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\"As the Zika virus continues to spread throughout North America, people need answers. What are the origins of this virus? How does it spread? Should we be concerned? How can we stop the spread of infected mosquitos? With the increasing prevalence of Zika, concrete answers are needed now more than ever - The Zika Prevention Handbook serves as the best reference for readers to stay informed about side-effects and symptoms, and to minimize your chance of contracting the virus. The Zika virus is a mosquito-borne infection that is estimated to have originated in Africa in the mid 1940's. In the last several years, the Zika virus has infected thousands of people around the world and has spread to over 60 countries. As of August 2016, Zika-infected mosquitoes have found a new home, the United States. The Zika virus has been reported in all 50 U.S. states, in addition to hundreds of reported cases throughout Mexico and Canada. With the assistance of infectious disease expert, Laura D. Kramer, PhD, author Alexander Webb has compiled the leading research from the U.S. Centers for Disease Control and Prevention (CDC). Whether you're an expectant mother worried about microcephaly (a side effect of Zika that causes babies to be born with abnormally small heads), planning a vacation to a tropical area, or living in an area where these contagious mosquitoes reside, this book is guaranteed to answer all your questions and ease your fears. Readers will learn about Zika's origins, transmission of the infection, leading prevention techniques, medical testing, symptoms and diagnosis, and much more.\" --Publisher's description.

The introduction of the bacterium Wolbachia (wMel strain) into Aedes aegypti mosquitoes reduces their capacity to transmit dengue and other arboviruses. Evidence of a reduction in dengue case incidence following field releases of wMel-infected Ae. aegypti has been reported previously from a cluster randomised controlled trial in Indonesia, and quasi-experimental studies in Indonesia and northern Australia. Following pilot releases in 2015-2016 and a period of intensive community engagement, deployments of adult wMel-infected Ae. aegypti mosquitoes were conducted in Niterói, Brazil during 2017-2019. Deployments were phased across four release zones, with a total area of 83 km2 and a residential population of approximately 373,000. A quasi-experimental design was used to evaluate the effectiveness of wMel deployments in reducing dengue, chikungunya and Zika incidence. An untreated control zone was pre-defined, which was comparable to the intervention area in historical dengue trends. The wMel intervention effect was estimated by controlled interrupted time series analysis of monthly dengue, chikungunya and Zika case notifications to the public health surveillance system before, during and after releases, from release zones and the control zone. Three years after commencement of releases, wMel introgression into local Ae. aegypti populations was heterogeneous throughout Niterói, reaching a high prevalence (>80%) in the earliest release zone, and more moderate levels (prevalence 40-70%) elsewhere. Despite this spatial heterogeneity in entomological outcomes, the wMel intervention was associated with a 69% reduction in dengue incidence (95% confidence interval 54%, 79%), a 56% reduction in chikungunya incidence (95%CI 16%, 77%) and a 37% reduction in Zika incidence (95%CI 1%, 60%), in the aggregate release area compared with the pre-defined control area. This significant intervention effect on dengue was replicated across all four release zones, and in three of four zones for chikungunya, though not in individual release zones for Zika. We demonstrate that wMel Wolbachia can be successfully introgressed into Ae. aegypti populations in a large and complex urban setting, and that a significant public health benefit from reduced incidence of Aedes-borne disease accrues even where the prevalence of wMel in local mosquito populations is moderate and spatially heterogeneous. These findings are consistent with the results of randomised and non-randomised field trials in Indonesia and northern Australia, and are supportive of the Wolbachia biocontrol method as a multivalent intervention against dengue, chikungunya and Zika.

The global emergence of Zika virus (ZIKV) revealed the unprecedented ability for a mosquito-borne virus to cause congenital birth defects. A puzzling aspect of ZIKV emergence is that all human outbreaks and birth defects to date have been exclusively associated with the Asian ZIKV lineage, despite a growing body of laboratory evidence pointing towards higher transmissibility and pathogenicity of the African ZIKV lineage. Whether this apparent paradox reflects the use of relatively old African ZIKV strains in most laboratory studies is unclear. Here, we experimentally compare seven low-passage ZIKV strains representing the recently circulating viral genetic diversity. We find that recent African ZIKV strains display higher transmissibility in mosquitoes and higher lethality in both adult and fetal mice than their Asian counterparts. We emphasize the high epidemic potential of African ZIKV strains and suggest that they could more easily go unnoticed by public health surveillance systems than Asian strains due to their propensity to cause fetal loss rather than birth defects. Here, the authors compare seven low passage Zika virus (ZIKV) strains representing the recently circulating viral genetic diversity of African and Asian strains and find that African ZIKV strains have higher transmissibility in mosquitoes and higher lethality in both adult and fetal mice.

Zika virus is rapidly spreading throughout the Americas and the Caribbean. The association with microcephaly has led the WHO to declare a public health emergency. This review describes our current understanding of the characteristics of Zika virus infection. In 1947, a study of yellow fever yielded the first isolation of a new virus, from the blood of a sentinel rhesus macaque that had been placed in the Zika Forest of Uganda. 1 Zika virus remained in relative obscurity for nearly 70 years; then, within the span of just 1 year, Zika virus was introduced into Brazil from the Pacific Islands and spread rapidly throughout the Americas. 2 It became the first major infectious disease linked to human birth defects to be discovered in more than half a century and created such global alarm that the World Health Organization (WHO) would . . .

One hundred and ten Zika virus genomes from ten countries and territories involved in the Zika virus epidemic reveal rapid expansion of the epidemic within Brazil and multiple introductions to other regions. Zika epidemiology Three papers in this issue present a wealth of new Zika virus (ZIKV) genome sequences and further insights into the genetic epidemiology of ZIKV. Nathan Grubaugh et al . provide 39 new ZIKV genome sequences from infected patients and Aedes aegypti mosquitoes in Florida. Phylogenetic analysis suggests that the virus has been introduced on multiple separate occasions, probably linked to travel from the Caribbean. They find a low probability of long-term persistence of ZIKV transmission chains within Florida, suggesting that the potential for future ZIKV outbreaks there will depend on transmission dynamics in the Americas. Nuno Faria et al . and Hayden Metsky et al . reconstruct the spread of ZIKV in Brazil and the Americas. Faria et al . provide 54 new ZIKV genomes, several sequenced in real time in a mobile genomics laboratory. They trace the spatial origins and spread of ZIKV in Brazil and the Americas and date the timing of the international spread of ZIKV from Brazil. They find that northeast Brazil had a crucial role in the establishment of the epidemic and the spread of the virus within Brazil and the Americas. Metsky et al . generate 110 ZIKV genomes from clinical and mosquito samples from ten regions. They also see rapid expansion of the epidemic within Brazil and multiple introductions to other geographic areas. In agreement with Faria et al ., they find that ZIKV circulated unobserved for many months before transmission was detected. Metsky et al . additionally describe ZIKV evolution and discuss how the accumulation of mutations might affect the performance of diagnostic tests in the future. Although the recent Zika virus (ZIKV) epidemic in the Americas and its link to birth defects have attracted a great deal of attention 1 , 2 , much remains unknown about ZIKV disease epidemiology and ZIKV evolution, in part owing to a lack of genomic data. Here we address this gap in knowledge by using multiple sequencing approaches to generate 110 ZIKV genomes from clinical and mosquito samples from 10 countries and territories, greatly expanding the observed viral genetic diversity from this outbreak. We analysed the timing and patterns of introductions into distinct geographic regions; our phylogenetic evidence suggests rapid expansion of the outbreak in Brazil and multiple introductions of outbreak strains into Puerto Rico, Honduras, Colombia, other Caribbean islands, and the continental United States. We find that ZIKV circulated undetected in multiple regions for many months before the first locally transmitted cases were confirmed, highlighting the importance of surveillance of viral infections. We identify mutations with possible functional implications for ZIKV biology and pathogenesis, as well as those that might be relevant to the effectiveness of diagnostic tests.

The explosive pandemic of Zika virus infection in South and Central America is the most recent of four unexpected arrivals of important arthropod-borne viral diseases in the Western Hemisphere over the past 20 years. Is this an important new disease-emergence pattern? The explosive pandemic of Zika virus infection occurring throughout South America, Central America, and the Caribbean (see map) and potentially threatening the United States is the most recent of four unexpected arrivals of important arthropod-borne viral diseases in the Western Hemisphere over the past 20 years. It follows dengue, which entered this hemisphere stealthily over decades and then more aggressively in the 1990s; West Nile virus, which emerged in 1999; and chikungunya, which emerged in 2013. Are the successive migrations of these viruses unrelated, or do they reflect important new patterns of disease emergence? Furthermore, are there secondary health consequences . . .

Zika is a mosquito-borne flavivirus that can cause congenital defects, including microcephaly. Although most Zika virus infections are asymptomatic, rash, fever, arthralgia, myalgia, and conjunctivitis can develop in some people. The Guillain–Barré syndrome occurs in 2 to 3 patients per 10,000 with Zika virus infection.

The placenta forms the foremost barrier that protects the developing fetus during pregnancy in eutherian organisms. However, diverse pathogens such as Toxoplasma gondii , rubella virus and cytomegalovirus can breach this barrier. In this Opinion article, Coyne and Lazear review mechanisms of vertical transmission, with a focus on the current Zika virus epidemic. The recent association between Zika virus (ZIKV) infection during pregnancy and fetal microcephaly has led to a renewed interest in the mechanisms by which vertically transmitted microorganisms reach the fetus and cause congenital disease. In this Opinion article, we provide an overview of the structure and cellular composition of the human placenta and of the mechanisms by which traditional 'TORCH' pathogens ( Toxoplasma gondii , other, rubella virus, cytomegalovirus and herpes simplex virus) access the fetal compartment. Based on our current understanding of ZIKV pathogenesis and the developmental defects that are caused by fetal ZIKV infection, ZIKV should be considered a TORCH pathogen and future research and public health measures should be planned and implemented accordingly.