R. H. Kokernot

Bio: R. H. Kokernot is an academic researcher. The author has contributed to research in topics: Virus & Aedes. The author has an hindex of 10, co-authored 18 publications receiving 262 citations.

Isolation of Bunyamwera virus from a naturally infected human being and further isolations from Aedes (Banksinella) circumluteolus theo.

Abstract: Summary 1. The isolation of a strain of Bunyamwera virus from the blood of a naturally infected human being is described. 2. Following infection there was a significant increase in titer of both neutralizing and hemagglutination-inhibiting antibodies in tests controlled by the inactivated acute serum from which the virus was isolated. 3. The significance of Bunyamwera virus as a causative agent of disease in human beings is discussed. 4. Three strains of this virus were isolated from Aedes (Banksinella) circumluteolus mosquitoes and two of these were from insects collected during the same time period and in the same locality where the human case acquired infection. 5. Evidence is discussed which would indicate that this mosquito species is a potential vector of Bunyamwera virus.

Isolation of viruses from mosquitoes collected at Lumbo, Mozambique. I. Lumbo virus, a new virus isolated from Aedes (Skusea) pembaensis Theobald.

Abstract: Summary Twelve strains of a hitherto unknown virus have been isolated from Aedes (Skusea) pembaensis collected in 1959 and 1960 at Lumbo in northeastern Mozambique. The name proposed for the agent is Lumbo. Lumbo virus is filterable and withstands lyophilization but is sensitive to sodium desoxycholate. It is pathogenic for adult mice and hamsters by the intracerebral but not the intraperitoneal inoculation route. Vervet monkey, yellow baboon, bushbaby and guinea pig develop an immune response to the virus without showing signs of illness. Viremia was detected on the 3rd and 4th postinoculation days in a vervet monkey. Of 128 human sera collected at Lumbo and Ndumu, northern Natal, in the tropical corridor in southeastern Africa, 16 contained neutralizing antibodies; all of 175 human sera collected in Angola and the Caprivi Strip were negative.

Rift Valley fever virus (Bunyaviridae: Phlebovirus): an update on pathogenesis, molecular epidemiology, vectors, diagnostics and prevention

Abstract: Rift Valley fever (RVF) virus is an arbovirus in the Bunyaviridae family that, from phylogenetic analysis, appears to have first emerged in the mid-19th century and was only identified at the begininning of the 1930s in the Rift Valley region of Kenya. Despite being an arbovirus with a relatively simple but temporally and geographically stable genome, this zoonotic virus has already demonstrated a real capacity for emerging in new territories, as exemplified by the outbreaks in Egypt (1977), Western Africa (1988) and the Arabian Peninsula (2000), or for re-emerging after long periods of silence as observed very recently in Kenya and South Africa. The presence of competent vectors in countries previously free of RVF, the high viral titres in viraemic animals and the global changes in climate, travel and trade all contribute to make this virus a threat that must not be neglected as the consequences of RVF are dramatic, both for human and animal health. In this review, we present the latest advances in RVF virus research. In spite of this renewed interest, aspects of the epidemiology of RVF virus are still not fully understood and safe, effective vaccines are still not freely available for protecting humans and livestock against the dramatic consequences of this virus. Rift Valley fever / molecular epidemiology / vector / pathogenesis / diagnostic

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

Abstract: 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. …

The Rift Valley fever epizootic in Egypt 1977–1978 1. Description of the epizootic and virological studies

Abstract: From October to December 1977, an extensive epizootic occurred in Egypt resulting in abortions and increased mortality in domestic animals, and severe clinical disease with fatalities in man. Rift Valley Fever (RVF) virus was isolated and identified as the causative agent. In humans, acute febrile, encephalitic, ocular and fatal haemorrhagic diseases were documented as resulting from RVF virus infection. A retrospective serological survey indicated RVF was recently introduced into the area. The 1977 epizootic extensively involved five Governorates. In the summer and autumn of 1978, epizootic RVF reappeared in Egypt and spread to previously uninfected areas. Virological, serological and epidemiological studies, and factors related to the spread of RVF are discussed.

Arthropod-borne viral infections of man in Nigeria, 1964-1970.

Abstract: During the years 1964 to 1970, 171 arboviruses of 15 different types were isolated from humans in Nigeria. Isolation rates were highest in 1969, and lowest in 1965 and 1967. Monthly arbovirus activity was highest in the rainy season months of June, July and August and lowest in the dry months of January and February. Viruses were isolated from all age groups, with the majority from children one to four years old. The viruses isolated in largest numbers were chikungunya and yellow fever, which caused epidemics in 1969, and dengue types 1 and 2 and Tataguine, which are endemic in Ibadan. Bwamba virus was isolated in 1964 and 1969, and Bunyamwera group viruses were encountered for the first time in 1969. Other viruses recovered less frequently were Zika, Igbo-Ora (an agent related to o'nyong-nyong), two viruses related to the Uganda mosquito virus Ug MP 359, Dugbe, Thogoto, Lebombo and Shuni. Several of these are new agents and have not previously been isolated from man. Clinical details are presented where available.

Mosquito-borne viruses in Europe

Abstract: The number of mosquito-borne viruses (‘moboviruses’) occurring in Europe since the twentieth century now stands at ten; they belong to three families—Togaviridae (Sindbis, Chikungunya), Flaviviridae (West Nile, Usutu, Dengue), and Bunyaviridae (Batai, Ťahyňa, Snowshoe hare, Inkoo, Lednice). Several of them play a definite role in human or animal pathology (Sindbis, Chikungunya, Dengue, West Nile, Ťahyňa). Mobovirus outbreaks are strictly determined by the presence and/or import of particular competent vectors of the disease. Ecological variables affect moboviruses considerably; the main factors are population density of mosquito vectors and their vertebrate hosts, intense summer precipitations or floods, summer temperatures and drought, and presence of appropriate habitats, e.g., wetlands, small water pools, or intravillan sewage systems. A surveillance for moboviruses and the diseases they cause in Europe is recommendable, because the cases may often pass unnoticed or misdiagnosed not only in free-living vertebrates but also in domestic animals and even in humans.