– and N-terminal domain–specific IgA observed in recipients of mRNA-1273. Antibodies eliciting neutrophil phagocytosis and natural killer cell activation were also increased in mRNA-1273 vaccine recipients as compared to BNT162b2 recipients. RBD-specific antibody depletion highlighted the different roles of non–RBD-specific antibody effector functions induced across the mRNA vaccines. These data provide insights into potential differences in protective immunity conferred by these vaccines.