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Biomedical subjects

J A Booth

Publications and source records attributed to J A Booth.

27 records · Page 2Linked to original sources

Aflatoxin inhibition of viral interferon induction.

The inhibitory effect of four basic aflatoxins on interferon induction by influenza virus in LLC-MK2 cell monolayers follows a structure-activity series with decreasing potency in the order aflatoxin B1 greater than G1 greater than B2 approximately G2. Of the four aflatoxins, B1 was the most deleterious to both cell growth and the viability of cells in confluent cultures. The fact that higher levels of influenza virus growth were attained in aflatoxin-treated cells than in normal cell monolayers was related to increased aflatoxin concentration in association with decreased interferon production. The ability of interferon to confer cellular resistance against viral infection, however, was not altered by aflatoxin. The inhibitory activity of aflatoxin on interferon production may be a factor contributing to impairment of host resistance to viral infections.

Aflatoxins↗

Antagonistic activity of poly (4-vinylpyridine-N-oxide) to the inhibition of viral interferon induction by asbestos fibres.

The depressive activity of both serpentine (Canadian and Rhodesian chrysotiles) and amphibole (amosite, crocidolite, and anthophyllite) asbestos fibres on interferon induction by influenza virus was significantly diminished or abolished completely when either asbestos fibres or LLC-MK2 cell monolayers were pretreated with poly(4-vinylpyridine-N-oxide). Maximal antagonistic activity of the polymer was time and concentration dependent. Pretreating asbestos fibres with the polymer was more rapid and effective in encouraging viral interferon synthesis than pretreating cell monolayers. Virus multiplication in the presence of asbestos fibre-treated cell monolayers attained a twofold higher level than that noted in normal cell monolayers or those containing polymer-pretreated asbestos fibres. These findings were related to the suppression of interferon production.

Asbestos↗

Quantitative assessment of hemadsorption by myxoviruses: virus hemadsorption assay.

The standardization and quantitative evaluation of an assay for myxoviruses, based on the enumeration of individual infected clone 1-5C-4 cells manifesting hemadsorption within 24 h of infection, are described. Hemadsorption was detectable earlier than immunofluorescence in infected cells or hemagglutinins in culture medium. The relationship between virus concentration and cells exhibiting hemadsorption was linear. The assay was highly precise, sensitive, and reproducible.

Animals↗

Cell attachment and penetration by influenza virus.

Attachment and penetration of influenza virus into clone 1-5C-4 cells were quantitatively determined by the immunofluorescent cell-counting assay. Aided by centrifugal force, more than 95% of virus inocula of five representative influenza virus strains (A(0)/PR8, A(1)/Ann Arbor, A(2)/Japan, B/Lee, B/Great Lakes) were attached to cells at a linear rate within 10 min, in contrast to approximately 35% after stationary incubation at 35 C for 2 h. By the former procedure, a proportionality between the number of infected cells and volume of inoculum was revealed which was not evident when stationary incubation was employed. Maximal binding of virus to cells occurred at 0.2 M NaCl. The salt requirement, added to evidence of pH dependence and temperature independence, indicated that the initial virus-cell union involved electrostatic forces. Virus penetration into cells, measured by the insensitivity of virus-cell complexes to antiviral serum, was linear and complete within 15 min at 35 C for all five virus strains tested. Maximal virus penetration occurred at 0.1 to 0.2 M NaCl; the process was pH- and temperature-dependent. Both virus attachment and penetration processes were partially inhibited in the presence of diethylaminoethyl-dextran.

Animals↗

Further studies on the anti-immunoglobulin G hemagglutination-inhibition test for influenza.

Incorporating species-specific anti-immunoglobulin G (IgG) serum into the hemagglutination-inhibition (HI) test for influenza markedly increased sensitivity without loss of specificity. The effectiveness of anti-IgG serum for augmenting antibody titers may be influenced by the variable potency of commercial anti-IgG preparations. Maximal enhancement of HI titers was achieved when anti-IgG serum and virus-antiserum mixtures were incubated at 23 C for 10 min. Precision and reproducibility of the test were within acceptable limits. Other conditions likely to affect the test were investigated.

Animals↗