Transmission cycles, host range, evolution and emergence of arboviral disease
Identifieur interne : 001424 ( Pmc/Checkpoint ); précédent : 001423; suivant : 001425Transmission cycles, host range, evolution and emergence of arboviral disease
Auteurs : Scott C. Weaver ; Alan D. T. BarrettSource :
- Nature Reviews. Microbiology [ 1740-1526 ] ; 2004.
Abstract
Many recent viral pandemics have been attributed to the ability of some RNA viruses, for example HIV, dengue virus and possibly the severe acute respiratory syndrome (SARS) coronavirus, to change their host range to include humans. The authors discuss the mechanisms of host-range alteration used by a selection of viruses, including Venezuelan equine and Japanese encephalitis viruses (VEEV and JEV, respectively), dengue virus and West Nile virus (WNV). Venezuelan equine encephalitis (VEE) was first recognized as a disease of horses, donkeys and mules in northern South America during the mid 1930s, but there has been renewed interest in this virus because of its potential as a biological weapon. Molecular analysis of epidemic strains — which exploit horses for amplification — and comparison with strains that do not cause epidemic disease, have shown that a few amino-acid mutations can affect host-range alteration. Changes on the surface of the VEE virion seem to be important for these host range changes. JEV causes epidemics of encephalitis in India, Korea, China, South-East Asia and Indonesia. The disease affects children, and is associated with a mortality rate of greater than 20%. However, unlike VEEV, there is no evidence that JEV undergoes mutation and selection to replicate in different hosts. Pigs amplify transmission in peridomestic settings, and migratory birds have a role in dispersion of JEV. Although different genotypes have been isolated, their relevance to pathology and host range is unclear. WNV is now endemic in the United States after first emerging in New York in 1999. WNV has a very broad host range. Forty-nine species of mosquitoes and ticks, and 225 species of birds are susceptible to infection. Other hosts include horses, cattle, llamas, alligators, cats, dogs, wolves and sheep. Transmission of WNV among these species has not been reported. Although humans are probably dead-end hosts, infection with WNV can cause severe disease. Dengue viruses are very important human arboviral pathogens and use humans as reservoir hosts. Finally, the authors discuss how host-range changes can be studied experimentally. Cell-culture model systems can be used to find mutations that correlate with virus fitness and adaptation in different host strains. Viruses that replicate in useful laboratory animal models can also be studied in whole animal hosts.
Url:
DOI: 10.1038/nrmicro1006
PubMed: 15378043
PubMed Central: 7097645
Affiliations:
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<front><div type="abstract" xml:lang="en"><title>Key Points</title>
<p id="Par3"><list list-type="bullet"><list-item><p id="Par4">Many recent viral pandemics have been attributed to the ability of some RNA viruses, for example HIV, dengue virus and possibly the severe acute respiratory syndrome (SARS) coronavirus, to change their host range to include humans. The authors discuss the mechanisms of host-range alteration used by a selection of viruses, including Venezuelan equine and Japanese encephalitis viruses (VEEV and JEV, respectively), dengue virus and West Nile virus (WNV).</p>
</list-item>
<list-item><p id="Par5">Venezuelan equine encephalitis (VEE) was first recognized as a disease of horses, donkeys and mules in northern South America during the mid 1930s, but there has been renewed interest in this virus because of its potential as a biological weapon. Molecular analysis of epidemic strains — which exploit horses for amplification — and comparison with strains that do not cause epidemic disease, have shown that a few amino-acid mutations can affect host-range alteration. Changes on the surface of the VEE virion seem to be important for these host range changes.</p>
</list-item>
<list-item><p id="Par6">JEV causes epidemics of encephalitis in India, Korea, China, South-East Asia and Indonesia. The disease affects children, and is associated with a mortality rate of greater than 20%. However, unlike VEEV, there is no evidence that JEV undergoes mutation and selection to replicate in different hosts. Pigs amplify transmission in peridomestic settings, and migratory birds have a role in dispersion of JEV. Although different genotypes have been isolated, their relevance to pathology and host range is unclear.</p>
</list-item>
<list-item><p id="Par7">WNV is now endemic in the United States after first emerging in New York in 1999. WNV has a very broad host range. Forty-nine species of mosquitoes and ticks, and 225 species of birds are susceptible to infection. Other hosts include horses, cattle, llamas, alligators, cats, dogs, wolves and sheep. Transmission of WNV among these species has not been reported. Although humans are probably dead-end hosts, infection with WNV can cause severe disease.</p>
</list-item>
<list-item><p id="Par8">Dengue viruses are very important human arboviral pathogens and use humans as reservoir hosts. <italic>Aedes aegypti</italic>
and <italic>Aedes albopictus</italic>
mosquitoes are the most common vectors in urban settings. It is thought that the human epidemic form of dengue virus evolved in the last 2000 years, and genetic analysis indicates that mutations have resulted in adaptation to the urban mosquito host. However, links between mutations and human pathogenicity have not been established.</p>
</list-item>
<list-item><p id="Par9">Finally, the authors discuss how host-range changes can be studied experimentally. Cell-culture model systems can be used to find mutations that correlate with virus fitness and adaptation in different host strains. Viruses that replicate in useful laboratory animal models can also be studied in whole animal hosts.</p>
</list-item>
</list>
</p>
</div>
</front>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Nat Rev Microbiol</journal-id>
<journal-id journal-id-type="iso-abbrev">Nat. Rev. Microbiol</journal-id>
<journal-title-group><journal-title>Nature Reviews. Microbiology</journal-title>
</journal-title-group>
<issn pub-type="ppub">1740-1526</issn>
<issn pub-type="epub">1740-1534</issn>
<publisher><publisher-name>Nature Publishing Group UK</publisher-name>
<publisher-loc>London</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">15378043</article-id>
<article-id pub-id-type="pmc">7097645</article-id>
<article-id pub-id-type="publisher-id">BFnrmicro1006</article-id>
<article-id pub-id-type="doi">10.1038/nrmicro1006</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Transmission cycles, host range, evolution and emergence of arboviral disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Weaver</surname>
<given-names>Scott C.</given-names>
</name>
<address><email>sweaver@utmb.edu</email>
</address>
<xref ref-type="aff" rid="Aff1">1</xref>
<bio><p id="Par1">Scott Weaver trained in entomology at Cornell University and in virology at the University of California, San Diego and Yale University. His interests include the ecology, evolution and pathogenesis of arboviral diseases, virus–vector interactions and vaccine development. He is Director of Tropical and Emerging Infectious Diseases at the University of Texas Medical Branch at Galveston.</p>
</bio>
</contrib>
<contrib contrib-type="author"><name><surname>Barrett</surname>
<given-names>Alan D. T.</given-names>
</name>
<xref ref-type="aff" rid="Aff2">2</xref>
<bio><p id="Par2">Alan Barrett is a professor in the Department of Pathology, and associate director of the Sealy Center for Vaccine Development at the University of Texas Medical Branch at Galveston. He has spent his career working on arthropod-borne viruses and is researching the development of vaccines against emerging viruses.</p>
</bio>
</contrib>
<aff id="Aff1"><label>1</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution>Department of Pathology,</institution>
<institution>Microbiology and Immunology, Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, 77555-0609 Texas USA</aff>
<aff id="Aff2"><label>2</label>
<institution-wrap><institution-id institution-id-type="GRID">grid.176731.5</institution-id>
<institution-id institution-id-type="ISNI">0000 0001 1547 9964</institution-id>
<institution>Department of Pathology,</institution>
<institution>Microbiology and Immunology, Center for Tropical Diseases, University of Texas Medical Branch,</institution>
</institution-wrap>
Galveston, 77555-0609 Texas USA</aff>
</contrib-group>
<pub-date pub-type="ppub"><year>2004</year>
</pub-date>
<volume>2</volume>
<issue>10</issue>
<fpage>789</fpage>
<lpage>801</lpage>
<permissions><copyright-statement>© Nature Publishing Group 2004</copyright-statement>
<license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p>
</license>
</permissions>
<abstract id="Abs1" abstract-type="KeyPoints"><title>Key Points</title>
<p id="Par3"><list list-type="bullet"><list-item><p id="Par4">Many recent viral pandemics have been attributed to the ability of some RNA viruses, for example HIV, dengue virus and possibly the severe acute respiratory syndrome (SARS) coronavirus, to change their host range to include humans. The authors discuss the mechanisms of host-range alteration used by a selection of viruses, including Venezuelan equine and Japanese encephalitis viruses (VEEV and JEV, respectively), dengue virus and West Nile virus (WNV).</p>
</list-item>
<list-item><p id="Par5">Venezuelan equine encephalitis (VEE) was first recognized as a disease of horses, donkeys and mules in northern South America during the mid 1930s, but there has been renewed interest in this virus because of its potential as a biological weapon. Molecular analysis of epidemic strains — which exploit horses for amplification — and comparison with strains that do not cause epidemic disease, have shown that a few amino-acid mutations can affect host-range alteration. Changes on the surface of the VEE virion seem to be important for these host range changes.</p>
</list-item>
<list-item><p id="Par6">JEV causes epidemics of encephalitis in India, Korea, China, South-East Asia and Indonesia. The disease affects children, and is associated with a mortality rate of greater than 20%. However, unlike VEEV, there is no evidence that JEV undergoes mutation and selection to replicate in different hosts. Pigs amplify transmission in peridomestic settings, and migratory birds have a role in dispersion of JEV. Although different genotypes have been isolated, their relevance to pathology and host range is unclear.</p>
</list-item>
<list-item><p id="Par7">WNV is now endemic in the United States after first emerging in New York in 1999. WNV has a very broad host range. Forty-nine species of mosquitoes and ticks, and 225 species of birds are susceptible to infection. Other hosts include horses, cattle, llamas, alligators, cats, dogs, wolves and sheep. Transmission of WNV among these species has not been reported. Although humans are probably dead-end hosts, infection with WNV can cause severe disease.</p>
</list-item>
<list-item><p id="Par8">Dengue viruses are very important human arboviral pathogens and use humans as reservoir hosts. <italic>Aedes aegypti</italic>
and <italic>Aedes albopictus</italic>
mosquitoes are the most common vectors in urban settings. It is thought that the human epidemic form of dengue virus evolved in the last 2000 years, and genetic analysis indicates that mutations have resulted in adaptation to the urban mosquito host. However, links between mutations and human pathogenicity have not been established.</p>
</list-item>
<list-item><p id="Par9">Finally, the authors discuss how host-range changes can be studied experimentally. Cell-culture model systems can be used to find mutations that correlate with virus fitness and adaptation in different host strains. Viruses that replicate in useful laboratory animal models can also be studied in whole animal hosts.</p>
</list-item>
</list>
</p>
</abstract>
<abstract id="Abs2"><p id="Par10">Many pandemics have been attributed to the ability of some RNA viruses to change their host range to include humans. Here, we review the mechanisms of disease emergence that are related to the host-range specificity of selected mosquito-borne alphaviruses and flaviviruses. We discuss viruses of medical importance, including Venezuelan equine and Japanese encephalitis viruses, dengue viruses and West Nile viruses.</p>
</abstract>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© Springer Nature Limited 2004</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Barrett, Alan D T" sort="Barrett, Alan D T" uniqKey="Barrett A" first="Alan D. T." last="Barrett">Alan D. T. Barrett</name>
<name sortKey="Weaver, Scott C" sort="Weaver, Scott C" uniqKey="Weaver S" first="Scott C." last="Weaver">Scott C. Weaver</name>
</noCountry>
</tree>
</affiliations>
</record>
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