Prevalence of asymptomatic Zika virus infection: a systematic review

Haby, Michelle M.; Pinart, Mariona; Elías, Vanessa; Revéiz, Ludovic

doi:10.2471/blt.17.201541

Cited by 125 publications

(108 citation statements)

References 65 publications

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“…In many infectious diseases, asymptomatic infection plays a critical role in determining the end of epidemic. For example, Zika virus infection involves 80% of asymptomatic infections ( Haby et al, 2018 ). To objectively determine the end of outbreak, the generation time, i.e.…”

Section: Discussionmentioning

confidence: 99%

Sexual transmission and the probability of an end of the Ebola virus disease epidemic

Lee

Nishiura

2019

Journal of Theoretical Biology

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a b s t r a c tThe criteria of zero Ebola cases defined by the World Health Organization did not explicitly account for the sexual transmission and led to multiple recrudescent events in West Africa from 2015 to 2016, partly indeed caused by sexual transmission from survivors. We devised a statistical model to compute the probability of the end of an Ebola virus disease epidemic, accounting for sexual transmission and underascertainment of cases. Analyzing the empirical data in Guinea, Liberia and Sierra Leone, the performance of the proposed model was compared with the existing criteria comprising a fixed waiting time of 42 days since the last case testing negative or burial. We showed that the waiting time can vary depending on the sexual behaviors of survivors and their adherence to refraining from unprotected sex is likely one of the key factors in determining the absence of additional cases after declaration. If the proportional weight of sexual transmission among all secondary transmission events was substantial, ascertaining the end could even require waiting 1 year from the purported last case. While our proposed method offers an objectively interpretable probability of the end of an epidemic, it highlights that the computation requires a good knowledge of sexual contact.

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Section: Discussionmentioning

confidence: 99%

Sexual transmission and the probability of an end of the Ebola virus disease epidemic

Lee

Nishiura

2019

Journal of Theoretical Biology

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“…Primary and secondary DENV infections in macaques are largely subclinical while in humans, approximately 25% of DENV infections are estimated to be symptomatic (55). Likewise, based on a meta-analysis that included 23 epidemiological studies by Haby et al in June of 2018, approximately 60% of human ZIKV infections are estimated to be symptomatic while most macaques show no signs of infection (24–30, 56). This suggests that findings in macaques may not entirely recapitulate disease observed in humans for either DENV, ZIKV, or sequential infections with both.…”

Section: Discussionmentioning

confidence: 99%

Primary infection with dengue or Zika virus does not affect the severity of heterologous secondary infection in macaques

Breitbach

Newman

Dudley

et al. 2019

Preprint

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33Zika virus (ZIKV) and dengue virus (DENV) are genetically and antigenically related 34 flaviviruses that now co-circulate in much of the tropical and subtropical world. The rapid 35 emergence of ZIKV in the Americas in 2015 and 2016, and its recent associations with 36 Guillain-Barré syndrome, birth defects, and fetal loss have led to the hypothesis that 37 DENV infection induces cross-reactive antibodies that influence the severity of 38 secondary ZIKV infections. It has also been proposed that pre-existing ZIKV immunity 39 3 could affect DENV pathogenesis. We examined outcomes of secondary ZIKV infections 40 in three rhesus and fifteen cynomolgus macaques, as well as secondary DENV-2 41 infections in three additional rhesus macaques up to a year post-primary ZIKV infection. 42 Although cross-binding antibodies were detected prior to secondary infection for all 43 animals and cross-neutralizing antibodies were detected for some animals, previous 44 DENV or ZIKV infection had no apparent effect on the clinical course of heterotypic 45 secondary infections in these animals. All animals had asymptomatic infections and, 46 when compared to controls, did not have significantly perturbed hematological 47 parameters. Rhesus macaques infected with DENV-2 approximately one year after 48 primary ZIKV infection had higher vRNA loads in plasma when compared with serum 49 vRNA loads from ZIKV-naive animals infected with DENV-2, but a differential effect of 50 sample type could not be ruled out. In cynomolgus macaques, the serotype of primary 51 DENV infection did not affect the outcome of secondary ZIKV infection. 52 53 Author summary 54 Pre-existing immunity to one of the four DENV serotypes is known to increase the risk 55 of severe disease upon secondary infection with a different serotype. Due to the 56 antigenic similarities between ZIKV and DENV, it has been proposed that these viruses 57 could interact in a similar fashion. Data from in vitro experiments and murine models 58 suggests that pre-existing immunity to one virus could either enhance or protect against 59 infection with the other. These somewhat contradictory findings highlight the need for 60 immune competent animal models for understanding the role of cross-reactive 61 4 antibodies in flavivirus pathogenesis. We examined secondary ZIKV or DENV infections 62 in rhesus and cynomolgus macaques that had previously been infected with the other 63 virus. We assessed the outcomes of secondary ZIKV or DENV infections by quantifying 64 vRNA loads, clinical and laboratory parameters, body temperature, and weight for each 65 cohort of animals and compared them with control animals. These comparisons 66 demonstrated that within a year of primary infection, secondary infections with either 67 ZIKV or DENV were similar to primary infections and were not associated with 68 enhancement or reduction in severity of disease based on the outcomes that we 69 assessed. 70 71 126 an effective vaccine for ZIKV, as well as the introduction of a tetravalent DENV va...

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“…This combination of low observation and high attack rates suggest great potential for asymptomatic infected individuals to transmit the virus. Indeed, Zika, as has dengue, has been shown to have a high proportion of asymptomatic cases (Haby et al, 2018;Ladhani et al, 2016), although it is not yet clear whether asymptomatic and symptomatic individuals have the same transmission potential (Duong et al, 2015;Moghadas et al, 2017;ten Bosch et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Inferring the ecological drivers of arboviral outbreaks

Tennant

McKinley

Recker

2019

Preprint

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The emergence and wide-spread circulation of mosquito-transmitted viral diseases, such as dengue, Zika and Chikungunya, is a global public health concern. In the absence of effective vaccines, current control measures are mostly targeted against the mosquito vector and have so far only shown limited success. The reliance on mosquitoes for transmission also imposes strong ecological constraints that can introduce significant spatial and temporal variations in disease incidence. However, the way that epidemiological and ecological factors interact and determine population-level disease dynamics is only partially understood. Here we fit a spatially-explicit individual based model defined within a Bayesian framework to Zika incidence data from Feira de Santana, allowing us to more precisely quantify the relationships between socioecological factors and arboviral outbreaks. Our results further demonstrated that the virus was likely introduced into multiple spatially segregated locations at the start of the outbreak, highlighting the benefits that spatio-temporal incidence data would bring in making modelling approaches more realistic for public health planning.where t is the individual's age in days, L is the location parameter of where infant and adult mortality coincide, {a H , b H } and {c H , d H } are the shape and scale parameters of infant and adult human mortality, respectively, and {c V , d V } are the shape and scale parameters of adult mosquito mortality, respectively.An arbovirus was introduced into the system by allowing every human individual to be either susceptible (S H ), exposed (E H ), infectious (I H ), or have recovered from (R H ) the disease. Similarly, individual mosquitoes were either susceptible (S V ), exposed (E V ) or infectious (I V ) with the virus. Mosquitoes bit at a constant rate β and infectious mosquitoes transmitted the virus with probability p H . Infected humans became infectious after 1/ H days and recovered after 1/γ days. Mosquitoes were then infected with probability p V given a bite on an infectious human, and became infectious after 1/ V days. To account for the introduction of the disease into the system, humans were also infected at an external infection rate, ι.We modelled the influence of temperature, humidity and rainfall on these transmission parameters similarly to Lourenço et al. (2017).

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Prevalence of asymptomatic Zika virus infection: a systematic review

Cited by 125 publications

References 65 publications

Sexual transmission and the probability of an end of the Ebola virus disease epidemic

Sexual transmission and the probability of an end of the Ebola virus disease epidemic

Primary infection with dengue or Zika virus does not affect the severity of heterologous secondary infection in macaques

Inferring the ecological drivers of arboviral outbreaks

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