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Mcintosh Bm

Bio: Mcintosh Bm is an academic researcher. The author has contributed to research in topics: Neutralization. The author has an hindex of 1, co-authored 1 publications receiving 19 citations.


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Journal ArticleDOI
TL;DR: Zika virus infection in humans appears to have changed in character as its geographical range has expanded from equatorial Africa and Asia, resulting in large outbreaks linked with neurological sequelae and congenital abnormalities.
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. …

451 citations

Journal ArticleDOI
TL;DR: The conclusion reached is that increased human population growth in decades ahead coupled with increased international travel and trade is likely to sustain and increase the threat of further geographical spread of current and new arboviral disease.
Abstract: Key aspects of 36 mosquito-borne arboviruses indigenous to Africa are summarized, including lesser or poorly-known viruses which, like Zika, may have the potential to escape current sylvatic cycling to achieve greater geographical distribution and medical importance. Major vectors are indicated as well as reservoir hosts, where known. A series of current and future risk factors is addressed. It is apparent that Africa has been the source of most of the major mosquito-borne viruses of medical importance that currently constitute serious global public health threats, but that there are several other viruses with potential for international challenge. The conclusion reached is that increased human population growth in decades ahead coupled with increased international travel and trade is likely to sustain and increase the threat of further geographical spread of current and new arboviral disease.

192 citations

Journal ArticleDOI
TL;DR: This review summarizes the literature on the main vectors of ZIKV (sylvatic and urban) across all the five continents with special focus on vector competence studies.

122 citations

Journal ArticleDOI
TL;DR: It is strongly suggested that arboviruses circulate and are common causes of disease in Guinea and improving surveillance and laboratory capacity forArbovirus diagnoses will be integral to understanding the burden posed by these agents in the region.
Abstract: Acute febrile illnesses comprise the majority of the human disease burden in sub-Saharan Africa. We hypothesized that arboviruses comprised a considerable proportion of undiagnosed febrile illnesses in Guinea and sought to determine the frequency of arboviral disease in two hospitals there. Using a standard case definition, 47 suspected cases were detected in approximately 4 months. Immunoglobulin M antibody capture enzyme-linked immunosorbent assays and plaque-reduction neutralization assays revealed that 63% (30/47) of patients were infected with arboviruses, including 11 West Nile, 2 yellow fever, 1 dengue, 8 chikungunya, and 5 Tahyna infections. Except for yellow fever, these are the first reported cases of human disease from these viruses in Guinea and the first reported cases of symptomatic Tahyna infection in Africa. These results strongly suggest that arboviruses circulate and are common causes of disease in Guinea. Improving surveillance and laboratory capacity for arbovirus diagnoses will be integral to understanding the burden posed by these agents in the region.

60 citations

Journal ArticleDOI
TL;DR: SPONV and ZIKV nucleotide and amino acid divergence coupled with differences in geographic distribution, ecology and vector species support previous reports that these viruses are separate species.
Abstract: Background Zika virus (ZIKV) has extended its known geographic distribution to the New World and is now responsible for severe clinical complications in a subset of patients While substantial genetic and vector susceptibility data exist for ZIKV, less is known for the closest related flavivirus, Spondweni virus (SPONV) Both ZIKV and SPONV have been known to circulate in Africa since the mid-1900s, but neither has been genetically characterized by gene and compared in parallel Furthermore, the susceptibility of peridomestic mosquito species incriminated or suspected in the transmission of ZIKV to SPONV was unknown Methodology/Principal Findings In this study, two geographically distinct strains of SPONV were genetically characterized and compared to nine genetically and geographically distinct ZIKV strains Additionally, the susceptibility of both SPONV strains was determined in three mosquito species The open reading frame (ORF) of the SPONV 1952 Nigerian Chuku strain, exhibited a nucleotide and amino acid identity of 978% and 992%, respectively, when compared to the SPONV 1954 prototype South African SA Ar 94 strain The ORF of the SPONV Chuku strain exhibited a nucleotide and amino acid identity that ranged from 683% to 690% and 746% to 750%, respectively, when compared to nine geographically and genetically distinct strains of ZIKV The ORF of the nine African and Asian lineage ZIKV strains exhibited limited nucleotide divergence Aedes aegypti, Ae albopictus and Culex quinquefasciatus susceptibility and dissemination was low or non-existent following artificial infectious blood feeding of moderate doses of both SPONV strains Conclusions/Significance SPONV and ZIKV nucleotide and amino acid divergence coupled with differences in geographic distribution, ecology and vector species support previous reports that these viruses are separate species Furthermore, the low degree of SPONV infection or dissemination in Ae albopictus, Ae aegypti and Cx quinquefasciatus following exposure to two geographically and genetically distinct virus strains suggest a low potential for these species to serve as vectors

42 citations