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Full-Text Articles in Life Sciences
Mechanisms Responsible For A Φx174 Mutant's Ability To Infect Escherichia Coli By Phosphorylation, Jennifer Cox, Catherine Putonti
Mechanisms Responsible For A Φx174 Mutant's Ability To Infect Escherichia Coli By Phosphorylation, Jennifer Cox, Catherine Putonti
Catherine Putonti
The ability for a virus to expand its host range is dependent upon a successful mode of viral entry. As such, the host range of the well-studied ΦX174 bacteriophage is dictated by the presence of a particular lipopolysaccharide (LPS) on the bacterial surface. The mutant ΦX174 strain JACS-K, unlike its ancestor, is capable of infecting both its native host Escherichia coli C and E. coli K-12, which does not have the necessary LPS. The conversion of an alanine to a very reactive threonine on its virion surface was found to be responsible for the strain's expanded host range.
A Case Study To Teach The Diagnostic Process: Determining The Cause Of Chlorosis In A Crop Of Cut Dicentra, Marci Spaw, Kimberley A. Williams, Laurie Hodges, Ellen T. Paparozzi, Ingrid L. Mallberg
A Case Study To Teach The Diagnostic Process: Determining The Cause Of Chlorosis In A Crop Of Cut Dicentra, Marci Spaw, Kimberley A. Williams, Laurie Hodges, Ellen T. Paparozzi, Ingrid L. Mallberg
Laurie Hodges
This universally accessible, Web-based decision case presents the challenge of determining the cause of foliar chlorosis in a crop of dicentra (Dicentra spectabilis) being forced as a cut flower for Valentine's Day sales. The case study serves as a tool to promote the development of diagnostic skills for production dilemmas, including nutritional disorders, disease problems, and evaluation of the appropriateness of cultural practices, Cut dicentra is a minor crop and standard production practices are not well established. Solving this case requires that students research production protocol, as well as nutritional and pest problems, and determine whether they have enough information …
Human Immunodeficiency Virus Type 1 Protease-Correlated Cleavage Site Mutations Enhance Inhibitor Resistance, Madhavi Kolli, Eric Stawiski, Colombe Chappey, Celia Schiffer
Human Immunodeficiency Virus Type 1 Protease-Correlated Cleavage Site Mutations Enhance Inhibitor Resistance, Madhavi Kolli, Eric Stawiski, Colombe Chappey, Celia Schiffer
Celia A. Schiffer
Drug resistance is an important cause of antiretroviral therapy failure in human immunodeficiency virus (HIV)-infected patients. Mutations in the protease render the virus resistant to protease inhibitors (PIs). Gag cleavage sites also mutate, sometimes correlating with resistance mutations in the protease, but their contribution to resistance has not been systematically analyzed. The present study examines mutations in Gag cleavage sites that associate with protease mutations and the impact of these associations on drug susceptibilities. Significant associations were observed between mutations in the nucleocapsid-p1 (NC-p1) and p1-p6 cleavage sites and various PI resistance-associated mutations in the protease. Several patterns were frequently …
Detection And Characterization Of A Distinct Bornavirus Lineage From Healthy Canada Geese (Branta Canadensis), John A. Baroch
Detection And Characterization Of A Distinct Bornavirus Lineage From Healthy Canada Geese (Branta Canadensis), John A. Baroch
John A Baroch
Avian bornaviruses (ABV), identified in 2008, infect captive parrots and macaws worldwide. The natural reservoirs of these viruses are unknown. Reverse transcription-PCR (RT-PCR) was used to screen oropha- ryngeal/cloacal swab and brain samples from wild Canada geese (Branta canadensis) for ABV. Approximately 2.9% of swab samples were positive for bornavirus sequences. Fifty-two percent of brain samples from 2 urban flocks also tested positive, and brain isolates were cultured in duck embryo fibroblasts. Phylogenetic analyses placed goose isolates in an independent cluster, and more notably, important regulatory sequences present in Borna disease virus but lacking in psittacine ABVs were present in …
Efficacy Of Orally Administered T-705 On Lethal Avian Influenza A (H5n1) Virus Infections In Mice, R. W. Sidwell, Dale L. Barnard, C. W. Day, Donald F. Smee, K. W. Bailey, M. H. Wong, John D. Morrey, Y. Furuta
Efficacy Of Orally Administered T-705 On Lethal Avian Influenza A (H5n1) Virus Infections In Mice, R. W. Sidwell, Dale L. Barnard, C. W. Day, Donald F. Smee, K. W. Bailey, M. H. Wong, John D. Morrey, Y. Furuta
John D. Morrey
T-705 (6-fluoro-3-hydroxy-2-pyrazinecarboxamide) was inhibitory to four strains of avian H5N1 influenza virus in MDCK cells, with the 90% effective concentrations ranging from 1.3 to 7.7 µM, as determined by a virus yield reduction assay. The efficacy was less than that exerted by oseltamivir carboxylate or zanamivir but was greater than that exerted by ribavirin. Experiments with mice lethally infected with influenza A/Duck/MN/1525/81 (H5N1) virus showed that T-705 administered per os once, twice, or four times daily for 5 days beginning 1 h after virus exposure was highly inhibitory to the infection. Dosages from 30 to 300 mg/kg of body weight/day …
In Vivo Activation Of Human Immunodeficiency Virus Type 1 Long Terminal Repeat By Uv Type A (Uv-A) Light Plus Psoralen And Uv-B Light In The Skin Of Transgenic Mice, John D. Morrey, S M. Bourn, T D. Bunch, M K. Jackson, R W. Sidwell, L R. Barrows, R A. Daynes, C A. Rosen
In Vivo Activation Of Human Immunodeficiency Virus Type 1 Long Terminal Repeat By Uv Type A (Uv-A) Light Plus Psoralen And Uv-B Light In The Skin Of Transgenic Mice, John D. Morrey, S M. Bourn, T D. Bunch, M K. Jackson, R W. Sidwell, L R. Barrows, R A. Daynes, C A. Rosen
John D. Morrey
UV irradiation has been shown to activate the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in cell culture; however, only limited studies have been described in vivo. UV light has been categorized as UV-A (400 to 315 nm), -B (315 to 280 nm), or -C (<280 nm); the longer wavelengths are less harmful but more penetrative. Highly penetrative UV-A radiation constitutes the vast majority of UV sunlight reaching the earth's surface but is normally harmless. UV-B irradiation is more harmful but less prevalent than UV-A. In this report, the HIV-1 LTR-luciferase gene in the skin of transgenic mice was markedly activated when exposed to UV-B irradiation. The LTR in the skin of transgenic mice pretreated topically with a photosensitizing agent (psoralen) was also activated to similar levels when exposed to UV-A light. A 2-h exposure to sunlight activated the LTR in skin treated with psoralen, whereas the LTR in skin not treated with psoralen was activated after 7 h of sunlight exposure. The HIV-1 LTR-β-galactosidase reporter genes have been used to demonstrate the in vivo UV-induced activation of the LTR and might be used to evaluate other environmental factors or pharmacologic substances that might potential activate the HIV-1 LTR in vivo