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Biomedical subjects

W Henle

Publications and source records attributed to W Henle.

251 records · Page 14Linked to original sources
PubMed1967

Herpes-type virus and chromosome marker in normal leukocytes after growth with irradiated Burkitt cells.

Cultured cells derived from male patients with Burkitt's lymphoma and harboring herpes-type virus particles were lethally irradiated. These irradiated cells induced normal peripheral leukocytes of female infants to grow within 2 to 4 weeks after mixed cultivation. Cells of a line free of this agent failed to stimulate growth. If either type of cell was cultured separately, it did not survive under the experimental conditions. Herpes-type viral antigen and C-group chromosomal marker previously described in cultured Burkitt cells were found in all of the female cell cultures that were obtained.

Burkitt Lymphoma↗
PubMed1967

Studies on persistent infections of tissue culture. VI. Reversible changes in Newcastle disease virus populations as a result of passage in L cells or chick embryos.

Populations of the Victoria strain of Newcastle disease virus (NDV), reisolated from persistently infected L-cell cultures and passed twice in the embryonated hen's egg (NDV(L-E-2)), were found to differ strikingly from the original, chick embryo-adapted virus (NDV(o)). After exposure of L cells to NDV(o) at high multiplicities of infection, all cells became abortively infected; they produced only small aggregates of viral antigen and few, if any, infectious virus particles, but they yielded large amounts of interferon. No cytopathic effects (CPE) were noted, and the cultures survived readily as viral carriers. In contrast, NDV(L-E-2) yielded under similar conditions large quantities of viral antigen and infectious virus particles, but no detectable interferon, and the cultures were rapidly destroyed. This change in "virulence" was at least partially reversible by further serial passages of NDV(L-E-2) in chick embryos, as was evident from a consecutive decrease in CPE with a concomitant increasingly rapid recovery of the L-cell cultures, gradually diminishing yields of infectious viral progeny, and the returning of a capacity to induce interferon synthesis. Thus, NDV(L-E-16) resembled NDV(o) in many aspects, except for a less striking reduction in its ability to replicate in L cells. Although a selection of viral variants under the given sets of conditions has not been entirely excluded, the establishment of "avirulence" appears to be largely explained by a gradual accumulation of noninfectious, interferon-inducing components in the course of serial passages in the embryonated hen's egg, and the acquisition of "virulence" by a loss of these components. The evidence is as follows. (i) By a step-wise decrease in the dose of virus and restriction of the analyses to the first infectious cycle, a multiplicity of infection was ultimately reached for all "avirulent" populations at which infected cells produced normal yields of infectious viral progeny; i.e., the interferon-inducing components were diluted to noneffective levels. The lowest multiplicity which resulted in a measurable reduction in infectious virus replication was also the last one to induce detectable interferon synthesis. (ii) All viral clones derived from "avirulent" populations behaved like NDV(L-E-2) rather than like the parent viral suspensions, except that some of them elicited small amounts of interferon in L cells. The interferon-inducing components were reduced or lost in the cloning procedures. The nature of the interferon-inducing components has not been established. These components, which were neutralized by rabbit sera against "virulent" NDV(L-E-2) populations, may represent largely inactive or incomplete virus particles; however, the infectious virus-hemagglutinin ratios of "avirulent" populations were mostly of an order similar to those of "virulent" populations. The interferon-inducing components aborted the infectious process in cells simultaneously invaded by infectious virus particles. The implications of these findings are discussed.

Animals↗
PubMed1967

Comparative study of cultured Burkitt tumor cells by immunofluorescence, autoradiography, and electron microscopy.

Cultured Burkitt cells were examined by immunofluorescence, autoradiography, and electron microscopy in an effort to identify the stainable cells with those harboring herpes-type virus particles. Immediately after a 2-hr pulse of (3)H-thymidine, from 30 to 60% of the cells revealed heavy nuclear labeling. In most cases the grains were evenly dispersed, but in about 3 to 5% the grains showed a focal distribution and occasionally they extended into the cytoplasm. Such nuclear foci were rarely seen at 8 hr after the pulse. When the analysis was restricted to preselected immunofluorescent cells, up to 80% showed label at 8 hr and cytoplasmic grains were prominent. To reduce cellular deoxyribonucleic acid (DNA) synthesis, cells were X-irradiated with 3,000 to 6,000 R, and the isotope pulse was applied 1, 4, or 7 days later. Whereas the total number of labeled cells decreased in roughly twofold steps at the respective intervals (from 40 to 10%), the incorporation of (3)H-thymidine into fluorescent cells was not affected by X irradiation. In each series, about 70% of the fluorescent cells contained label when they were examined at 24 and 48 hr after the pulse, whereas at 8 and 72 hr fewer were positive. At the earlier intervals, unlabeled fluorescent cells most likely represented cells which had completed viral DNA synthesis prior to the pulse; at the later intervals, unlabeled fluorescent cells were probably cells which commenced viral replication after the pulse. These data support the conclusion that the immunofluorescent cells are the ones which harbor virus, and also confirm the expectation that the virus is a DNA virus from a member of the herpes group. This conclusion was firmly established by sectioning and electron microscopic examination of individual fluorescent cells, all of which contained numerous virus particles, whereas the nonstained cells prepared in a similar manner were free of them.

Autoradiography↗
PubMed1966

Immunofluorescence in cells derived from Burkitt's lymphoma.

Henle, Gertrude (Children's Hospital of Philadelphia, Philadelphia, Pa.), and Werner Henle. Immunofluorescence in cells derived from Burkitt's lymphoma. J. Bacteriol. 91:1248-1256. 1966.-Indirect immunofluorescence tests led to the brilliant staining of a small proportion of the cells in five different cultures derived from Burkitt's (African) lymphomas. The reaction was not restricted to the 17 sera from cases of this disease but extended to many sera from American individuals, whether healthy donors or patients suffering from a variety of illnesses. The incidence of positive sera increased with age from about 30% in childhood to > 90% in adults. Fluorescein-isothiocyanate-conjugated human gamma-globulins were suitable for direct staining of the same proportion of cells. The stained cells appeared to be in varying stages of degeneration, but cultural conditions leading to an increase in the cellular death rates failed to result in a rise in fluorescent cells. Several observations suggest that the stainable cells might be those which are seen to harbor virus particles under the electron microscope. Two cell lines derived from leukemic patients in this country also contained a small fraction of stainable cells but two others, and numerous primary human leukocyte cultures, gave consistently negative results. Attempts to relate the staining to known viral antigens have failed to implicate herpes simplex, varicella, cytomegalo, and reo viruses types 1, 2, and 3. The nature of the virus carried by the lymphoma cells as well as of the staining reactions remains to be determined.

Adult↗
PubMed1966

Complement-fixation tests with cell lines derived from Burkitt's lymphoma and acute leukemias.

Armstrong, Donald (Children's Hospital of Philadelphia, Philadelphia, Pa.), Gertrude Henle, and Werner Henle. Complement-fixation tests with cell lines derived from Burkitt's lymphoma and acute leukemias. J. Bacteriol. 91:1257-1262. 1966.-Cells of various lines isolated from Burkitt's lymphomas and acute leukemias and disintegrated by freezing and thawing or sonic treatment were found to react in complement-fixation tests with a considerable proportion of human sera. At least 10(7) cells per milliliter were required for antigenic activity. All but one of 13 sera from Burkitt lymphoma patients were positive, with titers ranging from 1:8 to 1:320. About 20% of sera from American children and 60% of sera from adults, regardless of diagnosis, showed titers in a similar range. Sera giving positive tests with one of the neoplastic white cell antigens usually reacted also with many if not all of the others, but rarely with antigens derived from normal peripheral leukocyte cultures and not at all with HeLa or other human nonleukocytic cells. Various observations indicate that the complement-fixation test measures mainly antigens which are different from those detected by immunofluorescence. The nature of the reactions described remains obscure.

Adenocarcinoma↗
PubMed1966

Replication of mumps virus in human leukocyte cultures.

Duc-Nguyen, Huu (The Children's Hospital of Philadelphia, Philadelphia, Pa.), and Werner Henle. Replication of mumps virus in human leukocyte cultures. J. Bacteriol. 92:258-265. 1966.-Human peripheral leukocyte cultures maintained in the presence of phytohemagglutinin (PHA) were found to support to some extent the replication of mumps virus. When such cultures were exposed, within 24 hr after their initiation, to a high input multiplicity of virus, successful infection, as determined by immunofluorescence and plaque assays, did not become evident before the 3rd or 4th day. On exposure of cultures 4 to 5 days old, viral replication was detectable within 2 days. In both instances, peak immunofluorescence and virus titers were reached when the cultures were 7 to 9 days old and composed mainly of blast forms. With decreasing input multiplicities of infection, cells containing viral antigen and production of infectious viral progeny became detectable with increasing delay. No significant viral replication was noted in surviving cells maintained in the absence of PHA. These results indicate that mainly, if not solely, the PHA-stimulated cells of the lymphocytic series support viral multiplication. The extent of the infectious process was limited, however, because the life span of the cultures was not significantly shortened, the yields of infectious virus per immunofluorescent cell were at all times low, and most infected cells contained only a few well-delineated small masses of antigen, suggestive of an abortive infection. Only fresh cultures were capable of synthesizing interferon on stimulation by mumps, Newcastle disease, or Sendai viruses. When the cultures were set up in the presence of PHA, this capacity was lost within 24 hr. PHA per sefailed to induce detectable production of an interferon under the conditions used. The implications of these findings are discussed.

Antigens↗
PubMedDate not supplied

Post-perfusion syndrome due to Epstein-Barr virus. Report of two cases and review of the literature.

The post-perfusion syndrome is rarely due to Epstein-Barr virus (EBV), because most adult patients already carry protective neutralizing antibodies in their sera. Data are presented from two patients in whom heterophil-antibody-positive infectious mononucleosis developed 35 and 48 days after open-heart surgery. The diagnoses of their predominantly febrile illnesses were delayed because of late appearance of atypical lymphocytes and heterophil antibodies. EBV-specific antibody responses were also delayed, with peak titers appearing several weeks or months after onset. The differences in evolution of the present cases, compared to those of classic infectious mononucleosis, were presumably due to different portals of entry (blood stream versus oropharynx).

Antibodies, Viral↗