Background: Zika virus (ZIKV) is a mosquito-borne flavivirus distributed throughout much of Africa and Asia. Infection with the virus may cause acute febrile illness that clinically resembles dengue fever. A recent study indicated the existence of three geographically distinct viral lineages; however this analysis utilized only a single viral gene. Although ZIKV has been known to circulate in both Africa and Asia since at least the 1950s, little is known about the genetic relationships between geographically distinct virus strains. Moreover, the geographic origin of the strains responsible for the epidemic that occurred on Yap Island, Federated States of Micronesia in 2007, and a 2010 pediatric case in Cambodia, has not been determined. Methodology/Principal Findings: To elucidate the genetic relationships of geographically distinct ZIKV strains and the origin of the strains responsible for the 2007 outbreak on Yap Island and a 2010 Cambodian pediatric case of ZIKV infection, the nucleotide sequences of the open reading frame of five isolates from Cambodia, Malaysia, Nigeria, Uganda, and Senegal collected between 1947 and 2010 were determined. Phylogenetic analyses of these and previously published ZIKV sequences revealed the existence of two main virus lineages (African and Asian) and that the strain responsible for the Yap epidemic and the Cambodian case most likely originated in Southeast Asia. Examination of the nucleotide and amino acid sequence alignments revealed the loss of a potential glycosylation site in some of the virus strains, which may correlate with the passage history of the virus. Conclusions/Significance: The basal position of the ZIKV strain isolated in Malaysia in 1966 suggests that the recent outbreak in Micronesia was initiated by a strain from Southeast Asia. Because ZIKV infection in humans produces an illness clinically similar to dengue fever and many other tropical infectious diseases, it is likely greatly misdiagnosed and underreported.

/pdf/genetic-characterization-of-zika-virus-strains-geographic-3l36pxg54p.pdf

Genetic Characterization of Zika Virus Strains: Geographic Expansion of the Asian Lineage

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.

A total of 134 876 Diptera collected in Kenya during a 3-year period were tested in 3383 pools for Rift Valley fever (RVF) virus. Nineteen pools of unengorged mosquitoes were found positive for RVF. All isolations were made from specimens collected at or near the naturally or artificially flooded grassland depressions that serve as the developmental sites for the immature stages of many mosquito species. The isolation of virus from adult male and female A. lineatopennis which had been reared from field-collected larvae and pupae suggests that transovarial transmission of the virus occurs in this species.

/pdf/rift-valley-fever-virus-family-bunyaviridae-genus-2r4rptgbyp.pdf

Rift Valley fever virus (family Bunyaviridae, genus Phlebovirus). Isolations from Diptera collected during an inter-epizootic period in Kenya

Background: Lassa fever is caused by a viral haemorrhagic arenavirus that affects two to three million people in West Africa, causing a mortality of between 5,000 and 10,000 each year. The natural reservoir of Lassa virus is the multi-mammate rat Mastomys natalensis, which lives in houses and surrounding fields. With the aim of gaining more information to control this disease, we here carry out a spatial analysis of Lassa fever data from human cases and infected rodent hosts covering the period 1965–2007. Information on contemporary environmental conditions (temperature, rainfall, vegetation) was derived from NASA Terra MODIS satellite sensor data and other sources and for elevation from the GTOPO30 surface for the region from Senegal to the Congo. All multi-temporal data were analysed using temporal Fourier techniques to generate images of means, amplitudes and phases which were used as the predictor variables in the models. In addition, meteorological rainfall data collected between 1951 and 1989 were used to generate a synoptic rainfall surface for the same region. Methodology/Principal Findings: Three different analyses (models) are presented, one superimposing Lassa fever outbreaks on the mean rainfall surface (Model 1) and the other two using non-linear discriminant analytical techniques. Model 2 selected variables in a step-wise inclusive fashion, and Model 3 used an information-theoretic approach in which many different random combinations of 10 variables were fitted to the Lassa fever data. Three combinations of absence:presence clusters were used in each of Models 2 and 3, the 2 absence:1 presence cluster combination giving what appeared to be the best result. Model 1 showed that the recorded outbreaks of Lassa fever in human populations occurred in zones receiving between 1,500 and 3,000 mm rainfall annually. Rainfall, and to a much lesser extent temperature variables, were most strongly selected in both Models 2 and 3, and neither vegetation nor altitude seemed particularly important. Both Models 2 and 3 produced mean kappa values in excess of 0.91 (Model 2) or 0.86 (Model 3), making them ‘Excellent’. Conclusion/Significance: The Lassa fever areas predicted by the models cover approximately 80% of each of Sierra Leone and Liberia, 50% of Guinea, 40% of Nigeria, 30% of each of Coˆ te d’Ivoire, Togo and Benin, and 10% of Ghana.

/pdf/risk-maps-of-lassa-fever-in-west-africa-4wt9t1t706.pdf

Risk maps of Lassa fever in West Africa.

Lassa fever is a severe febrile illness of man, first recognized in West Africa in 1969 During an epidemic in Sierra Leone, Lassa virus was isolated for the first time from wild rodents of Mastomys natalensis A high prevalence of infected Mastomys was found in houses occupied by patients with Lassa fever The data presented provide the first demonstration of an extra-human cycle of Lassa virus transmission and suggest that rodent control may be an effective method of limiting the disease

http://science.sciencemag.org/content/sci/185/4147/263.full.pdf

Lassa Virus Isolation from Mastomys natalensis Rodents during an Epidemic in Sierra Leone

Lassa virus was isolated from specimens collected from 12 of the 13 patients involved in an epidemic of Lassa Fever which occurred in Jos during 1970. Sero-epidemiological studies indicate that Lassa virus infection occurs over a wide area of western Africa extending at least from Guinea to Nigeria.

Lassa fever virological and serological studies

The isolation in Kenya of arboviruses from mosquitoes and patients is reported. Middelburg and Semliki Forest virus (group A), Banzi virus (group B), Bunyamwera and Beliefe virus (Bunyamwera group), Sango virus (Simbu group), Pongola virus (Bwamba group), Tahyna virus (California group), ungrouped AR 1169/64 and a number of viruses still to be identified were isolated from mosquitoes. Of the latter some may be hitherto undescribed viruses. Bunyamwera, Rift Valley Fever and 2 unidentified viruses were isolated from patients. The isolates are discussed against the background of information from isolations and serology performed elsewhere. Attempts are made to define their role in human disease. Some superficial suggestions about the ecology are made.

Isolation of arboviruses in Kenya, 1966–1971

Virus isolations from ixodid ticks in Uganda. Part I. Isolation and characterisation of ten strains of a virus not previously described from eastern Africa.

Virus isolations from Ixodid ticks in Uganda. Part II. Kadam virus-a new member of arbovirus group B isolated from Rhipicephalus pravus Donitz.

Recent research on yellow fever in Kenya.

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