Biomedical subjects
Publications and source records attributed to H Gelderblom.
Chicken anaemia agent (CAA) was characterized as a virion with 25 nm in diameter, with a buoyant density in CsCl of 1.36-1.37 g/cm3, and containing a circular, single-stranded DNA genome. The virus is composed of 32 hollow morphological units representing a regular T = 3 icosahedron.
Six cases of oral hyperpigmentation in HIV-infected patients are reported. While in two patients the lesions could be related to systemic clofazimine or ketoconazole therapy, in the other patients the cause remained unknown. Clinically, the pigmentations were characterized by a sudden onset and the appearance of well-defined, brown-black macules in the buccal mucosa, the gingiva, the hard palate, or the lateral borders of the tongue. In one patient, longitudinal hyperpigmented striae were observed on all fingernails and toenails. Histologically, hyperpigmentations associated with systemic medication revealed accumulation of melanin in phagocytes and extracellularly within the connective tissue. In those lesions with unknown cause, melanin was restricted to keratinocytes of the basal cell layer or to extracellular foci in the lamina propria. The clinical and histologic findings, as well as differential diagnosis, are discussed.
De novo infection of Rous sarcoma virus (RSV) strains of receptor subgroups A, B, C, and D is inhibited by low doses of chick interferon. Adsorption and penetration into the cell are not marginally impaired by interferon treatment. Since the level of proviral DNA synthesis is strongly reduced in the interferon-treated cell it is concluded that uncoating or reverse transcription of the viral genome is inhibited. This inhibition of proviral DNA synthesis is not caused by an arrest of CEF in the stationary phase. Chronic infection of SR-RSV-A, -B, -C, but not SR-RSV-D is also sensitive to interferon. Chick interferon treatment (50 u/ml) also had no inhibitory effect on the amount of transcripts of the RSV-specific oncogene src or the cellular oncogenes src and myc.
Twelve biopsies of clinically normal oral mucosa taken from HIV seropositive patients have been investigated by means of light- and electron microscopy. Vascular abnormalities were found in all biopsies, regardless of the clinical stage of the HIV infection. In particular slit-like vascular channels, sparseness of intercellular junctions and swollen, protruded endothelial cells with an increased quantity of Weibel-Palade bodies were noticed. These findings were similar to those described in lesions of early stage Kaposi's sarcoma.
Oral hyperpigmentation has been observed in six HIV-infected patients, in two of whom systemic medication (ketokonazole, clofazimine) was supposed to be etiologically involved. Histologically, pigment was found in epithelial basal cells and particularly in subepithelial connective tissue. Ultrastructurally, the presence of premature melanosomes in subepithelial keratinocytes was of interest. Stimulation of melanocytes during HIV infection may occur in association with immunopathologic changes in the oral mucosa.
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Seventeen biopsies taken from oral mucosa of HIV infected patients were analysed for the distribution of CD4+/CD8+ T-lymphocytes and Langerhans cells. The results were evaluated statistically. An increase in the absolute number of CD4+ and CD8+ cells in HIV infected patients without clinical symptoms, ARC or AIDS was seen in the connective tissue stroma when compared with normal oral mucosa from sero-negative patients. However, the ratio between CD4+/CD8+ cells was decreased due to the disproportionate increase of CD8+ cells. These findings did not show statistical correlation with the clinical status of the infection. In contrast to the increase in absolute number of CD4+/CD8+ cells the number of Langerhans cells was unchanged when compared with the control group. Using four different monoclonal antibodies against virus structural proteins (2 X anti p24, gp41, gp120) two of 26 patients showed labelled cells in consecutive sections in the same connective tissue areas. It was assumed that latently infected mononuclear cells invaded the oral mucosa together with uninfected cells of the cellular immune system.
Three cases of HL from the lateral border of the tongue of male homosexual AIDS patients were investigated by thin section electron microscopy. Keratinocytes contained condensed chromatin in their pyknotic nuclei and a few organelles in the oedematous cytoplasm. Chromatin was in close association to the nuclear membrane and showed a punched-out appearance. Particles typical of the herpes virus group were abundant in the upper two thirds of the epithelium in all three cases. Virus particles were seen frequently in the nuclei of the ballooned keratinocytes, but rarely in cells containing Candida albicans. Viral nucleocapsids were observed budding at the inner nuclear membrane, thereby acquiring the prospective viral envelope. Complete, enveloped virions were found in the endoplasmic reticulum and in the extracellular space. These virions were identified immunohistochemically as Epstein-Barr virus (EBV) using two monoclonal antibodies directed against EBV capsid and membrane antigen, respectively. Candida albicans was observed in the stratum corneum and in the upper layer of the stratum spinosum. Special cytoplasmic tubular structures arranged in parallel bundles were found in koilocytotic cells in addition to characteristic membrane structures composed of undulating convoluted membranes. Epithelial basement membranes were always intact.
The production and properties of monoclonal antibodies raised against herpes simplex virus type 1 (HSV-1)-infected cell nuclei are described. Biological and immunochemical assays revealed that these antibodies recognize four different proteins in HSV-1-infected cells. Four antibodies reacted with the major DNA-binding protein (ICP8) and six with the 65K DNA-binding protein. Two antibodies detected the ICP35 family of proteins and one antibody bound to a protein with an apparent mol. wt. of 60K. Immune electron microscopy showed that the major DNA-binding protein had a patchy distribution, whereas the 65K DNA-binding protein was evenly spread in the infected cell nuclei. The 60K protein as well as the polypeptides of the ICP35 family were preferentially found associated with the viral capsid.
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Retroviruses are small, RNA-containing enveloped viruses which are widely distributed in nature. They exist in many animal species as well as in man. Exogenous virus strains are horizontally transmitted between individuals of a given species, like all other virus groups. Endogenous virus strains have managed some time during evolution to infect germ line cells like oocytes and spermatocytes and are thus transmitted vertically from parents to offspring. Several retrovirus strains possess oncogenes, i.e., acutely tumor-inducing genes. There are four human retrovirus strains so far. The initially discovered strain, HTLV-I, is accepted to be a co-factor in the development of an acute T-cell leukemia in adults. HTLV-II has repeatedly been isolated from cells of patients with hairy cell leukemia. Its etiological significance is unclear at present. HTLV-III/LAV-1, now designated HIV-1, is the causative agent of AIDS. HTLV-IV and LAV-2 are additional HIV-1 related strains and are supposed to cause AIDS as well. What is known about the pathogenicity of the human retrovirus strains will be discussed.
The toxic effect of insect iridescent virus type 6 - chilo iridescent virus - (CIV) was investigated using Balb/c mice (strain ByJ Ico and Kisslegg). The animals were inoculated with CIV intraperitoneally (1 X 10(9) to 9.2 X 10(11) TCID50/animal). The animals which were administered with 1 X 10(11) to 9 X 10(11) TCID50 of CIV per animal, developed acute clinical illness and died during 18 to 80 h post infection. Histopathological and electronmicroscopic examinations of the liver tissues of those animals which died and/or were sacrificed when moribund showed acute degenerative hepatitis leading to death. No evidence for viral replication was found in the liver cells affected. A mortality rate between 21.1% and 100% was recorded for CIV, depending on the strain and number of mice used and the dose of virus administered. The toxic effect of CIV was eliminated or reduced extensively using heat denaturation or treatment of CIV with sodium dodecylsulphate or proteinase K. This indicates that the nature of the factor causing toxic degenerative cell damage is a protein.
The HFEM strain of HSV-1 is apathogenic for the tree shrew by the intraperitoneal (i.p.) route because of a deletion in the genome coordinates 0.762-0.789. Insertion of the MluI DNA fragment (coordinates 0.7615-0.789) cloned from HSV-1 strain F, which is pathogenic for the tree shrew, restored the i.p. pathogenicity to strain HFEM. The recombinant designated R-M1-C1 was highly pathogenic for the tree shrew, but slightly virulent for inbred mouse strain A. It thus appears that the viral DNA sequence involved in the i.p. pathogenicity of HSV-1 is located within the genome coordinates 0.761-0.796. This sequence is recognized differently by the cellular elements involved in HSV-1 infection in the tree shrew and the mouse.
Liver tumor biopsies of a 9-year-old moribund Tupaia (tree shrew) were explanted and cultured in vitro. The cell cultures degenerated spontaneously. A virus was isolated from the cell-free supernatant of these cultures and subsequent electron microscopy revealed rhabdovirus-like particles. Negative staining showed typical bullet-shaped particles 125-220 nm in length with a diameter of 68 nm studded with a dense layer of surface projections 9-11 nm in length. One end of the virion was flat, the other end was open; a distinct ribonucleoprotein (RNP) core was visible. The pitch of the RNP was 4.5 nm. Virus was assembled and matured by budding primarily into regions of dilated endoplasmic reticulum. The dimensions of the virion also were determined in ultrathin sections: the diameter and length of the virion were 52 and 125-255 nm, respectively, those of the RNP core were 39 and 120-240 nm. Only tupaia embryonic fibroblasts and kidney cells were susceptible to the rhabdovirus. The virus, when plaque-assayed on tupaia embryonic fibroblasts, grew to a titer of 1 X 10(6) PFU.
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