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Biomedical subjects

R Wigand

Publications and source records attributed to R Wigand.

At least 127 records · Page 7Linked to original sources
PubMed1976

[Studies on the mechanism of L-agglutination (author's transl)].

The mechanism of L-agglutination (LA) was studied by fractionating human sera by means of Sephadex G 200 gel filtration. LA was found to be mediated by 2 factors: the rheumatoid factor (RF) as a macroglobulin, occuring only in sera from patients with rhematoid arthritis, and an IgG globulin, found also in normal sera, probably a highly prevalent incomplete streptococcal antibody. RF-containing IgM fractions, by themselves devoid of LA activity, can be rendered positive not only by IgG from the same serum, but also by IgG from normal sera or by commercial human IgG. After absorption of sera containing the RF with streptococci LA disappears; by addition of normal serum, IgG from normal serum or human IgG LA titers were attained similar to those of the respective native serum. A treatment of RF-containing sera with mercaptoethanol leads to a largely parallel disapperance of LA and latex fixation. Three substrains of Streptococcus pyogenes SF 130 (type) 1), Varying in their endowment with type-specific antigens, reacted similarly in LA.

Antibodies, Bacterial↗
PubMed1975

Terminal dilution purification of adenovirus prototypes, and the antigenic relationship between types 4, 16 and 14.

Two terminal dilution purifications in HEK cells were performed with adenovirus prototypes of types 1 to 7, 12, 16, 19 and 9-15, and one terminal dilution with a freshly isolated type 8 strain. The antisera prepared against viruses after terminal dilution neutralized the original and the purified virus to the same extent, indicating the antigenic purity of the respective prototypes. Cross-reactions in neutralization with other types within the subgroup were also identical. Only the prototype of type 16 (Ch 79) showed a cross-neutralization with type 4, while four type 16 wild strains showed cross-neutralization with type 14, but none with type 4. The prototype (CH 79) is a "prime strain" in relation to the type 16 wild strains.

Adenoviridae↗
PubMed1975

Virus isolation and titration at 33 degrees and 37 degrees C.

Various prototype viruses and original specimens were comparatively titrated in cell cultures at 33 degrees and 37 degrees C. Higher titers at 37 degrees were consistently obtained with adenoviruses; for other viruses (enteroviruses, herpesvirus hominis, vaccinia virus, parainfluenza viruses) the titers were mostly identical at either temperature. Original specimens and prototye strains showed the same behavior. The habit to cultivate viruses from throat swabs at 33 degrees C is unsatisfactory for adenoviruses.

Adenoviridae↗
PubMed1975

[Laboratory procedures in adenoviruses. II. Sensitivity of various cell cultures as determined by endpoint titration (author's transl)].

The sensitivity of human embryonic kidney (HEK), human amnion (HAm) and HeLa cells for human adenoviruses was investigated by means of endpoint titrations of 13 prototype strains and numerous original specimens from patients. Prototypes and original specimens showed the same behavior. Adenoviruses of subgrouppp III produced nearly identical titers in all 3 cell cultures, while for subgroup I HAm cells showed a 10- to 100-fold lower titer. On the other hand, HAm cells are nearly as sensitive as HEK cells for type 8, whereas HeLa cells are less sensitive. For other viruses of subgroup II and for subgrou IV, HAm (for type 12 also HeLa) cells are less sensitive than HEK cells. Out of three HeLa cell strains tested the Bristol strain was inferior to the other two in its sensitivity. Concerning the speed of the CPE development, HEK cells are superior for all types, the difference being greatest for subgroup I towards HAm and HeLa and for type 8 towards HeLa cells. The length of incubation necessary for the appearance of CPE even with minimal amounts of virus is 40 days for type 8 in all kinds of cell cultures, whereas for adenoviruses of sub-groups I and III, which are predominantly isolated in the routine laboratory, 25 days for HEK and 30 days for HAm and HeLa cells may suffice in most cases. When endpoint titrations are compared with titers obtained by immunofluorescence, it appears that this technique may be applied as a screening method; thus long incubation periods of negative specimens can be saved. The amounts of infectious virus present in original specimens are reported; the highest quantity was found in specimens containing subgroup I viruses.

Adenoviridae↗
PubMed1975

[The etiology of epidemic keratoconjunctivities (author's transl)].

In 93 patients (mostly sporadic cases) with suspected EKC an infection with adenoviruses was proved by virological and serological methods in 54 cases. Types 8, 3, 7, 19, 4, and 14 were found in 38, 6, 5, 3, 1, and 1 cases respectively. 33 out of 48 patients with clinically typical EKC had an infection with type 8. From the patients without adenoviral infection, the absence of which having been proved by extensive serological tests, 7 showed a typical EKC. The symptoms considered as relatively typical (hyperemia and oedema of the plica and caruncle, subepithelial corneal infiltrates) were not confined to patients with adenovirus infection; thus they cannot be considered as characteristic for this group of viruses. The results indicate the need for a specific diagnosis in cases of suspected EKC, which should include virus isolation from conjunctival swabs as well as the demonstration of antibody titer rises by various serological tests. EKC is to be considered as a clinical and epidemiological rather than as an etiological entity.

Adenoviridae↗
PubMed1975

The effect of purine and pyrimidine analogues and virazole on adenovirus replication.

The multiplication of adenovirus 19 in HeLa cells was inhibited by various purine and pyrimidine analogues and by virazole. The formation of infectious virus and of capsid proteins (haemagglutin, group-specific complement-fixing antigen) was inhibited to the same degree, while the viral cytopathic effect (CPE) was not inhibited. The reversibility of the inhibition after removal of the substances was more complete for purine than for pyrimidine analogues. The inhibition was counteracted by simulataneous addition of the corresponding nucleosides. Adenosine was more effected than guanosine against purine analogues; both were partially effective against virazole, but none of them against arabinofuranosyladenine. The time-dependence of inhibition, the ensuing eclipse period after removal of the inhibitors, and the successive application of two inhibitors led to the conclusion that most of them affect the viral multiplication mainly by inhibition of DNA synthesis. Azacytidine inhibits the synthesis of structural proteins as well.

Adenoviridae↗