Zika virus increases risk of dengue disease

doi:10.1126/science.abd5922

GSTDTAP > 气候变化

DOI	10.1126/science.abd5922
	Zika virus increases risk of dengue disease
	Hannah Clapham
	2020-08-28
发表期刊	Science
出版年	2020
英文摘要	The dengue flavivirus (DENV) is a mosquito-borne virus that occurs in more than 100 countries and is known for inducing complex immunity in human infections. The first infection with one of the four DENV serotypes generally has a low risk of severe outcome. Subsequently, it is thought that there is a period of cross-protection in which infection with any serotype results in even lower risk of severe disease. After this period, an infection with a different serotype has a higher risk of severe disease ([ 1 ][1]). In 2015 to 2016, Zika virus (ZIKV, also mosquito-borne) spread rapidly across Central and South America and the Caribbean, where DENV is also endemic ([ 2 ][2]). Because ZIKV is also a flavivirus, whether prior infection with DENV alters Zika disease risk and vice versa became an important question as ZIKV spread. On page 1123 of this issue, Katzelnick et al. ([ 3 ][3]) studied the long-running dengue cohort in Nicaragua and found evidence that prior ZIKV infection increases dengue disease risk. DENV infection can result in a range of outcomes, including asymptomatic, mild flu-like illness and severe dengue, which is characterized by complications of bleeding and organ damage. ZIKV infections are mostly mild, except for a small proportion that result in Guillain-Barre syndrome (autoimmunity to peripheral nerves) or birth defects in infants born to mothers infected during pregnancy. An initial DENV infection generates high levels of serotype cross-reactive neutralizing antibodies. However, these antibodies wane over time and are thought to reach “subneutralizing” levels. The more severe disease in subsequent infections is thought to arise in part from antibody-dependent enhancement, whereby these antibodies are able to bind to, but not neutralize, the virus, which can promote virus cell entry. To study the relationship between prior DENV infections and subsequent dengue outcome, a long-running cohort study is ideal. The cohort study in Managua, Nicaragua, running since 2004, has led to numerous insights into dengue immunity and disease. With the arrival of ZIKV, this study effectively expanded to include ZIKV infections, leading to the findings of Katzelnick et al. For ZIKV infection after a DENV infection, in vitro testing of sera showed that previous DENV infection led to both neutralizing and enhancing responses to ZIKV ([ 4 ][4]). In nonhuman primates, DENV infection did not affect the outcome of subsequent ZIKV infection ([ 5 ][5]). However, population studies showed that previous DENV immunity correlated with lower risk of ZIKV infection ([ 6 ][6]). In the Nicaraguan cohort, there was evidence that previous DENV infection may protect against subsequent symptomatic ZIKV infection. However, there was no relationship with DENV immunity, and no enhancing effect was observed ([ 7 ][7]). Therefore, studies on how DENV infection affects subsequent ZIKV infection outcome have shown varied results. The reasons for this could include differences in the number of prior DENV exposures and serotypes; time between DENV and ZIKV infections; and differences between animal model, in vitro, and human responses. In addition, the range of outcomes for Zika disease is not as wide as for dengue, so differences due to any enhancement could be harder to detect. There are also remaining questions about how prior DENV infection modulates the risk of birth defects to infants born to mothers infected with ZIKV during pregnancy. What about how ZIKV infection modulates subsequent DENV infection outcome? Before the 2015–2016 outbreak, there had been little research on ZIKV and few reported cases, so the long-term impact of ZIKV infection could not be assessed. Initially after the outbreak, it was possible to show that individuals who were exposed to ZIKV generated both neutralizing and enhancing antibodies for DENV ([ 8 ][8]). In nonhuman primates, there was some evidence of enhancement upon infection with DENV a short time after ZIKV infection ([ 9 ][9]). Now, 5 years after the outbreak, it is possible to assess the longer-term effects of ZIKV on subsequent dengue disease risk in humans. A previous modeling study using reported dengue cases from Colombia and Brazil estimated that ZIKV infection led to cross-protection to DENV, resulting in low reported dengue case numbers in the 2 years after the ZIKV outbreak ([ 10 ][10]). This study predicted future higher numbers of dengue cases after this period, which will need to be assessed. The study of Katzelnick et al. similarly shows very low DENV transmission in the 2 years after the ZIKV outbreak. The important aspect of this study is in the assessment of individual disease risk in the 2019 dengue outbreak, the largest on record. During this epidemic, Katzelnick et al. clearly show that on an individual level, there is an increased risk of symptomatic and severe dengue disease in individuals with prior ZIKV immunity. Together, these data show that ZIKV infection modulates the disease severity of subsequent DENV infection in both negative and positive ways, on an individual and population level. This suggests that previous ZIKV infection acts similarly to previous DENV infection. However, there are still unknowns, such as whether risk differs by DENV sero-type and the longer-term impact of ZIKV infection on dengue. Another reason this is an important result is for vaccination. Follow-up of participants in the Dengvaxia vaccine trial showed that dengue-unexposed individuals who were vaccinated showed an increased risk of severe disease in the longer term upon the next DENV infection, similar to individuals experiencing a second natural DENV infection ([ 11 ][11]). Dengvaxia is the only licensed dengue vaccine to date, but there are others in development. For ZIKV, there are also several vaccines currently in development, but none are licensed. It is now important to establish whether dengue vaccine efficacy varies according to previous ZIKV infection. For Dengvaxia, vaccination in the initial trials was before the 2015–2016 ZIKV outbreak. It is also possible that ZIKV vaccination could lead to more severe subsequent DENV infections. It would therefore seem prudent for both DENV and ZIKV vaccine studies to measure immunity to both viruses before and after vaccination and to follow up for both diseases within any trial. Because viral immunity will be changing over time, long-term follow-up will be required. For other flaviviruses, this interaction with vaccination and risk has also been considered, such as for Japanese encephalitis virus and DENV ([ 12 ][12]). Interactions with the yellow fever flavivirus and vaccinations should also be considered in relevant countries. More generally, the cross-reactive properties of viral immunity, how to measure it, how it changes over time, and the impact on disease risk are important for a number of viral infections, and the study of Katzelnick et al. serves as a reminder that issues of cocirculation and cross-immunity should remain in view for understanding transmission dynamics and vaccination. 1. [↵][13]1. W. Dejnirattisai et al ., Science 328, 745 (2010). [OpenUrl][14][Abstract/FREE Full Text][15] 2. [↵][16]WHO, Zika virus and complications: 2016 Public Health Emergency of International Concern; [www.who.int/emergencies/zika-virus-tmp/en/][17]. 3. [↵][18]1. 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领域	气候变化 ; 资源环境
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文献类型	期刊论文
条目标识符	http://119.78.100.173/C666/handle/2XK7JSWQ/293213
专题	气候变化资源环境科学
推荐引用方式 GB/T 7714	Hannah Clapham. Zika virus increases risk of dengue disease[J]. Science,2020.
APA	Hannah Clapham.(2020).Zika virus increases risk of dengue disease.Science.
MLA	Hannah Clapham."Zika virus increases risk of dengue disease".Science (2020).