The Effect of Colonization upon Aedes Aegypti Susceptibility to Oral Infection with Yellow Fever Virus *

Lorenz, Leslie H.; Bj, Beaty; Th, Aitken; Gp, Wallis; Wj, Tabachnick

doi:10.4269/ajtmh.1984.33.690

Cited by 73 publications

(68 citation statements)

References 10 publications

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“…It has been demonstrated that infection rates tend to increase with the number of laboratory generations of mosquitoes. 42,43 Using a different method of virus titration and a colony of Ae. albopictus from Cariacica, Brazil, Miller and Ballinger 44 demonstrated a lower infection rate for dengue virus type 2 (38%) and higher rates for yellow fever virus (36-57%) than we found using F 1 females from the same locality (47.0% and 6.3%, respectively).…”

Section: Discussionmentioning

confidence: 99%

Large Genetic Differentiation and Low Variation in Vector Competence for Dengue and Yellow Fever Viruses of Aedes Albopictus From Brazil, the United States, and the Cayman Islands

Oliveira¹,

Vazeille²,

Filippis³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

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Abstract. We conducted a population genetic analysis of Aedes albopictus collected from 20 sites in Brazil, the United States (Florida, Georgia, and Illinois), and the Cayman Islands. Using isoenzyme analysis, we examined genetic diversity and patterns of gene flow. High genetic differentiation was found among Brazilian samples, and between them and North American samples. Regression analysis of genetic differentiation according to geographic distances indicated that Ae. albopictus samples from Florida were genetically isolated by distance. Infection rates with dengue and yellow fever viruses showed greater differences between two Brazilian samples than between the two North American samples or between a Brazilian sample and a North American sample. Introductions and establishments of new Ae. albopictus populations in the Americas are still in progress, shaping population genetic composition and potentially modifying both dengue and yellow fever transmission patterns.

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Section: Discussionmentioning

confidence: 99%

Large Genetic Differentiation and Low Variation in Vector Competence for Dengue and Yellow Fever Viruses of Aedes Albopictus From Brazil, the United States, and the Cayman Islands

Oliveira¹,

Vazeille²,

Filippis³

et al. 2003

The American Journal of Tropical Medicine and Hygiene

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“…Considerable microevolution of dengue virus strains found in studies employing monoclonal antibody analysis (Vazeille et al, 1999), RNA finger printing (Lorenz et al, 1984) or sequencing of selected regions of the genome. As variants with similar genetic structure have been found within a specific geographic location, the studies elucidating the movements of dengue viruses and source of epidemics suggest that genetic variation in virus strains may determine virulence and explain the changing patterns of disease.…”

Section: Dengue Virus Strain Variationmentioning

confidence: 99%

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

Seema

Jain

2005

Indian J Clin Biochem

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Dengue fever is one of the major health problems in India. Interaction with specific receptor(s) at the cell surface is one of the first events in the pathogenesis of Dengue virus. However, relatively little is known about these receptors. Cellular receptors in human monocytes and mouse neural cells are main target for the viral infection. The envelope protein of the virus (E-protein) plays important role in attachment of virus to target cells and their interaction with cellular receptors. The modulation of receptor gene(s) and/or protein(s) can be used as a method for interfering with virus entry and can thus become a new method for disease prevention. The receptors can be purified by affinity chromatography using E-protein as ligand. It has been reported that addition of highly sulfated heparan sulfate prevents E-protein binding to target cells suggesting that heparan sulfate is utilized by dengue envelope protein to bind to target cells.

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“…17,18 Laboratory colonies of insects are often accepted as being representative of field populations from which they have been derived, but this assumption may be challenged because colonies frequently incorporate only a fraction of the genetic variability present in the original populations. 19 It has been reported that laboratory colonization of sand flies reduces natural genetic variability, and might foster selection for certain traits that are normally suppressed in field populations. [20][21][22] The loss of genetic variation as a result of colonization might figure prominently in the protection observed in mice preimmunized with SGH of long-term colonized P. papatasi and challenged with L. major co-inoculated with the same type of SGH.…”

mentioning

confidence: 99%

Lack of Protection of Pre-Immunization with Saliva of Long-Term Colonized Phlebotomus papatasi against Experimental Challenge with Leishmania major and Saliva of Wild-Caught P. papatasi

Ahmed¹,

Kaabi²,

Chelbi³

et al. 2010

The American Society of Tropical Medicine and Hygiene

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Several studies have shown that pre-immunization of mice with needle-injected saliva or pre-exposure to uninfected bites of Phlebotomus papatasi provided protection against infection with Leishmania major , the etiologic agent of zoonotic cutaneous leishmaniasis (ZCL).1-3 These studies were performed by using long-term laboratory colonized sand flies mainly because of the difficulty of working with wild-caught flies. A puzzling fact is that people in leishmaniasis-endemic areas succumb of ZCL despite the high frequency of uninfected bites compared with infected ones. 4 We showed in a previous study that pre-immunization of mice with salivary gland homogenate (SGH) of wild-caught P. papatasi does not confer protection against L. major co-inoculated with the same type of SGH compared with a significant protection obtained when pre-immunization and challenge were performed with SGH of long-term colonized flies. 5 It was reported that colonized and wild-caught Lutzomyia longipalpis differ in the composition and the amount of salivary proteins and these differences may account for the lower effect observed on the modulation of experimental Leishmania infection by wild-caught SGH. 6,7 Thus, these studies provide good evidence that the outcome of Leishmania infection differs significantly between colonized and wild-caught salivary gland proteins. Our aim in this study was to assess the protective effect of pre-immunization with SGH of long-term colonized P. papatasi on experimental L. major challenge co-inoculated with SGH of wild-caught P. papatasi .Phlebotomus papatasi (Tunisian strain that originated in the Governorate of Sidi Bouzid) have been reared at the Vector Ecology Laboratory of the Institut Pasteur de Tunis since 2003. 8 This colony is maintained without being supplemented periodically with wild-caught P. papatasi . Generation F 39 was used in this study. Wild sand flies were collected using CDC light traps from animal shelters located in the village of Felta (Governorate of Sidi Bouzid), a focus highly endemic for ZCL.9 Preparation of SGH from laboratory-reared and wild-caught P. papatasi was performed as described. 5 A highly virulent strain of L. major , MHOM/TN/95/GLC94, isolated from a patient in Tunisia was used in this study. 5 We used female BALB/c mice (6-8 weeks of age) bred in the animal facility of the Institut Pasteur de Tunis.Mice were immunized intradermally in the right ear with the equivalent of two pairs of salivary glands in 10 µL of phosphate-buffered saline (PBS). Two groups of 10 mice each were pre-immunized with SGH of long-term colonized female P. papatasi (F 39 ), once a week for two weeks. In the fourth week, the first [CSGH (F 39 )-L.m+CSGH (F 39 )] and the second [CSGH (F 39 )-L.m+WSGH] groups were challenged with 10 6 stationary phase L. major promastigotes in 50 µL of PBS co-inoculated subcutaneously in the right hind footpads with SGH of long-term, colonized and SGH of wild-caught, female P. papatasi , respectively. Three control groups of 10 mice each were used in this stud...

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The Effect of Colonization upon Aedes Aegypti Susceptibility to Oral Infection with Yellow Fever Virus *

Cited by 73 publications

References 10 publications

Large Genetic Differentiation and Low Variation in Vector Competence for Dengue and Yellow Fever Viruses of Aedes Albopictus From Brazil, the United States, and the Cayman Islands

Large Genetic Differentiation and Low Variation in Vector Competence for Dengue and Yellow Fever Viruses of Aedes Albopictus From Brazil, the United States, and the Cayman Islands

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

Lack of Protection of Pre-Immunization with Saliva of Long-Term Colonized Phlebotomus papatasi against Experimental Challenge with Leishmania major and Saliva of Wild-Caught P. papatasi

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