DOCSLIB.ORG

Rift Valley and West Nile Virus Antibodies in Camels, North Africa

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Rift Valley and West Nile Virus Antibodies in Camels, North Africa LETTERS 4°75′Ε) during May–June 2010. All 2. Fijan N, Matasin Z, Petrinec Z, Val- Rift Valley and larvae were euthanized as part of an potiç I, Zwillenberg LO. Isolation of an iridovirus-like agent from the green frog West Nile Virus invasive species eradication project (Rana esculenta L.). Vet Arch Zagreb. and stored at –20°C until further 1991;3:151–8. Antibodies use. At necropsy, liver tissues were 3. Cunningham AA, Langton TES, Bennet in Camels, collected, and DNA was extracted PM, Lewin JF, Drury SEN, Gough RE, et al. Pathological and microbiological North Africa by using the Genomic DNA Mini fi ndings from incidents of unusual mor- Kit (BIOLINE, London, UK). PCR tality of the common frog (Rana tempo- To the Editor: Different to detect ranavirus was performed as raria). Philos Trans R Soc Lond B Biol arboviral diseases have expanded described by Mao et al. (10). Sci. 1996;351:1539–57. doi:10.1098/ rstb.1996.0140 their geographic range in recent times. Three samples showed positive 4. Hyatt AD, Gould AR, Zupanovic Z, Of them, Rift Valley fever, West Nile results with this PCR. These samples Cunningham AA, Hengstberger S, Whit- fever, and African horse sickness were sequenced by using primers tington RJ, et al. Comparative studies of are of particular concern. They are M4 and M5 described by Mao et al. piscine and amphibian iridoviruses. Arch Virol. 2000;145:301–31. doi:10.1007/ endemic to sub-Saharan Africa but (10) and blasted in GenBank. A 100% s007050050025 occasionally spread beyond this area. homology with the common midwife 5. Balseiro A, Dalton KP, Del Cerro A, Mar- Trade and transport of animals and toad (A. obstetricans) ranavirus partial quez I, Cunningham AA, Parra F, et al. animal products, along with wildlife major capsid protein gene (GenBank Pathology, isolation and molecular char- acterisation of a ranavirus from the com- movements, are considered the accession no. FM213466.1) was mon midwife toad Alytes obstetricans on driving factors in the spread of these found (5). Despite the low prevalence the Iberian Peninsula. Dis Aquat Organ. pathogens. of Ranavirus infection (0.75%) in 2009;84:95–104. doi:10.3354/dao02032 In wide regions of Africa, the bullfrog tadpoles examined, this 6. Ficetola GF, Coic C, Detaint M, Berro- neau M, Lorvelec O, Miaud C. Pattern 1-humped camels (Camelus study shows that invasive bullfrogs, a of distribution of the American bullfrog dromedarius) are valuable livestock known reservoir of chytridiomycosis, Rana catesbeiana in Europe. Biol In- appreciated as a meat source and as are also a likely carrier of ranaviral vasions. 2007;9:767–72. doi:10.1007/ a means for transportation of goods. disease in Europe. s10530-006-9080-y 7. Schloegel LM, Ferreira CM, James TY, Camels are susceptible to infection by Hipolito M, Longcore JE, Hyatt AD, et al. Rift Valley fever virus (RVFV), West This study was partly performed The North American bullfrog as a reser- Nile virus (WNV), and African horse in the framework of European Union voir for the spread of Batrachochytrium sickness virus (AHSV), although their Interreg IVA project IVA-VLANED-2.31 dendrobatidis in Brazil. Anim Conserv. epidemiologic role in these diseases is “Invasieve exoten in Vlaanderen en Zuid- 2010;13(S1):53–61. doi:10.1111/j.1469- 1795.2009.00307.x uncertain (1–3). Movements of camels Nederland–INVEXO.” 8. Daszak P, Strieby A, Cunningham AA, across the Sahara Desert could carry Longcore JE, Brown CC, Porter D. Ex- these pathogens to northern Africa. To Mojdeh Sharifi an-Fard, perimental evidence that the bullfrog (Rana catesbeiana) is a potential carrier test this hypothesis, we conducted a Frank Pasmans, of chytridiomycosis, an emerging fungal serologic survey in 1-humped camels Connie Adriaensen, disease of amphibians. Herpetolog J. intercepted at different points by the Sander Devisscher, 2004;14:201–7. Moroccan Veterinary Services in Tim Adriaens, Gerald Louette, 9. Miller DL, Gray MJ, Rajeev S, Schmutzer AC, Burton EC, Merril A, et al. Pathologi- 2009. The camels were coming from and An Martel cal fi ndings in larval and juvenile anurans the southeastern part of the Sahara Author affi liations: Ghent University, inhabiting farm ponds in Tennessee, USA. Desert going to the northwest. Merelbeke, Belgium (M. Sharifi an-Fard, F. J Wildl Dis. 2009;45:314–24. 10. Mao J, Hedrick RP, Chichar VB. Molecu- Serum samples were obtained Pasmans, C. Adriaensen, A. Martel); and lar characterization, sequence analysis, in Smara-Laayoune, Dakhla, and Research Institute for Nature and Forest, and taxonomic position of newly isolated Tata (Table). Most samples (71 of Brussels, Belgium (S. Devisscher, T. fi sh iridoviruses. Virology. 1997;229:212– 100 total samples) were from male Adriaens, G. Louette) 20. doi:10.1006/viro.1996.8435 camels. Samples were also grouped by age of the camels (Table). RVFV DOI: http://dx.doi.org/10.3201/eid1712.110236 Address for correspondence: An Martel, antibodies were detected by using a Department of Pathology, Bacteriology and competitive ELISA (4), and samples References Avian Diseases, Faculty of Veterinary Medicine, yielding positive ELISA results were Ghent University, Salisburylaan 133, B-9820 1. Ariel E, Kielgast J, Svart HE, Larsen K, confi rmed by virus-neutralization Tapiovaara H, Jensen BB, et al. Ranavi- Belgium; email: [email protected] rus in wild edible frogs Pelophylax kl. test. WNV-specifi c antibodies were esculentus in Denmark. Dis Aquat Organ. detected by ELISA (5), and positive 2009;85:7–14. doi:10.3354/dao02060 results were confi rmed by virus- 2372 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 12, December 2011 LETTERS neutralization test. AHSV-specifi c 15 RVFV-positive samples, 12 were these are known to reemerge under antibodies were detected by using also positive for WNV antibodies, and certain circumstances in locations the ELISA prescribed by the World 12 of 29 WNV-positive samples were where they have occurred in the past. Organisation for Animal Health. also positive for RVFV (χ2 = 8.37, The results of this study support Fifteen of 100 samples were df = 1, p < 0.05). that camels moving across the Sahara positive for RVFV-specifi c antibodies Antibodies to 2 zoonotic have contact with RVFV and WNV, by competitive ELISA, all of which arboviruses, i.e., RVFV and WNV, and frequently the same animals have were confi rmed by virus-neutralization were present in camels moving to been infected by both agents. In a test, with neutralization titers ranging the northwestern part of the Sahara particularly dry environment such as from 40 to 1,280 (geometric mean Desert, and antibodies to AHSV were the desert, particular attention should titer = 229). With regard to WNV absent in the populations examined. be paid to singular wet areas such antibodies, the ELISA detected 44 Despite the higher percentage of as oases. The presence of water in positive samples and 1 doubtful seropositivity for WNV than for these areas results in an abundance sample, of which 29 were confi rmed RVFV, the epidemiologic consequence of competent mosquitoes and hosts, as positive by virus-neutralization test of RVFV-specifi c antibodies in this which in turn makes these viruses (virus-neutralization test titers ranging population could be higher than that likely to cycle and infect domestic from 10 to 640; geometric mean for WNV antibodies. Camels can act animals such as camels coming to titer = 20). As for AHSV antibodies, as reservoir hosts for RVFV (6) but drink and rest. none of the samples was positive by are unlikely to do so for WNV, which ELISA. Prevalence data were analyzed cycles between mosquitoes and wild Acknowledgments by generalized linear model with birds with mammals usually being We thank the Ministry of Agriculture locality (Dakhla or Smara), sex, and dead-end hosts. High prevalence of of Morocco for technical assistance on age as fi xed factors. No differences by antibodies to RVFV in camels has been sample collection. origin or sex were found in prevalence described in different sub-Saharan and for WNV (p>0.14) but antibodies Sahelian countries (7–9). Camels have This research was supported by were more prevalent in camels >3 been involved in the spread of disease Biopharma and INIA-MARM agreement years of age (χ2 = 14.04, 3 df, p = in some instances (10). Immunity to no. CC08-020. 0.003). No differences in prevalence RVFV indicates previous infection. of RVFV antibodies were found by Our results showed that seroprevalence Mehdi El-Harrak, sex (p = 0.29), but prevalence was of RVFV was higher among older Raquel Martín-Folgar, higher in Smara (χ2 = 3.74, p = 0.05) than younger camels, indicating Francisco Llorente, and among camels >6 years of age that contact could have occurred Paloma Fernández-Pacheco, (χ2 = 8.37, df = 3, p = 0.04) (Table). some years ago. Nevertheless, these Alejandro Brun, Jordi Figuerola, We also examined the co-occurrence populations should be monitored for and Miguel Ángel Jiménez- of antibodies to RVFV and WNV. Of RVFV and other arboviroses because Clavero Author affi liations: Biopharma, Rabat, Table. Results of testing of camels for virus antibodies, by location, age group, and sex Morocco (M. El-Harrak); Centro de of camels examined, North Africa, 2009* Investigación en Sanidad Animal, No. No. positive for antibody Valdeolmos, Spain (R. Martín-Folgar, F. Camel characteristic samples RVFV WNV AHSV RVFV and WNV Llorente, P. Fernández-Pacheco, A. Brun, Origin M.Á. Jiménez-Clavero); and Estación Tata 2 0 0 0 0 Biológica de Doñana, Seville, Spain (J. Smara-Laayoune 58 13 20 0 11 Figuerola). Dakhla 40 2 9 0 1 Age group, y DOI: http://dx.doi.org/10.3201/eid1712.110587 <1 18 1 1 0 1 1–2 25 0 1 0 0 3–5 7 1 3 0 1 6–10 27 6 12 0 10 References >10 23 7 12 0 0 1.
Load more

Recommended publications
  • Executive Orders and Emergency Declarations for the West Nile Virus: Applying Lessons from Past Outbreaks to Zika
    Executive Orders and Emergency Declarations for the West Nile Virus: Applying Lessons from Past Outbreaks to Zika Government leaders are often given the authority to issue executive orders (EOs), proclamations, or emergency declarations to address public health threats, such as that posed by the Zika virus.1 Local, state, and federal executive branch leaders have used these powers to address public health threats posed by other mosquito-borne diseases.2 While existing laws and regulations may allow localities, states, and the federal government to take action to combat mosquito-borne threats absent an EO or emergency declaration, examining such executive actions provides a snapshot of how some jurisdictions have responded to past outbreaks. As of February 21, 2016, only one territory and two states (Puerto Rico, Florida, and Hawaii) have issued emergency declarations that contemplate the threats posed by the Zika virus.3, 4 Historically, however, many US jurisdictions have taken such actions to address other mosquito-borne illnesses, such as West Nile virus. The following provides a brief analysis of select uses of local, state, and federal executive powers to combat West Nile virus. Examining the use of executive powers to address West 1 L Rutkow et al. The Public Health Workforce and Willingness to Respond to Emergencies: A 50-State Analysis of Potentially Influential Laws, 42 J. LAW MED. & ETHICS 64, 64 (2014) (“In the United States, at the federal, state, and local levels, laws provide an infrastructure for public health emergency preparedness and response efforts. Law is perhaps most visible during an emergency when the president or a state’s governor issues a disaster declaration establishing the temporal and geographic parameters for the response and making financial and other resources available.”).
    [Show full text]
  • A New Orbivirus Isolated from Mosquitoes in North-Western Australia Shows Antigenic and Genetic Similarity to Corriparta Virus B
    viruses Article A New Orbivirus Isolated from Mosquitoes in North-Western Australia Shows Antigenic and Genetic Similarity to Corriparta Virus but Does Not Replicate in Vertebrate Cells Jessica J. Harrison 1,†, David Warrilow 2,†, Breeanna J. McLean 1, Daniel Watterson 1, Caitlin A. O’Brien 1, Agathe M.G. Colmant 1, Cheryl A. Johansen 3, Ross T. Barnard 1, Sonja Hall-Mendelin 2, Steven S. Davis 4, Roy A. Hall 1 and Jody Hobson-Peters 1,* 1 Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia 4072, Australia; [email protected] (J.J.H.); [email protected] (B.J.M.); [email protected] (D.W.); [email protected] (C.A.O.B.); [email protected] (A.M.G.C.); [email protected] (R.T.B.); [email protected] (R.A.H.) 2 Public Health Virology Laboratory, Department of Health, Queensland Government, P.O. Box 594, Archerfield 4108, Australia; [email protected] (D.W.); [email protected] (S.H.-M.) 3 School of Pathology and Laboratory Medicine, The University of Western Australia, Nedlands 6009, Australia; [email protected] 4 Berrimah Veterinary Laboratory, Department of Primary Industries and Fisheries, Darwin 0828, Australia; [email protected] * Correspondence: [email protected]; Tel.: +61-7-3365-4648 † These authors contributed equally to the work. Academic Editor: Karyn Johnson Received: 19 February 2016; Accepted: 10 May 2016; Published: 20 May 2016 Abstract: The discovery and characterisation of new mosquito-borne viruses provides valuable information on the biodiversity of vector-borne viruses and important insights into their evolution.
    [Show full text]
  • Wnv-Case-Definition.Pdf
    Draft Case Definition for West Nile Fever Animal and Plant Health Inspection Service West Nile Fever Veterinary Services October 2018 Case Definition (Notifiable) 1. Clinical Signs 1.1 Clinical Signs: West Nile Fever (WNF) is a zoonotic mosquito-borne viral disease caused by the West Nile virus (WNV), a Flavivirus of the family Flaviviridae. Many vertebrate species are susceptible to natural WNV infection; however, fatal neurological outbreaks have only been documented in equids, humans, geese, wild birds (particularly corvids), squirrels, farmed alligators, and dogs. Birds serve as the natural host reservoir of WNV. The incubation period is estimated to be three to 15 days in horses Ten to 39 percent of unvaccinated horses infected with WNV will develop clinical signs. Most clinically affected horses exhibit neurological signs such as ataxia (including stumbling, staggering, wobbly gait, or incoordination) or at least two of the following: circling, hind limb weakness, recumbency or inability to stand (or both), multiple limb paralysis, muscle fasciculation, proprioceptive deficits, altered mental status, blindness, lip droop/paralysis, teeth grinding. Behavioral changes including somnolence, listlessness, apprehension, or periods of hyperexcitability may occur. Other common clinical signs include colic, lameness, anorexia, and fever. 2. Laboratory criteria: 2.1 Agent isolation and identification: The virus can be identified by polymerase chain reaction (PCR) and virus isolation (VI). Preferred tissues from equids are brain or spinal cord. 2.2 Serology: Antibody titers can be identified in paired serum samples by IgM and IgG capture enzyme linked immunosorbent assay (ELISA), plaque reduction neutralization test (PRNT), and virus neutralization (VN). Only a single serum sample is required for IgM capture ELISA, and this is the preferred serologic test in live animals.
    [Show full text]
  • Potential Arbovirus Emergence and Implications for the United Kingdom Ernest Andrew Gould,* Stephen Higgs,† Alan Buckley,* and Tamara Sergeevna Gritsun*
    Potential Arbovirus Emergence and Implications for the United Kingdom Ernest Andrew Gould,* Stephen Higgs,† Alan Buckley,* and Tamara Sergeevna Gritsun* Arboviruses have evolved a number of strategies to Chikungunya virus and in the family Bunyaviridae, sand- survive environmental challenges. This review examines fly fever Naples virus (often referred to as Toscana virus), the factors that may determine arbovirus emergence, pro- sandfly fever Sicilian virus, Crimean-Congo hemorrhagic vides examples of arboviruses that have emerged into new fever virus (CCHFV), Inkoo virus, and Tahyna virus, habitats, reviews the arbovirus situation in western Europe which is widespread throughout Europe. Rift Valley fever in detail, discusses potential arthropod vectors, and attempts to predict the risk for arbovirus emergence in the virus (RVFV) and Nairobi sheep disease virus (NSDV) United Kingdom. We conclude that climate change is prob- could be introduced to Europe from Africa through animal ably the most important requirement for the emergence of transportation. Finally, the family Reoviridae contains a arthropodborne diseases such as dengue fever, yellow variety of animal arbovirus pathogens, including blue- fever, Rift Valley fever, Japanese encephalitis, Crimean- tongue virus and African horse sickness virus, both known Congo hemorrhagic fever, bluetongue, and African horse to be circulating in Europe. This review considers whether sickness in the United Kingdom. While other arboviruses, any of these pathogenic arboviruses are likely to emerge such as West Nile virus, Sindbis virus, Tahyna virus, and and cause disease in the United Kingdom in the foresee- Louping ill virus, apparently circulate in the United able future. Kingdom, they do not appear to present an imminent threat to humans or animals.
    [Show full text]
  • Rift Valley Fever for Host Innate Immunity in Resistance to a New
    A New Mouse Model Reveals a Critical Role for Host Innate Immunity in Resistance to Rift Valley Fever This information is current as Tânia Zaverucha do Valle, Agnès Billecocq, Laurent of September 25, 2021. Guillemot, Rudi Alberts, Céline Gommet, Robert Geffers, Kátia Calabrese, Klaus Schughart, Michèle Bouloy, Xavier Montagutelli and Jean-Jacques Panthier J Immunol 2010; 185:6146-6156; Prepublished online 11 October 2010; Downloaded from doi: 10.4049/jimmunol.1000949 http://www.jimmunol.org/content/185/10/6146 Supplementary http://www.jimmunol.org/content/suppl/2010/10/12/jimmunol.100094 http://www.jimmunol.org/ Material 9.DC1 References This article cites 46 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/185/10/6146.full#ref-list-1 Why The JI? Submit online. by guest on September 25, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American
    [Show full text]
  • West Nile Virus (WNV) Fact Sheet
    West Nile Virus (WNV) Fact Sheet What Is West Nile Virus? How Does West Nile Virus Spread? West Nile virus infection can cause serious disease. WNV is ▪ Infected Mosquitoes. established as a seasonal epidemic in North America that WNV is spread by the bite of an infected mosquito. flares up in the summer and continues into the fall. This Mosquitoes become infected when they feed on fact sheet contains important information that can help infected birds. Infected mosquitoes can then spread you recognize and prevent West Nile virus. WNV to humans and other animals when they bite. What Can I Do to Prevent WNV? ▪ Transfusions, Transplants, and Mother-to-Child. In a very small number of cases, WNV also has been The easiest and best way to avoid WNV is to prevent spread directly from an infected person through blood mosquito bites. transfusions, organ transplants, breastfeeding and ▪ When outdoors, use repellents containing DEET, during pregnancy from mother to baby. picaridin, IR3535, some oil of lemon eucalyptus or para- Not through touching. menthane-diol. Follow the directions on the package. ▪ WNV is not spread through casual contact such as ▪ Many mosquitoes are most active from dusk to dawn. touching or kissing a person with the virus. Be sure to use insect repellent and wear long sleeves and pants at these times or consider staying indoors How Soon Do Infected People Get Sick? during these hours. People typically develop symptoms between 3 and 14 days after they are bitten by the infected mosquito. ▪ Make sure you have good screens on your windows and doors to keep mosquitoes out.
    [Show full text]
  • Interaction of TIA-1/TIAR with West Nile and Dengue Virus Products in Infected Cells Interferes with Stress Granule Formation and Processing Body Assembly
    Interaction of TIA-1/TIAR with West Nile and dengue virus products in infected cells interferes with stress granule formation and processing body assembly Mohamed M. Emara and Margo A. Brinton* Department of Biology, Georgia State University, Atlanta, GA 30302 Communicated by Hilary Koprowski, Thomas Jefferson University, Philadelphia, PA, April 11, 2007 (received for review February 23, 2007) -The West Nile virus minus-strand 3؅ terminal stem loop (SL) RNA cells and tissues (8, 9). TIA-1 and TIAR contain three N was previously shown to bind specifically to cellular stress granule terminal RNA recognition motifs (RRM) (10) and a glutamine- (SG) components, T cell intracellular antigen-1 (TIA-1) and the rich C-terminal domain, called prion-related domain (PRD), related protein TIAR. In vitro TIAR binding was 10 times more that shares structural and functional characteristics with the efficient than TIA-1. The 3؅(؊)SL functions as the promoter for aggregation domains of mammalian and yeast prion proteins genomic RNA synthesis. Colocalization of TIAR and TIA-1 with the (11). A recombinant TIA-1 protein lacking the three RNA- viral replication complex components dsRNA and NS3 was ob- binding domains was unable to bind poly(A)ϩ RNA and recruit served in the perinuclear regions of West Nile virus- and dengue it to SGs (2). Deletion of the TIA-1 PRD inhibited protein virus-infected cells. The kinetics of accumulation of TIAR in the aggregation and SG assembly (11). PRD aggregation is regulated perinuclear region was similar to those of genomic RNA synthesis. by the molecular chaperone heat shock protein 70 (HSP70), and In contrast, relocation of TIA-1 to the perinuclear region began only overexpression of HSP70 prevented cytosolic aggregation of after maximal levels of RNA synthesis had been achieved, except PRD (11).
    [Show full text]
  • Transmission of Dengue Virus Without a Mosquito Vector: Nosocomial
    BRIEF REPORT Transmission of Dengue Virus had recently returned from Peru; the presumed mechanism of transmission was mucocutaneous exposure that occurred dur- without a Mosquito Vector: ing medical care. We describe both cases of dengue fever and Nosocomial Mucocutaneous review the ways that dengue virus can be transmitted without mosquito vectors. Transmission and Other Routes Case reports. Patient 1, a 48-year-old female traveler, pres- of Transmission ented in November 2002 with a 5-day history of fever, myalgia, Downloaded from https://academic.oup.com/cid/article/39/6/e56/359683 by guest on 30 September 2021 and headache. She had recently returned from Iquitos, Peru Lin H. Chen1,2,3 and Mary E. Wilson1,3 (on a trip that lasted from 1 through 10 November), where 1Harvard Medical School, and 2Travel Medicine Center and 3Division of she worked as a nurse on a medical mission and traveled Infectious Diseases, Mount Auburn Hospital, Cambridge, Massachusetts through the Amazon jungles. She stayed in a hotel that had unscreened, open windows. The patient had received hepatitis A virus, hepatitis B virus, and oral typhoid vaccines prior to We report a case of dengue fever in a Boston-area health travel, and she took mefloquine hydrochloride for malaria pro- care worker with no recent history of travel but with mu- phylaxis. She had received yellow fever vaccine in 1997. cocutaneous exposure to infected blood from a febrile trav- At examination, the patient’s temperature was 37.9ЊC. Ab- eler who had recently returned from Peru. Serologic tests normal findings included marked erythroderma, especially on confirmed acute dengue virus infection in both the traveler the patient’s back, and a maculopapular rash along her hairline.
    [Show full text]
  • Single Mosquito Metatranscriptomics Identifies Vectors, Emerging Pathogens and Reservoirs in One Assay
    TOOLS AND RESOURCES Single mosquito metatranscriptomics identifies vectors, emerging pathogens and reservoirs in one assay Joshua Batson1†, Gytis Dudas2†, Eric Haas-Stapleton3†, Amy L Kistler1†*, Lucy M Li1†, Phoenix Logan1†, Kalani Ratnasiri4†, Hanna Retallack5† 1Chan Zuckerberg Biohub, San Francisco, United States; 2Gothenburg Global Biodiversity Centre, Gothenburg, Sweden; 3Alameda County Mosquito Abatement District, Hayward, United States; 4Program in Immunology, Stanford University School of Medicine, Stanford, United States; 5Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, United States Abstract Mosquitoes are major infectious disease-carrying vectors. Assessment of current and future risks associated with the mosquito population requires knowledge of the full repertoire of pathogens they carry, including novel viruses, as well as their blood meal sources. Unbiased metatranscriptomic sequencing of individual mosquitoes offers a straightforward, rapid, and quantitative means to acquire this information. Here, we profile 148 diverse wild-caught mosquitoes collected in California and detect sequences from eukaryotes, prokaryotes, 24 known and 46 novel viral species. Importantly, sequencing individuals greatly enhanced the value of the biological information obtained. It allowed us to (a) speciate host mosquito, (b) compute the prevalence of each microbe and recognize a high frequency of viral co-infections, (c) associate animal pathogens with specific blood meal sources, and (d) apply simple co-occurrence methods to recover previously undetected components of highly prevalent segmented viruses. In the context *For correspondence: of emerging diseases, where knowledge about vectors, pathogens, and reservoirs is lacking, the [email protected] approaches described here can provide actionable information for public health surveillance and †These authors contributed intervention decisions.
    [Show full text]
  • West Nile Virus
    West Nile Virus Frequently Asked Questions What is West Nile virus? West Nile virus is a viral infection that is spread by the bite of an infected mosquito. Mosquitoes get infected with the West Nile virus by feeding on infected birds. The infected mosquitoes then spread the virus by biting humans and other animals, such as horses. Identified in the United States in 1999, West Nile virus is seen most often during the summer and early fall months. Who gets West Nile virus? Anyone can get infected with the West Nile virus. The virus can affect anyone bitten by an infected mosquito. People over the age of 50 and people with weak immune systems are at greater risk of developing severe illness. How do people get West Nile virus? The virus is spread by the bite of a mosquito infected with the West Nile virus. What are the symptoms of West Nile virus? Many people infected with West Nile virus do not become ill and may not develop symptoms. About 20% of infected people will develop West Nile fever. When symptoms do occur, they may be mild or severe and show up 3 to 15 days after being bitten by an infected mosquito. • Mild symptoms inlcude flu-like illness with fever, headache, body aches, nausea and sometimes swollen lymph glands or a skin rash on the chest, stomach and back. • Severe symptoms include high fever, neck stiffness and swelling of the brain (encephalitis) which can lead to coma, convulsions and death. Less than 1% of infected people will develop severe symptoms.
    [Show full text]
  • Systematic Review of Important Viral Diseases in Africa in Light of the ‘One Health’ Concept
    pathogens Article Systematic Review of Important Viral Diseases in Africa in Light of the ‘One Health’ Concept Ravendra P. Chauhan 1 , Zelalem G. Dessie 2,3 , Ayman Noreddin 4,5 and Mohamed E. El Zowalaty 4,6,7,* 1 School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban 4001, South Africa; [email protected] 2 School of Mathematics, Statistics and Computer Science, University of KwaZulu-Natal, Durban 4001, South Africa; [email protected] 3 Department of Statistics, College of Science, Bahir Dar University, Bahir Dar 6000, Ethiopia 4 Infectious Diseases and Anti-Infective Therapy Research Group, Sharjah Medical Research Institute and College of Pharmacy, University of Sharjah, Sharjah 27272, UAE; [email protected] 5 Department of Medicine, School of Medicine, University of California, Irvine, CA 92868, USA 6 Zoonosis Science Center, Department of Medical Biochemistry and Microbiology, Uppsala University, SE 75185 Uppsala, Sweden 7 Division of Virology, Department of Infectious Diseases and St. Jude Center of Excellence for Influenza Research and Surveillance (CEIRS), St Jude Children Research Hospital, Memphis, TN 38105, USA * Correspondence: [email protected] Received: 17 February 2020; Accepted: 7 April 2020; Published: 20 April 2020 Abstract: Emerging and re-emerging viral diseases are of great public health concern. The recent emergence of Severe Acute Respiratory Syndrome (SARS) related coronavirus (SARS-CoV-2) in December 2019 in China, which causes COVID-19 disease in humans, and its current spread to several countries, leading to the first pandemic in history to be caused by a coronavirus, highlights the significance of zoonotic viral diseases.
    [Show full text]
  • West Nile Virus Restriction in Mosquito and Human Cells: a Virus Under Confinement
    Review West Nile Virus Restriction in Mosquito and Human Cells: A Virus under Confinement Marie-France Martin and Sébastien Nisole * Viral Trafficking, Restriction and Innate Signaling Team, Institut de Recherche en Infectiologie de Montpellier (IRIM), CNRS, 34090 Montpellier, France; [email protected] * Correspondence: [email protected] Received: 7 May 2020; Accepted: 27 May 2020; Published: 29 May 2020 Abstract: West Nile virus (WNV) is an emerging neurotropic flavivirus that naturally circulates between mosquitoes and birds. However, WNV has a broad host range and can be transmitted from mosquitoes to several mammalian species, including humans, through infected saliva during a blood meal. Although WNV infections are mostly asymptomatic, 20% to 30% of cases are symptomatic and can occasionally lead to severe symptoms, including fatal meningitis or encephalitis. Over the past decades, WNV-carrying mosquitoes have become increasingly widespread across new regions, including North America and Europe, which constitutes a public health concern. Nevertheless, mosquito and human innate immune defenses can detect WNV infection and induce the expression of antiviral effectors, so-called viral restriction factors, to control viral propagation. Conversely, WNV has developed countermeasures to escape these host defenses, thus establishing a constant arms race between the virus and its hosts. Our review intends to cover most of the current knowledge on viral restriction factors as well as WNV evasion strategies in mosquito and human cells in order to bring an updated overview on WNV–host interactions. Keywords: West Nile virus; restriction factors; interferon; innate immunity; mosquito; viral countermeasures; viral evasion 1. Introduction 1.1. West Nile Virus Incidence West Nile virus (WNV) belongs to the Flaviviridae family, from the Flavivirus genus, which also comprises Zika virus (ZIKV), dengue virus (DENV), tick-borne encephalitis virus (TBEV), and yellow fever virus (YFV).
    [Show full text]