1994
 

 

 

Abbassy, M.M.; K. Stein; M. Osman. New artificial feeding technique for experimental infection of Argas ticks (Acari: Argasidae). Journal of Medical Entomology. Mar 1994. v. 31 (2) p. 202-205. ISSN: 0022-2585.

NAL Call No.:  421 J828

Descriptors: Argas, ticks, birds, membranes, blood, artificial rearing, West Nile virus, disease vectors, artificial feeding, fetal bovine serum.

Abstract: An artificial feeding technique using fetal bovine serum as a food source was established for the demonstration of West Nile virus transmission by Argas ticks in susceptibility studies. Fetal bovine serum does not coagulate and is free from contaminating microorganisms, antibodies, and anticoagulants, which are all known to reduce virus titers. This technique also compensates for the lack of suitable laboratory hosts as well as problems associated with disease agents, such as viruses that may not produce illness or antibodies after virus exposures.


Halevy, M; Akov, Y; Ben-Nathan, D; Kobiler, D; Lachmi, B; Lustig, S. Loss of active neuroinvasiveness in attenuated strains of West Nile virus: pathogenicity in immunocompetent and SCID mice. Archives of Virology. 1994; 137(3-4): 355-70. ISSN: 0304-8608.

NAL Call No.: 448.3 Ar23

Descriptors: neuropathogenicity of WN25 and WN25A, ICR and SCID mice, comparison of serology and RNA fingerprints between WNV and WN25, viral envelope proteins, IC and IP inoculations, attenuated strains.

Abstract: The neuropathogenicity of West Nile virus (WNV) and two derived attenuated strains WN25 and WN25A, was studied in young adult ICR mice and in severe combined immunodeficient (SCID) mice. Similarity in serology and RNA fingerprints were found between WNV and WN25. The viral envelope proteins of the attenuates differed from WNV in their slower mobility in SDS-PAGE due probably to the presence of N-linked glycan. The three strains were lethal to ICR mice by intracerebral (IC) inoculation, but when inoculated intraperitoneally (IP), WNV caused viremia, invaded the CNS and was lethal, whereas the attenuates showed no viremia or invasion of the CNS. The attenuates elicited antibodies to comparable levels as WNV in IP-infected mice, conferring upon them immunity to IC challenge with the wild type. In IP-inoculated SCID mice the three strains exhibited similar high viremiae that lasted until death of the animals. All strains invaded the CNS and proliferated in the mouse brain to similar high titers, but differed largely in the time of invasion: WNV invaded the CNS of SCID mice (and two other mouse strains) much earlier than the attenuates, which showed large intervals in their time of invasion into individual mouse brains within the group. The data presented for SCID mice indicate that WN25 and WN25A have truly lost the neuroinvasive property, and that this property materialized by a prescribed, active process specific for WNV.


Ilkal, MA; Prasanna, Y; Jacob, PG; Geevarghese, G; Banerjee, K. Experimental studies on the susceptibility of domestic pigs to West Nile virus followed by Japanese encephalitis virus infection and vice versa. Acta Virologica. 1994 Jun; 38(3): 157-61. ISSN: 0001-723X.

NAL Call No.: 448.3 Ac85

Descriptors: disease susceptibility, swine, WNV, JEV, experimental infections, antibody, inoculation and mosquito bites, Culex vishnui, virus levels, pigs poor hosts.

Abstract: A study on the susceptibility of domestic pigs to West Nile virus (WNV) and Japanese encephalitis virus (JEV) infection was carried out. One batch of pigs was inoculated with WNV followed by JEV and another batch was inoculated vice versa. The first batch developed low level of viraemia and haemagglutination-inhibition (HI) antibodies to both viruses. There was a booster effect on the already existing WNV antibodies after challenging with JEV. In the second batch the animals developed high level of JE viraemia but did not develop WN viraemia. They developed HI antibodies to both JEV and WNV with low booster effect of WNV infection on JEV antibodies. Fresh batches of pigs were infected through bite of WNV- and JEV-infected Culex vishnui mosquitoes. WNV-infected pigs did not show viraemia, whereas JEV-infected ones developed JE viraemia. The study indicated that pigs were poor hosts for WNV but good ones for JEV. However, WNV antibodies reduced the level of JE viraemia and JEV infection boosted the already existing WNV antibodies.


Traore-Lamizana, M.; H. Zeller; M. Mondo; J. Hervy; F. Adam; J. Digoutte. Isolations of West Nile and Bagaza viruses from mosquitoes (Diptera: Culicidae) in central Senegal (Ferlo). Journal of Medical Entomology. Nov 1994. v. 31 (6) p. 934-938. ISSN: 0022-2585.

NAL Call No.:  421 J828

Descriptors: Culicidae, West Nile virus, flaviviridae, infections, mosquitoes, disease vectors, disease survey, Senegal.

Abstract: During October-November 1990, 31,497 mosquitoes consisting of 25 different species were collected in Barkedji, Ferlo area (Senegal), and tested for virus infection. Viruses were isolated from 55 of 407 pools. Eighteen pools were found positive for both Bagaza virus (BGA) and West Nile virus (WN). One alphavirus (Babanki [BBK] and 72 flaviviruses (19 BGA, 53 WN) were isolated from Culex poicilipes Theobald (29 WN, 8 BGA), C. neavei Theobald (3 WN, 1 BGA), Mimomyia hispida Theobald (8 WN, 6 BGA, and 1 BBK), M. lacustris Edwards (4 WN,1 BGA), M. splendens Theobald (6 WN,2 BGA), Mimomyia. spp. (2 WN), and Aedeomyia africana Neveu-Lemaire (1 WN). These were the first isolations of arboviruses from A. africana and Mimomyia species. C. poicilipes and possibly Mimomyia spp. may be involved in an avian-mosquito cycle of West Nile virus transmission in Senegal.


Yamshchikov, VF; Compans, RW. Processing of the intracellular form of the west Nile virus capsid protein by the viral NS2B-NS3 protease: an in vitro study. Journal of Virology. 1994 Sep; 68(9): 5765-71. ISSN: 0022-538X.

NAL Call No.: QR360.J6

Descriptors: mature capsid protein, in vitro expression cassettes, prM protein, C-prM precursor, viral protease components, characterized their translation products.

Abstract: According to the existing model of flavivirus polyprotein processing, one of the cleavages in the amino-terminal part of the flavivirus polyprotein by host cell signalases results in formation of prM (precursor to one of the structural proteins, M) and the membrane-bound intracellular form of the viral capsid protein (Cint) retaining the prM signal sequence at its carboxy terminus. This hydrophobic anchor is subsequently removed by the viral protease, resulting in formation of the mature viral capsid protein found in virions (Cvir). We have prepared in vitro expression cassettes coding for both forms of the capsid protein, for the prM protein, for the C-prM precursor, and for the viral protease components of West Nile flavivirus and characterized their translation products. Using Cint and Cvir translation products as molecular markers, we have observed processing of the intracellular form of the West Nile capsid protein by the viral protease in vitro both upon cotranslation of the C-prM precursor and the viral protease-encoding cassette and by incubation of C-prM translation products with a detergent-solubilized extract of cells infected with a recombinant vaccinia virus expressing the active viral protease. The cleavage of Cint by the viral protease at the predicted dibasic site was verified by introduction of point mutations into the cleavage site and an adjacent region. These studies provide the first direct demonstration of processing of the intracellular form of the flavivirus capsid protein by the viral protease.


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February 26, 2003