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Zika: An Ancient Virus Incipient into New Spaces
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Bennet Angel, Neelam Yadav, Jagriti Narang, Surender Singh Yadav, Annette Angel, Vinod Joshi
In humans, Zika fever first appeared in Nigeria in 1954. Some of the outbreaks were documented in tropical Africa and in South East Asia. The major epidemic with 185 ZIKV cases affected Yap Island of the Federal States of Micronesia. About 108 affected cases were validated by either PCR or serological tests, while 72 cases were suspected. Persons infected with ZIKV showed symptoms such as rashes, fever, arthralgia, and conjunctivitis, but no casualty was reported. In the Yap epidemic, Aedes hensilli was the chief vector for the transmission of ZIKV, and this was the beginning phase of ZIKV infection in the exterior of Africa and Asia (Fig. 6.1). In French Polynesia, the second major outbreak was documented in 2013 (Macnamara, 1954).
Out of Nowhere
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
Meanwhile, in east central South America, Brazil was enjoying a time of relative infectious disease tranquility following the successful anti-mosquito campaigns of the last century. With yellow fever apparently vanquished, those mosquito control programs had been largely dismantled. Infectious disease threat response shifted from building basic public health infrastructure and capacities for prevention as the first line of defense to the use of surveillance to pick up early signals of an outbreak and then mounting an emergency response. It was in this setting that doctors in north-eastern Brazil first began seeing patients with a characteristic disease pattern in the summer of 2014: almost all had the same symptoms of fever, bloodshot eyes, flat, pink, itchy rash, and headache. Dengue was very common in this area and the symptoms were similar, but serological tests excluded dengue as well as chikungunya. Although patients were not severely ill, their numbers were alarming and after investigation, authorities confirmed that the previously unknown disease was an ongoing outbreak of Zika fever, proven by RT-PCR by researchers from Brazil’s Federal University of Bahia in May 2015. Zika had never previously been seen in South America. Local authorities linked the outbreak to the recent increased flow of foreign visitors prompted by a series of sporting events, coupled with the large population of the mosquito vectors, Aedes aegypticus and A. albopictus, that inhabit the region.60
Medical microbiology
Published in Lois N. Magner, Oliver J. Kim, A History of Medicine, 2017
In the 2010s, the virus spread rapidly through Central and South America, especially Brazil. According to Brazilian authorities, close to 9,000 babies with birth defects—primarily microcephaly (abnormally small heads)—attributed to the Zika virus were reported between October 2015 and August 2016. In the previous year, only 150 microcephaly cases had been reported. Babies with this rare condition typically suffer from profound cognitive and developmental problems. It is, of course, possible that sporadic cases of microcephaly in infants occurred before 2007 in isolated areas in Sub-Saharan Africa where high infant mortality rates would have obscured their existence. The panic caused by the initial suggestive reports stimulated intensive research on the possible relationship between Zika virus and birth defects. Zika virus is spread by the Aedes genus of mosquitoes, which includes Aedes aegypti and Aedes albopictus. In previous outbreaks, the virus rarely caused serious symptoms, but a few cases of Zika fever seemed to be associated with Guillain-Barré syndrome (GBS) and researchers suspect that the virus might also affect adult brains.
Defining Zika virus infection in pregnant women
Published in Pathogens and Global Health, 2019
Zika fever is an acute illness clinically similar to other diseases due to mosquito-borne infections caused by flavivirus or alphaviruses circulating in tropical and sub-tropical areas of the Americas, but it may have severe consequences, such as fetal and birth defects in the offspring of infected pregnant women. The most striking feature of Congenital Zika Syndrome (CZS) is microcephaly, which is characterized by a widespread damage to the developing brain as a consequence of a specific tropism of the virus for the neural cortical progenitor cells. It has been estimated that the vertical maternal-fetal transmission rate of Zika virus is 26% and that fetal loss and CZS may occur in 14% and 21% of infected fetuses, respectively [1]. Maternal infection in the first trimester carries the highest risk of CZS, even though CZS can also develop when the mother becomes infected later in pregnancy [2]. For these reasons it is extremely important for both clinicians and epidemiologists to formulate a clear case definition of Zika virus infection in pregnancy, which is not an easy goal, since up to 80% of Zika infections are asymptomatic, and even symptomatic illness is usually mild and characterized by nonspecific clinical manifestations.
The new European invader Aedes (Finlaya) koreicus: a potential vector of chikungunya virus
Published in Pathogens and Global Health, 2018
Silvia Ciocchetta, Natalie A. Prow, Jonathan M. Darbro, Francesca D. Frentiu, Sandro Savino, Fabrizio Montarsi, Gioia Capelli, John G. Aaskov, Gregor J. Devine
Globalization of trade and travel often results in the introduction of new species into non-native territories [1–4]. Arthropod-borne virus (arbovirus) outbreaks of public health significance have occurred as a consequence [5–12]. In 2012, an Aedes aegypti population that had established in Madeira (Portugal) in 2004 [13,14] was responsible for the largest outbreak of dengue in Europe since 1928 [15]. More than 2000 cases were recorded [16] (Figure 1). Similarly, the continuing expansion of Aedes albopictus and Ae. aegypti [17–19] might aggravate the ongoing pandemic of Zika fever through South and Central America and the Caribbean [20]. A mutation in the chikungunya virus (CHIKV) that facilitates enhanced transmission by Ae. albopictus was introduced from India to Ravenna Province, Italy in 2007. The local presence of Ae. albopictus set off an epidemic of over 200 human cases [9]. The establishment of Ae. albopictus across southern Europe has also led to autochthonous outbreaks of dengue and chikungunya in France in 2010 and 2014 (Figure 1). Further chikungunya outbreaks were reported in France and Italy during 2017 [10–12]. In recent years, a new invader: Aedes koreicus has entered Europe, with the largest populations found in Italy [21–24].
Salivary extracellular vesicles inhibit Zika virus but not SARS-CoV-2 infection
Published in Journal of Extracellular Vesicles, 2020
Carina Conzelmann, Rüdiger Groß, Min Zou, Franziska Krüger, André Görgens, Manuela O Gustafsson, Samir El Andaloussi, Jan Münch, Janis A. Müller
Over the last 12 years, Zika virus (ZIKV) re-emerged and caused several epidemics in the Americas [1]. Infection with ZIKV remains asymptomatic, manifests as self-resolving Zika fever [2], or results in severe diseases like Guillain-Barré syndrome, a neurological disorder that can be fatal [3,4]. Devastatingly, ZIKV infection during pregnancy can induce teratogenic effects, including foetal death, microcephaly [5], and congenital complications that may impair future neurodevelopmental function [6]. Until now, no vaccine nor drugs are available, thus ZIKV poses a risk especially for pregnant women. ZIKV is mainly spread via the Aedes aegypti and albopictus mosquitos and transmissions have been recorded in 87 countries and territories [7] and still occur in different regions [8,9]. Independent of mosquitos, ZIKV can be transmitted via body fluids [10]. In infected individuals, the virus has been detected in plasma, cerebrospinal fluid, amniotic fluid, urine, semen, vaginal excretions, breast milk, and saliva [10,11]. Transmissions via some of these body fluids, i.e. during blood transfusion [10,12], intrauterine [10,13], sexual intercourse [10,14–16] or breastfeeding [17] have been recorded. Even though there is no evidence at present that ZIKV can be transmitted through saliva, i.e. during deep kissing [18–20], this route of transmission cannot be excluded as there have been cases of unresolved human-to-human non-sexual transmissions [21,22]. ZIKV RNA is regularly detected in saliva [10,11,23–28] which might be relevant for diagnostic purposes as RNA levels are as high as up to ~106 per ml [24] and remain detectable up to 91 days [25]. Importantly, infectious virus has been isolated from saliva [24,28] suggesting that this body fluid represents a potential source of viral transmission. Animal studies confirmed that ZIKV is present in saliva and suggested that rhesus macaque saliva may contain anti-ZIKV activity [29]. In addition, rhesus macaques that were repeatedly challenged with saliva from ZIKV-positive animals remained uninfected [29], suggesting a low risk of oral mucosal transmission. As human saliva was previously reported to contain antimicrobial and antiviral activity [30] we here analysed the effect of human saliva on ZIKV infection. We found that saliva inhibits ZIKV infection by preventing ZIKV attachment to target cells. The responsible factors are extracellular vesicles (EVs) that are highly abundant in saliva and compete with ZIKV for cellular interaction, representing a novel antiviral defence mechanism. Intriguingly, we found that the currently pandemic SARS-CoV-2 is not inhibited by either saliva or purified salivary EVs, matching its dominant mode of transmission by saliva-containing respiratory droplets.