Introduction Zika, a flavivirus transmitted mainly by mosquitos in the genus Aedes, was discovered in 1947 in Uganda. (1) From the 1960s to 1980s, human infections were found across Africa and Asia, typically accompanied by mild illness. The first large outbreak of disease caused by Zika infection was reported from the island of Yap (Federated States of Micronesia) in 2007, as the virus moved from south-east Asia across the Pacific. During an outbreak in French Polynesia in 2013-2014, Guillain-Barre syndrome was linked to Zika infection and cases of microcephaly in newborn children were also retrospectively linked to this outbreak. The World Health Organization (WHO) received the first reports of locally-transmitted infection from Brazil in May 2015. In July 2015, health ministry officials from Brazil reported an association between Zika virus infection and Guillain-Barre syndrome in adults. In October 2015, WHO received reports from Brazil of microcephaly in babies whose mothers had been exposed to Zika during pregnancy. At this time, there was no proof of a causal link between Zika infection and these neurological complications. In February 2016, as infection moved rapidly through the range occupied by Aedes mosquitos in the Americas, WHO declared that Zika infection associated with microcephaly and other neurological disorders constituted a Public Health Emergency of International Concern (PHEIC). By the start of February 2016, local transmission of Zika infection had been reported from more than 20 countries and territories in the Americas and an outbreak numbering thousands of cases was under way in Cabo Verde in western Africa. Beyond the range of its mosquito vectors, Zika virus infections are expected to be carried worldwide by people as they travel and be transmitted by travellers to sexual partners who have not been to places where the virus is endemic. Methods To illustrate the spread of Zika virus and associated neurological complications, we did a literature search in PubMed using "Zika" and "ZIKV" as the search terms and cross-checked our findings for completeness against other published reviews. (2, 3) In addition, we drew on formal notifications to WHO under the International Health Regulations (IHR), (4) which are archived in the WHO Event Information Site (EIS). EIS contains information about public health events of potential international concern notified to WHO as required by the IHR. EIS notifications sometimes contain confidential patient information and therefore are not publicly available. Other details of specific events can be provided by the authors on request. Results The first reported case of Zika virus dates to 1947 when the virus was isolated in samples taken from a captive sentinel rhesus monkey by scientists conducting routine surveillance for yellow fever in the Zika forest of Uganda. (1) The virus was recovered from Aedes (Stegomyia) africanus, caught on a tree platform in the forest. (1) Laboratory infection experiments showed the virus to be neurotropic in mice. (5) The timeline presented in this paper includes numerous serological surveys that purportedly detected antibodies to Zika virus in the 1950s and 1960s in Africa and Asia. Because serological (antibody detection) tests for Zika cross-react with antibodies stimulated by other viral infections, the presence of Zika virus is ideally confirmed by the detection of viral nucleic acids by polymerase chain reaction (PCR) testing or by virus isolation. A chronological map of the presence of Zika in those countries for which there is evidence of autochthonous transmission by mosquitos is presented in Fig. 1. The map excludes the many countries from which imported Zika infections have been reported. The country-by-country spread of Zika virus infections, from the earliest published report in 1947 to a World Health Organization, avenue Appia 20, 1211 Geneva 27, Switzerland. January 2014 is summarized in Table 1. …

Zika: the origin and spread of a mosquito-borne virus.

Zika virus is a mosquitoborne flavivirus that is the focus of an ongoing pandemic and public health emergency. Previously limited to sporadic cases in Africa and Asia, the emergence of Zika virus in Brazil in 2015 heralded rapid spread throughout the Americas. Although most Zika virus infections are characterized by subclinical or mild influenza-like illness, severe manifestations have been described, including Guillain-Barre syndrome in adults and microcephaly in babies born to infected mothers. Neither an effective treatment nor a vaccine is available for Zika virus; therefore, the public health response primarily focuses on preventing infection, particularly in pregnant women. Despite growing knowledge about this virus, questions remain regarding the virus's vectors and reservoirs, pathogenesis, genetic diversity, and potential synergistic effects of co-infection with other circulating viruses. These questions highlight the need for research to optimize surveillance, patient management, and public health intervention in the current Zika virus epidemic.

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A Literature Review of Zika Virus.

2 – Antigenic Characteristics and Classification of Togaviridae

Objective
To review the state of knowledge about diagnostic testing for Zika virus infection and identify areas of research needed to address the current gaps in knowledge.

Background review for diagnostic test development for Zika virus infection

A retrospective serological survey for dengue immunity was conducted in Nigeria to determine the prevalence of infection in man and non-human primates. Preliminary haemagglutination-inhibition (HI) tests revealed that 63% of persons tested had HI antibodies against one or more of the following flaviviruses: dengue type 1, yellow fever, West Nile and Wesselsbron. Parallel HI and neutralization (N) tests on 179 human sera showed that six of 20 sera (30%) negative for flavivirus HI antibody contained dengue N antibody. This finding emphasized the advantage of the N test over HI in screening for dengue virus immunity. Neutralization tests performed on 1,816 human sera from different geographical locations in Nigeria showed that 45% of Nigerians were immune to dengue type 2 virus. The percentage of immunity in adults aged 20 years and older (51%) was significantly higher than in children (37%) (P less than 0-01). In all four ecological zones sampled, the highest percentage of dengue N antibody was observed in the derived Savannah zone (63%) followed by the rain forest zone (42%). The Southern Guinea savannah and plateau zones had lower percentages of dengue-immune persons. There was a higher prevalence of antibodies in urban (48%) than in rural communities (37%). Tests on dengue-immune sera showed that 35% of such sera contained N antibodies to dengue only or to dengue and one other virus. Therefore, dengue immunity cannot be explained by heterologous cross reactions within the flavivirus group. In addition, evidence of dengue infection was found in monkeys and galagos. 48% of monkeys and 25% of galagos contained dengue N antibody. The presence of specific dengue N antibodies in a few sera suggests that the occurrence of a forest cycle of dengue is possible in Nigeria.

Dengue virus infections in Nigeria: a survey for antibodies in monkeys and humans.

Serological studies of persons infected with yellow fever (YF) during the 1970 epidemic in Okwoga District, Nigeria, indicated that epidemic YF occurred despite a high prevalence of pre-existing group B arbovirus immunity, which increased with age. The viruses involved were primarily dengue, Zika, and Wesselsbron. Patterns of responses of haemagglutination-inhibiting, complement-fixing, and neutralizing antibodies in primary YF and in superinfections are defined in this paper.

The 1970 yellow fever epidemic in Okwoga District, Benue Plateau State, Nigeria. 3. Serological responses in persons with and without pre-existing heterologous group B immunity.

D. C. Wilson

Papers

The 1970 yellow fever epidemic in Okwoga District, Benue Plateau State, Nigeria. 3. Serological responses in persons with and without pre-existing heterologous group B immunity.