According to the Statutes of the European Society for Virology, the election to the Advisory Council of the European Society for Virology should take place this year.

As a first step, the list of candidates has to be set up. Each full member of the Society is eligible for service on the Society’s Advisory Council and therefore can run as a candidate.

All full members are therefore invited to let us know if they are willing to run as a candidate for the election to the Advisory Council by writing an e-mail to info@eusv.eu  by May 15, 2016.

Please note that only candidates who have expressed their willingness until May 15 can be put on the ballot list.

According to the Statutes of the European Society for Virology, the Advisory Council consists of 12 elected regular members of the Society and the chairmen of the committees. They participate in meetings of the Executive Board in an advisory capacity. The elected members serve for a term of three years. A place on the Advisory Council also ends upon termination of membership in the Society.

The pre-election will be held electronically from June 20 to July 03, 2016. Those 12 candidates are elected who have received the most number of votes and who accept. In case of an equality of votes for position 12, all candidates with the same number of votes are considered to be elected. The results of the pre-elections will be reconciled in the Final Elections in the course of the Assembly of Members during the 6^th European Congress of Virology in Hamburg, Germany in October 2016.

The 6th European Congress of Virology (ECV2016) is taking shape!

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Three years have passed since ESV’s last elections were held in 2013. This year, it’s election year again, and all full and corporate members of the Society will be asked to elect the representatives of the Executive Board and the Advisory Council for the next term of office. Pre-Elections will be conducted electronically in the period from April to October 2016. Final elections will be held in the course of the Assembly of Members during the 6^th European Congress of Virology in Hamburg in October 2016.

Dates and Procedures of the Elections 2016 – Overview

Members eligible to vote will be informed electronically. We hope for an active voter participation.

Ab Osterhaus and Leslie Reperant, ‘Artemis One Health’ Utrecht, The Netherlands and ‘RIZ’, Hannover, Germany

Complex relationships between the human and animal species have never ceased to evolve since the emergence of the human species and have resulted in a human-animal interface that has promoted the cross-species transmission, emergence and eventual evolution of a plethora of infectious pathogens. Remarkably, most of the characteristics of the human-animal interface -as we know it today- have been established long before the end of our species pre-historical development took place, to be relentlessly shaped throughout the history of our species. More recently, changes affecting the modern human population worldwide as well as their dramatic impact on the global environment have taken domestication, agriculture, urbanization, industrialization, and colonization to unprecedented levels. This has created a unique global multi-faceted human-animal interface, associated with a major epidemiological transition that is accompanied by an unexpected rise of new and emerging infectious diseases.

Until the beginning of the last century, infectious diseases were the major cause of mortality of humankind. Around 1900 infectious diseases caused an estimated fifty percent of all deaths in the western world. In the following decades, this percentage decreased to a few percent. This was largely due to the implementation of public health measures such as the installment of sewage and clean drinking water systems, but also to the development of vaccines and antimicrobial compounds. A major success in this regard was the eradication of smallpox through a worldwide vaccination campaign orchestrated by the World Health Organization (WHO). Stimulated by these successes certain policymakers and scientists predicted that all infectious diseases of humankind would be brought under control. Paradoxically the following decades confronted the world with an ever-increasing number of emerging or re-emerging infectious diseases, some causing true pandemics. A complex mix of predisposing factors in our globalizing world, linked to major changes in our social environment, technology and global ecology, collectively created opportunities for viruses to infect new hosts. Subsequent adaptation to the newly invaded species then paved the way for an unprecedented spread with dramatic consequences for public health, animal health, animal welfare, food supply, economies, and biodiversity. Striking examples were the emergence of AIDS, Avian flu, SARS, MERS, Ebola and most recently Zika. Viruses spilling over from animal reservoirs have all caused these disease outbreaks.

HIV, the causative agent of the AIDS pandemic that started about thirty years ago, with changes in bush meat consumption, behaviour, demography, human mobility, medical practises and rapidly adapting viruses as main drivers, has now infected more than 55 million people of whom more than 20 million have died. The identification of HIV as the causative agent took more than two years after the recognition of AIDS as a new disease entity. Since then virus discovery techniques have evolved drastically with the advent of an ever-increasing range of new generation molecular techniques. This allowed us to rapidly identify dozens of new viruses of animals and humans, some of which were indeed newly emerging viruses, while others were viruses that had just not been discovered before due to technical limitations. Avian influenza viruses were first shown to sporadically infect humans in Hong Kong in the late 90ies of the last century, without subsequent efficient human-to-human transmission. However more recently it was shown that not more than a handful of mutations would allow such avian influenza viruses to become transmissible among mammals, thus creating a pandemic threat. In the light of the four influenza pandemics that have occurred in the last century, and together have cost the lives of more than 50 million people, this is an alarming observation. The emergence of severe acute respiratory syndrome (SARS) in China at the beginning of the 21^st century, proved to be caused by a newly discovered coronavirus that most probably spilled over from a bat reservoir, an was transmitted via carnivores to humans. SARS coronavirus started to spread efficiently among humans, rapidly creating a pandemic threat. Through an international WHO-coordinated collaborative pathogen discovery and intervention network, this virus was identified and characterized within a month after the start of this collaboration and the emerging pandemic was subsequently rapidly controlled. A decade later yet another coronavirus of probable bat origin spilled over to humans in the Middle East, causing Middle East respiratory syndrome (MERS). The identification and characterization of MERS coronavirus was performed in a matter of weeks, whereas the dromedary camel proved to be the intermediate species that transferred the virus to humans. Different outbreaks in the Middle East and sporadic cases and outbreaks elsewhere, have indicated predominantly nosocomial human-to-human transmission. It is not clear at present whether this virus has the potential to cause a pandemic. Most recently the emergence of Zika virus, a flavivirus that had been discovered in Africa in the middle of the last century, emerged outside Africa and Asia in the last decade. Zika virus that is transmitted by Aedes mosquitos, was initially shown to cause a mild and self-limiting disease, and was until recently considered to be a relatively innocuous pathogen. However an increased incidence of microcephaly in unborn babies that coincided since last year with the emergence of Zika virus in South America, has created an ongoing public health emergency.

Importantly, the unprecedented emergence of these and other viruses is largely paralleled by medical, technological, and scientific progress, continuously spurred by our never-ending combat against pathogens. Investment in a better understanding of the human-animal interface will therefore offer humankind a future head start in the never-ending battle against emerging infectious diseases.

*Reperant LA, Cornaglia G, Osterhaus AD. Curr Top Microbiol Immunol. 2013

Christian Drosten, Institute of Virology, University of Bonn, Germany

Please refer to the Zika facts summary by the Society for Virology in Germany

To virologists, Zika virus is a long known subject (1). Experienced labs consider the infection among the differential diagnoses in cases of fever after travel to tropical Africa and, more lately, Asia. Reports on the occurrence of this typical Old World virus in Brazil in May 2015 were admittedly surprising, but did not come totally unexpected in light of the introduction of chikungunya virus to the Americas one year earlier (2). It seemed that Zika was just another aedes-transmitted and primate-associated arbovirus that made it into the virgin soil-environment of the neotropics. Ensuing reports of cases of Guillain-Barré syndrome associated with Zika virus infection caused little concern, as the syndrome is non-specifically associated with a whole range of pathogens. A whole new and very different aspect was added in October 2015, when the Brazil Ministry of Health expressed concern about an increased incidence of microcephaly in newborns in the northeastern part of the country that followed the arrival and spread of Zika virus with a delay corresponding to the duration of a human pregnancy.

Virologists know a whole number of viruses causing this and similar neurological fetopathies in humans. Rubella virus, the most notorious representative, has been virtually eliminated as a cause of fetopathy through vaccination programs in Europe and the Americas. The One Health perspective provides epidemiological scenarios not normally considered in humans. In Europe, we have just witnessed the devastating consequences of a fetopathogenic virus that is transmitted by blood-feeding insects. The Schmallenberg virus was recognized in Germany in 2011 and spread across Europe within less than 2 years, causing dramatic malformations including severe cerebral fetopathies in ruminants (3). We did not dare at that time to project an equivalent scenario for a human disease.

The threat posed by Zika virus is difficult to express in numbers. The emotional component, the uncertainty, as well as the possibility to miss a window of opportunity for study and intervention have already triggered ad-hoc funding programs and pragmatic approaches to extract information from available data. It is not in spite of the emotional component, but because of it, that virologists should look at the problem from a scientific perspective – and communicate a conservative perspective to the public via the media.

Most virus infections that cause fetopathy have a low manifestation index. Certainly, also the Zika virus will cause harm in only a small proportion of the many pregnant women now exposed to the virus. Of note, the attack rate in the 2007 outbreak on Yap island (Micronesia) may have been as high as 73% in the population aged >3 years. In the much larger outbreak in French Polynesia the attack rate was 11.5% according to retrospective analyses (1). In the affected regions in South America, where people are similarly exposed and immunologically naïve toward the infection, very high rates of unnoticed infection are to be expected – including in pregnant women. Even if truly associated with Zika virus infection, the 5640 cases of microcephaly reported in Brazil by end of February 2016 will only represent a tiny fraction of the many pregnant women who got infected during 2015. A more severe issue is the reporting and classification of microcephaly. The perception of an increased incidence of microcephaly came up in an area notably affected by Zika virus. Beginning in autumn 2015, the Brazilian MOH strengthened and emphasized microcephaly surveillance, whereas notifications prior to this time occurred on a more routine basis. The media coverage of the Zika/microcephaly connection contributed an additional stimulus for reporting. A recent research manuscript suggests that the MOH reporting criterion for suspected cases of microcephaly, based on cranial circumference of 32 cm, may be inappropriate for the most affected population in northeastern Brazil. This criterion may trigger the formal notification of up to 10% of all newborns as suspected cases of microcephaly (4). Of the 5,640 suspected cases notified so far, 3,935 remain under investigation (5). Among the remaining 1705 cases, 950 have not been confirmed as cases of microcephaly (5).

The literature now contains several reports on Zika virus detection in amniotic fluid, blood, and even central nervous tissue of fetuses with signs of microcephaly. With every new case report that is published, we perceive the link between Zika virus infection and microcephaly to become stronger. There is probably truth to this. However, as scientists we should emphasize that case reports do not establish a causative link between virus and microcephaly. As always at the beginning of epidemics, studies tend to focus on cases but not controls. What fraction of healthy pregnancies and babies might reveal evidence for Zika virus infection if sampled at the peak of an outbreak, assuming attack rates of 10% or even higher in the adult population? Up to now, 583 cases of microcephaly in Brazil have been completely investigated including objective neurological criteria and virological laboratory tests. Only 67 (11.5%) tested positive for Zika virus infection (5). An extrapolation of this proportion to all notified cases fails to explain the reported >20-fold increase of incidence of microcephaly in northeastern Brazil compared to other populations.

The increase of microcephaly may represent a complex effect on the local population that could include other factors such as unrecognized pathogens or environmental causes. These factors may manifest as microcephaly alone or in concert with Zika virus infection. The WHO Zika Open resource carries a research manuscript that follows the incidence of microcephaly from 2012 to 2015 in Paraiba, the Brazilian federal state that was second most affected (6). Using data from prospectively-designed birth cohorts, the study reveals a stark increase of microcephaly incidence already by end of 2012 and a second peak by mid 2014, pre-dating the presumed introduction of Zika virus into the country. A third peak of incidence recorded for the second half of 2015 is the strongest peak. Only this peak plausibly correlates with Zika outbreaks. We should remain open for additional or even alternative explanations for the increased incidence of microcephaly observed in northeastern Brazil. Interestingly, the outbreak in French Polynesia, which according to ongoing retrospective analyses may have involved fetopathies, co-incided with a dengue virus outbreak (1). Dengue is also endemic in many of the regions now affected by the Zika outbreak in Brazil.

Having summarized concerns regarding the true incidence of Zika-associated microcephaly, we should not forget to mention that virally-induced fetopathies can involve many other symptoms that are not easily objectified. Along with microcephaly, retinal malformations have already been noted in 2 cases (1). Zika´s association with Guillain Barré Syndrome can be regarded as confirmed based on a recent revisit of the French Polynesia outbreak (7). However, GBS should not be regarded as predictive for other severe neurological sequelae as many other pathogens that are not specifically neurotropic are associated with the syndrome (e.g., campylobacter). Co-endemic arboviroses including dengue and chikungunya virus infection are thought to trigger Guillain Barré syndrome, typically with low incidence. Much more worrying with regard to Zika virus infection is the perspective of sequelae effective on higher neurological functions, involving deficits that may come to show as kids develop. The clear reports of fetal neurotropic infection (e.g., 8) call for neuro-psychiatric follow-up of birth cohorts.

Given the epidemiological uncertainties regarding the causation of microcephaly, animal experiments will be utilized to compensate for pressing information needs. Newborn mice can be readily infected with a range of arboviruses, but the pathology observed in adult mouse models does usually not compare to the situation in primates for most human arboviruses. Mouse-adapted adult disease models for Zika virus infection are not available. Even if they were, it is questionable whether these models could reliably depict syndromes that show a very low incidence among cases with normal courses of infection. Experiments on pregnant macaques are being conducted as this text is being written. However, the results of these experiments may not come in time to provide first evidence of causation of microcephaly. Nature is presenting us with a large-scale, cruel study scenario in humans. We will be able to observe over the next coming months whether the incidence of microcephaly will increase in areas that have been newly affected by Zika virus since the end of 2015. Next to the implementation of prophylactic measures such as mosquito control, it is our prime responsibility to secure epidemiological evidence by careful design of prospective, controlled observational trials.

References

1. Kindhauser MK, Allen T, Frank V, Santhana RS & Dye C. Zika: the origin and spread of a mosquito-borne virus [Submitted]. Bull World Health Organ E-pub: 9 Feb 2016.
2. Leparc-Goffart I, Nougairede A, Cassadou S, Prat C, de Lamballerie X. Chikungunya in the Americas. Lancet. 2014 Feb 8;383(9916):514. doi: 10.1016/S0140-6736(14)60185-9
3. Wernike K, Elbers A, Beer M. Schmallenberg virus infection. Rev Sci Tech. 2015 Aug;34(2):363-73
4. Rocha HAL, Correia LL, Leite AJM, Campos JS, Cavalcante e Silva A, Machado MMT, Rocha SGMO, Saraiva de Almeida NMG, Alves da Cunha AJL. Microcephaly: normality parameters and its determinants in northeastern Brazil: a multicentre prospective cohort study [Submitted]. Bull World Health Organ E-pub: 8 Feb 2016. doi: http://dx.doi.org/10.2471/BLT.16.171215
5. Pan American Health Organization / World Health Organization. Zika Epidemiological Update – 24 February 2016. Washington, D.C.: PAHO/WHO; 2016
6. Soares de Araújo JS, Regis CT, Gomes RGS, Tavares TR, Rocha dos Santos C, Assunção PM, et al. Microcephaly in northeast Brazil: a review of 16 208 births between 2012 and 2015 [Submitted]. Bull World Health Organ E-pub: 4 Feb 2016. doi: http://dx.doi.org/10.2471/BLT.16.170639
7. Van-Mai Cao-Lormeau, Alexandre Blake, Sandrine Mons, Stéphane Lastère, Claudine Roche, Jessica Vanhomwegen, Timothée Dub,
Laure Baudouin, Anita Teissier, Philippe Larre, Anne-Laure Vial, Christophe Decam, Valérie Choumet, Susan K Halstead, Hugh J Willison, Lucile Musset, Jean-Claude Manuguerra, Philippe Despres, Emmanuel Fournier, Henri-Pierre Mallet, Didier Musso, Arnaud Fontanet, Jean Neil, Frédéric Ghawché. Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. The Lancet 2016 Published online February 29, 2016 http://dx.doi.org/10.1016/S0140-6736(16)00562-6
8. Mlakar J, Korva M, Tul N, Popović M, Poljšak-Prijatelj M, Mraz J, Kolenc M, Resman Rus K, Vesnaver Vipotnik T, Fabjan Vodušek V, Vizjak A, Pižem J, Petrovec M, Avšič Županc T. Zika Virus Associated with Microcephaly. N Engl J Med. 2016 Feb 10.

The registration to the 4th European Seminar in Virology, “Oncogenic and oncolytic viruses”,  Bertinoro, Italy, June 10-12 2016, will close on April 15.

For info on the meeting, please visit the website
http://www.eusev2016.lima-city.de/.

Contributed by the working gorup “pregnancy-associated virus infections” of the Gesellschaft für Virologie (GfV).

The Virus

Zika virus is a mosquito-transmitted flavivirus belonging to the Spondweni virus group. It has a single-stranded plus-strand RNA-genome of 10.617 base pairs surrounded by a capsid and envelope (Baronti et al., 2014). An African and an Asian genetic lineage are known. The virus presently circulating in the Americas belongs to the Asian lineage.

Epidemiology

Zika virus was first isolated in 1947 from a rhesus macaque that was kept for studies on yellow fever in Zika forest near Entebbe, Uganda. Primates including humans are considered natural hosts. In addition, there is evidence for sporadic mosquito-borne transmission to other vertebrates. Human cases have long been known in Africa and Asia. Significant outbreaks occurred in 2007 and 2008 in Micronesia (Yap islands) as well as in 2013 in French Polynesia, from where the virus subsequently spread to New Caledonia. Imported cases from these epidemics were reported in several European countries, Japan, as well as the Easter islands (Marano et al., 2015).

A change in the general perception of Zika virus distribution occurred in early 2015, when Brazil reported first patients who had acquired their infection in the country (autochthonous cases). The autochthonous circulation in Brazil extended to 18 federal states through December 2015. On February 18^th autochthonous transmissions were reported from 32 countries or regions (www.cdc.gov). In large parts of South- and Middle America the virus meanwhile present. WHO declared the Zika outbreak a public health emergency of international concern (PHEIC) on February 1^st, 2016.

Transmission

Zika virus is transmitted by mosquitos of the species Aedes aegypti, which also transmit dengue and yellow fever virus (Marconedes and Ximenes, 2015). Zika virus has occasionally been found in other species of the same genus of mosquitos (Ae. polynesiensis, Ae. dalzieli, Ae. africanus, Ae. luteocephalus, Ae. vittatus, Ae. apicoargenteus, Ae. furcifer). In a study conducted in 2007 in Gabon, Zika virus RNA was found in pools of Ae. albopictus, a species that is also endemic in large parts of southern Europe (Grard et al., 2014). However, these results do not prove vector competence of Ae. albopictus as mosquitos were sampled in a natural context in an endemic area where they could have taken up the virus via blood meal but might not be able to transmit the virus further.

Another study showed replication and salivary secretion of Zika virus in Ae. albopictus under defined laboratory conditions (Wong et al. 2013). However, the appropriate experimental conditions to represent virus uptake from infected humans are unknown, and the virus dose used in mosquito infection studies has very strong influence on the result. Further studies using appropriate control settings with dose titration, as well as transmission trials in primates will be necessary to define vector competence for Ae. albopictus and other mosquito species endemic in temperate climate zones.

There are rare descriptions of direct human-to-human transmission including reports of 2 newborns with perinatal infection during the outbreak in French Polynesia (Besnard et al., 2014). The mothers in both cases had an acute infection at the time of birth. There is evidence for the presence of virus in semen and sexual transmission via semen (Foy et al. 2011; Musso et al., 2015). In all cases reported so far, males had symptomatic disease and females showed symptoms 10 to 14 days after sexual intercourse.

In spite of a short time of viremia, transmission via blood donations cannot be excluded. During the outbreak in French Polynesia, viral RNA was detected in 2.8 % of 1,505 blood donors by RT-PCR (Musso et al., 2014). Blood donations from donors infected with the related dengue- and West Nile virus are known to transmit the disease to recipients (Petersen and Busch, 2010).

Clinical Features

(I) Clinical Presentation in Children and Adults

Symptoms appear after a short incubation period of 3 to 12 days and are usually mild and self-limiting. Up to 80 percent of infections are clinically silent. Symptoms can include fever, arthralgia, headaches, retro-orbital pain, conjunctival injection, digestive disorder and pruritic maculopapular rash usually spreading from face to limbs, including soles and palms. Other complications of Zika virus infection are rare. In Brazil, one patient who was on corticosteroid treatment and another patient without known underlying disease died after Zika virus infection.

During the outbreak in French Polynesia 2013-2014 health authorities reported an increase of Guillain-Barré-Symdrome (GBS) cases. The association of acute Zika virus infection with GBS was recently demonstrated by a case-control study conducted in French Polynesia (Cao-Lormeau, 2016). An increase of GBS cases has also been reported during the ongoing outbreak in Brazil, Colombia, Venezuela and El Salvador. The pathogenesis of GBS after Zika virus infection is not yet clear.

(II) Congenital Disease

In October 2015 the Brazilian Ministry of Health reported an increase of the number of cases of microcephaly over the past months, coinciding with the expanding outbreak of Zika virus infection. Until the end of February 2016 almost 6,000 cases of suspected microcephaly were notified, mainly in the northeastern regions of Brazil. During the past weeks, Brazilian health authorities started re-examinations to confirm microcephaly in these children. These examinations are still ongoing. At present, in about one third of 1.687 case that had been re-examined microcephaly was confirmed. In 12.8% of confirmed microcephalic children diagnostic markers for Zika virus infection were observed (Ministry of Health, Brazil). Several case reports implicating Zika virus infection to cause microcephaly were published. A recent publication presents data of Zika virus genomes to be detectable by RT-PCR in brain tissue of an aborted fetus suffering from microcephaly. In addition, flavivirus-like particles were detected by electron microscopy. During springtime and summer 2015, the pregnant woman had lived in Natal (Brasilia) and reported an episode of high fever, myalgia and arthralgia in combination with an itchy exanthema during week 13 of gestation. After returning to Europe (Slovenia), ultrasound examination performed at week 29 of gestation showed microcephaly in combination with several further abnormalities indicative of severe impairment of brain function. As a consequence of these findings, pregnancy was terminated (Mlakar et al., 2016). In a fetus with induced abortion in week 32 due to microcephaly, intracranial calcifications and hydrops fetalis, Zika virus was found in amniotic fluid and brain tissue, but not in any other tissue (Sarno et al., 2016).

Another report describes the presence of Zika virus genomes in amniotic fluid obtained from two pregnant women during weeks of gestation 29 and 30, respectively, when cerebral abnormalities and microcephaly had been recognized (Oliviera Melo et al. 2016). An additional report that is not yet formally published described viral RNA detection in a newborn child with microcephaly that died shortly after birth. Prospective analyses are planned to further clarify these observations. As of February 17^th, the US CDC has been notified of 9 pregnant women with confirmed Zika virus infection after exposure in endemic regions. 7 of 9 reported high fever during early pregnancy. 2 of 9 had spontaneous early abortion, and in another 2 cases, pregnancies were terminated. Of 3 children born so far, 1 had microcephaly. 2 pregnancies proceed without complications. Zika virus in child or fetus was detectable only in 1 case of early spontaneous abortion.

The etiological link between Zika virus infection and microcephaly has not been established. In general, microcephaly is a fetopathy that manifests in late pregnancy or at the time of birth based on small head circumference. Data from the US and Germany show that 12 or 16 of 10,000 births, respectively, show symptoms of microcephaly (National Birth Defects Prevention Network/USA 2013; Baltzer et al., 2016). In early pregnancy, infections (cytomegalovirus, rubella virus, toxoplasma), malnutrition, drug abuse, environmental factors, as well as genetic aberrations can cause microcephaly.

As recommended by the Centers of Disease Control (CDC, Atlanta, USA), laboratory diagnosis should be performed when pregnant women returning from countries with Zika virus circulation report at least two symptoms indicative for Zika disease (sudden onset of fever, itchy exanthema, conjunctivitis and/or arthralgia). If markers for recent and/or acute infection are observed, follow-up by ultrasound examination is recommended in four weekly intervals. In addition, laboratory diagnosis should be performed if ultrasound testing reveals cerebral calcifications and/or microcephaly symptoms in pregnant women with plausible travel history. For pregnant women without travel history, laboratory testing is not recommended (Staples et al., 2016).

Since sexual transmission may occur, testing for Zika virus infection may be recommended for partners of pregnant women after returning from epidemic regions. Until the Zika virus infection status is cleared, transmission may be omitted by the use of condoms. This recommendation is based on plausible hypotheses. Until now, is is not known how long infectious virus is secreted in present in seminal fluid following acute infection.

Risk for Pregnant Women in Endemic Areas

At present, there is a relatively high risk to be bitten by a Zika virus-infected mosquito in Brazil and several other Latin American countries. Since neural development occurs between the 8^th and 15^th week of pregnancy, Zika virus infection should be particularly likely to lead to neurologic damage during this period of fetal development. As long as a causal link between these infections and severe fetal damage cannot be excluded, traveling of pregnant women to affected countries is not recommended, particularly during the first trimester. In the case of travelling to affected areas nonetheless, usage of repellents, adequate clothing, mosquito nets etc. is highly recommended to minimize exposure to the mosquito vectors which are active during daytime and dawn.

Risk for Pregnant Women in Germany

There is no risk of an infection with the Zika virus in Germany at the present time. The probability of importing an infected mosquito that could transmit the virus to a pregnant woman in Germany, is negligible. Continuous presence and spread of Ae. aegypti in Germany and Central Europe is highly unlikely under the current climatic conditions. Whether other Aedes species that already occur in Southern Germany, such as Ae. albopictus and Ae. japonicus, can be efficient vectors for the Zika virus requires investigation. Small-scale epidemics and local transmission events following importation of the Zika virus by infected travelers could be more likely in Southern European countries harboring larger Ae. albopictus populations during summer. It would be important to know whether animals may be involved in Zika virus transmission cycles to make more precise risk assessments.

Laboratory Diagnostics

During the first days of Zika virus disease viral RNA can be detected in blood samples, and up to 4 weeks in urine. Specialized laboratories have already established the appropriate molecular detection methods (qRT-PCRs). The detection of virus-specific antibodies should be performed in reference laboratories. There is a validated, commercial ELISA available for the detection of IgG and IgM against Zika virus. Due to the antigenic relationship to other flaviviruses (dengue, yellow fever, West Nile virus, TBE) there is a serological cross-reactivity. This is relevant if the patient had already undergone infections with other flaviviruses or has been vaccinated against yellow fever (Lanciotti et al., 2008). If there is a positive result for the detection of antiviral antibodies in indirect immunofluorescence assays or ELISA, it needs to be confirmed by a virus neutralization test (VNT); while the VNT results for ZIKV should be at least four titers above those obtained for a comparative dengue virus VNT (Petersen et al., 2016).

A detailed procedure for laboratory diagnostic evaluation of possible ZIKV infections is available from the Bernhard Nocht Institute in Hamburg, Germany

(https://www.bnitm.de/aktuelles/mitteilungen/954-empfehlungen-zur-diagnostik-der-zika-virus-infektion/).

References and further reading

Jörg Baltzer, Klaus Friese, Michael Graf, Friedrich Wolff (Hrsg.): Praxis der Gynäkologie und Geburtshilfe. Thieme, Stuttgart 2006, ISBN 978-3-13-144261-1, S. 314 f.

Baronti C, Piorkowski G, Charrel RN, Boubis L, Leparc-Goffart I, de Lamballerie X. Complete coding sequence of zika virus from a French Polynesia outbreak in 2013. Genome Announc. 2014 Jun 5;2(3). pii: e00500-14. doi: 10.1128/genomeA.00500-14. PubMed PMID: 24903869; PubMed Central PMCID: PMC4047448.

Bernhard-Nocht-Institut, Hamburg. https://www.bnitm.de/aktuelles/mitteilungen/954-empfehlungen-zur-diagnostik-der-zika-virus-infektion/

Besnard M, Lastere S, Teissier A, Cao-Lormeau V, Musso D. Evidence of perinatal transmission of Zika virus, French Polynesia, December 2013 and February 2014. Euro Surveill. 2014 Apr 3;19(13). pii: 20751. PubMed PMID: 24721538.

Cao-Lormeau V-M., Blake A, Mons S, Lastère S, Roche C, Vanhomwegen J, Dub T, Baudouin L, Teissier A, Larre P, Vial A-L, Decam C, Choumet V, Halstead SK, Willison HJ, Musset L, Manuguerra J-C, Despres P, Fournier E, Mallet H-P, Musso D, Fontanet A, Neil J, Ghawché F. Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. The Lancet 2016 Published online February 29, 2016 http://dx.doi.org/10.1016/S0140-6736(16)00562-6

Foy BD, Kobylinski KC, Chilson Foy JL, Blitvich BJ, Travassos da Rosa A, Haddow AD, Lanciotti RS, Tesh RB. Probable non-vector-borne transmission of Zika virus, Colorado, USA. Emerg Infect Dis. 2011 May;17(5):880-2. doi: 10.3201/eid1705.101939. PubMed PMID: 21529401; PubMed Central PMCID: PMC3321795.

Gesundheitsministerium Brasilien, 27. January 2016. http://portalsaude.saude.gov.br/index.php/cidadao/principal/agencia-saude/22032-saude-investiga-3-670-casos-suspeitos-de-microcefalia-no-pais

Grard G., Caron M., Mombo I. M., Nkoghe D., Ondo S. M., Jiolle Davy, Fontenille Didier, Paupy Christophe, Leroy Eric. Zika virus in Gabon (Central Africa) – 2007: a new threat from Aedes albopictus ?. Plos Neglected Tropical Diseases , 2014, 8 (2), art. e2681 [6 p.] ISSN 1935-2735

Lanciotti RS, Kosoy OL, Laven JJ, Velez JO, Lambert AJ, Johnson AJ, Stanfield SM, Duffy MR. Genetic and serologic properties of Zika virus associated with an epidemic, Yap State, Micronesia, 2007. Emerg Infect Dis. 2008 Aug;14(8):1232-9. doi: 10.3201/eid1408.080287. PubMed PMID: 18680646; PubMed Central PMCID: PMC2600394.

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The European Society for Virology provides five fellowships for young scientists who are actively participating in the 4^th European Seminars in Virology: Viral Oncology and Virotherapy to be held from 10-12 June, 2016 in Bertinoro, Italy.

The fellowships include the all-inclusive-registration-fee. Further information will be provided soon on the official EuSeV2016 website.

The 1^st WAidid Congress will be held in Milan, on February 18-20, 2016.

The organizers of the congress are very pleased to offer a free registration to the Congress for five ESV members, who could be interested in participating.

The Congress scientific programme will consist of plenary and parallel sessions and will focus on the following topics: Infectious diseases & Vaccines, Pneumology & Allergology, Autoimmune & Rheumatic diseases. A wide range of subjects will be covered, for example: emerging pathogens, new antinfective therapies, old and new vaccines, tuberculosis, asthma & COPD, new technologies, biologics and biosimilars, chronic pain.

ESV  members who would like to participate should just write an e-mail to the Organizing Secretariat (waidid2016@aimgroup.eu) by February 5, 2016. In case of more than five interested persons, selection will be on the first come, first selected basis.

The 4^th European Seminars in Virology: Viral Oncology and Virotherapy will take place in Bertinoro from 10 – 12 June, 2016 in Bertinoro, Italy.

The European Seminars in Virology are short meetings dedicated to dissect one topic – or two related topics. The idea is to gather expert personalities on the selected topic from Europe, and occasionally from US, and to bring young students and post-docs in contact with the leaders in the field. The meeting lasts a weekend (from Friday noon to Sunday noon), and is held in Italy, in a facility of the University of Bologna. The facility includes a renovated fortress and nearby buildings. All meals are taken together, to further foster informal contacts and the discussion. This years’ seminar will focuse on “Viral Oncology and Virotherapy ”.

Detailed information can be found on the official website: http://www.eusev2016.lima-city.de/