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Title: EXPERIMENTAL INFECTION OF BEAGLES WITH ECHO VIRUS TYPE 6

Authors:
;
Publication Date:
Research Org.:
Lovelace Foundation for Medical Education and Research, Albuquerque, N. Mex.
OSTI Identifier:
4618387
Report Number(s):
LF-25
NSA Number:
NSA-19-031632
DOE Contract Number:
AT(29-2)-1013
Resource Type:
Technical Report
Resource Relation:
Other Information: Orig. Receipt Date: 31-DEC-65
Country of Publication:
United States
Language:
English
Subject:
GENERAL AND MISCELLANEOUS; BLOOD; DETECTION; DOGS; FECES; IMMUNITY; QUANTITY RATIO; URINE; VIRUSES

Citation Formats

Pindak, F.F., and Clapper, W.E.. EXPERIMENTAL INFECTION OF BEAGLES WITH ECHO VIRUS TYPE 6. United States: N. p., 1965. Web. doi:10.2172/4618387.
Pindak, F.F., & Clapper, W.E.. EXPERIMENTAL INFECTION OF BEAGLES WITH ECHO VIRUS TYPE 6. United States. doi:10.2172/4618387.
Pindak, F.F., and Clapper, W.E.. Sat . "EXPERIMENTAL INFECTION OF BEAGLES WITH ECHO VIRUS TYPE 6". United States. doi:10.2172/4618387. https://www.osti.gov/servlets/purl/4618387.
@article{osti_4618387,
title = {EXPERIMENTAL INFECTION OF BEAGLES WITH ECHO VIRUS TYPE 6},
author = {Pindak, F.F. and Clapper, W.E.},
abstractNote = {},
doi = {10.2172/4618387},
journal = {},
number = ,
volume = ,
place = {United States},
year = {Sat May 01 00:00:00 EDT 1965},
month = {Sat May 01 00:00:00 EDT 1965}
}

Technical Report:

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  • The interaction between nitrogen dioxide (NO/sub 2/) exposure and human susceptibility to respiratory virus infection was investigated in a placebo-controlled, randomized, blinded trial conducted in an environmentally controlled research chamber. Healthy, nonsmoking volunteers, 18 to 35 years old, who were seronegative to influenza A/Korea/82 (H/sub 3/N/sub 2/) virus, breathed either filtered air or NO/sub 2/ for two hours a day for three consecutive days. Live, attenuated cold-adapted influenza A/Korea/82 reassortant virus was administered intranasally to all subjects after the second day of exposure. No adverse changes in pulmonary function or nonspecific airway reaction to methacholine were observed after NO/sub 2/more » exposure, virus infection, or both. Although the differences were not statistically significant, the groups exposed to NO/sub 2/ in year 3 became infected more often (91%) than those exposed only to air (71%).« less
  • The main objective for this study was the development of a rapid diagnostic method for IHN virus in fish tissue samples. The rationale for developing new techniques for diagnosing IHNV infection was that present methods were time consuming and dependent on virus neutralization by specific antisera, a reagent that was not readily available or reliable. Fish pathologists required a rapid detection method which was sensitive enough to detect virus strain differences so that they could provide data for effective management decisions in controlling the spread of IHNV. Bonneville Power Administration's (BPA) role in efforts in fish diseases and more genericallymore » the protection, mitigation, and enhancement of Columbia River salmon and steelhead populations, is mandated by Congress through the Pacific Northwest Electric Power Planning and Conservation Act (Regional Act), Pub. L. 96-501. Section 4 (h) of the Regional Act directs the Northwest Power Planning Council to develop a Fish and Wildlife Program. BPA's Administrator is authorized in Section 4 (h) (10) (A) to ''use funds and the authorities available to the extent affected by the development and operation of any hydroelectric project of the Columbia River and its tributaries''. The fund is to be used to implement measures that are consistent with the Council's Fish and Wildlife Program. The research detailed in this final report is consistent with these objectives. This final report has been prepared as part of BPA's policy to encourage the preservation and dissemination of research results by publication in scientific journals.« less
  • Our research on Turnip crinkle virus (TCV) has shown that the viral capsid protein (CP) is both a virulence factor as well as the elicitor of a hypersensitive resistance response (HR) to the virus in Arabidopsis. Initially, we identified a protein from Arabidopsis that specifically interacted with the viral CP using a yeast two-hybrid screen. This protein, designated TIP for TCV-Interacting Protein, is a member of the NAC family of plant transcription factors implicated in the regulation of development and senescence. When TCV CP was mutated to eliminate its ability to interact with TIP, the corresponding virus mutants broke themore » HR-mediated resistance conferred by the HRT resistance (R) gene in Arabidopsis ecotype Dijon (Di)-17. This result suggested that TIP is a component of the signal transduction pathway that leads to the genetically specified TCV resistance. We next confirmed that TIP and the viral CP interact in plant cells and that this interaction prevents nuclear localization of this transcription factor. We demonstrated that TCV CP suppresses post-transcriptional gene silencing (PTGS), a newly discovered RNA-mediated defense system in plants. Together these results suggest that the CP is a virulence factor that could well be functioning through its interaction with TIP. We have proposed a model involving the role of TIP and CP in triggering HR mediated plant defense that fits with the current thinking about how gene-for-gene resistance may function. A unique component of our system is the opportunity to link R-gene function with the newly discovered RNA silencing pathway that is not only a potent defense against viral pathogens, but also regulates early development in plants. In the current funding period we made several significant findings: First, we completed an array analysis comparing gene expression in Arabidopsis infected with TCV and a mutant virus unable to bind TIP. Second, we produced transgenic lines that over-express and inducibly under-express TIP. These accomplishments now form the basis for our continued effort towards providing a complete understanding of molecular events leading to susceptible and resistant interactions between TCV and Arabidopsis plants. Our data strongly suggest that TIP is involved in activating the SA-mediated defense pathway and that TCV CP acts to repress this role of TIP.« less