Characterization of novel bacteriochlorophyll-a-containing red filaments from alkaline hot springs in Yellowstone National Park.

Novel red, filamentous, gliding bacteria formed deep red layers in several alkaline hot springs in Yellowstone National Park. Filaments contained densely layered intracellular membranes and bacteriochlorophyll a. The in vivo absorption spectrum of the red layer filaments was distinct from other phototrophs, with unusual bacteriochlorophyll a signature peaks in the near-infrared (IR) region (807 nm and 911 nm). These absorption peaks were similar to the wavelengths penetrating to the red layer of the mats as measured with in situ spectroradiometry. The filaments also demonstrated maximal photosynthetic uptake of radiolabeled carbon sources at these wavelengths. The red layer filaments displayed anoxygenic photoheterotrophy, as evidenced by the specific incorporation of acetate, not bicarbonate, and by the absence of oxygen production. Photoheterotrophy was unaffected by sulfide and oxygen, but was diminished by high-intensity visible light. Near-IR radiation supported photoheterotrophy. Morphologically and spectrally similar filaments were observed in several springs in Yellowstone National Park, including Octopus Spring. Taken together, these data suggest that the red layer filaments are most similar to the photoheterotroph, Heliothrix oregonensis. Notable differences include mat position and coloration, absorption spectra, and prominent intracellular membranes.

The calcium channel blocker used with cyclosporin has an effect on gingival overgrowth.

BACKGROUND/AIMS: To investigate whether the choice of calcium channel blocker, used in conjunction with cyclosporin A, affected the prevalence of gingival overgrowth. METHOD: A cohort of 135 renal transplant recipients who had been medicated with cyclosporin A in combination with either nifedipine (89) or amlodipine (46) since transplant, took part in the study. The inclusion criteria were that eligible subjects had been in receipt of a kidney transplant for at least 12 months, had at least 10 teeth and had not received specialist periodontal treatment. The age, gender, current drug regimen and dosage were recorded for each participant and alginate impressions taken of both arches. The presence and severity of gingival overgrowth were scored from plaster models. RESULTS: A higher proportion (72%) of the amlodipine group were categorised as having gingival overgrowth compared with only 53% of the nifedipine group, chi square=4.5, p<0.05. Logistic regression analysis was used to explore the relationship between the presence or absence of gingival overgrowth (dependent variable) and age, gender, time since transplant, dose of cyclosporin A, centre in which the patient was treated, and the calcium channel blocker used (independent variables). Independent predictors of gingival overgrowth in this multivariate analysis were whether the individual was treated with amlodipine or nifedipine (p=0.01) and whether the individual was young or old (p=0.01). Within the multivariate analysis, the odds ratio for amlodipine to be associated with gingival overgrowth compared with nifedipine was 3.0 (confidence interval 1.3-6.9). CONCLUSIONS: The prevalence of gingival overgrowth in renal transplant recipients maintained on cyclosporin A and nifedipine is lower than those treated with cyclosporin A and amlodipine.

Reduction in gingival overgrowth associated with conversion from cyclosporin A to tacrolimus.

BACKGROUND: Unsightly gingival overgrowth affects many individuals immunosuppressed with cyclosporin A (CsA). Current management involves repeated periodontal surgery and intensive hygienist support. Tacrolimus is an effective alternative immunosuppressive agent for renal transplantation which does not appear to produce gingival enlargement. AIMS: The purpose of the present study was to monitor the gingival response of 4 renal transplant patients (RTPs), with clinically significant CsA-induced gingival overgrowth, after their immunosuppressive therapy was switched to tacrolimus. METHODS: Intra-oral photographs and alginate impressions were taken both prior to the drug conversion and again, 6 to 9 months later. Gingival overgrowth scores were determined, from plaster models on both these occasions. RESULTS: All of the RTPs experienced significant resolution of their gingival enlargement within the time period studied; however, only one had complete regression. CONCLUSION: It is concluded that conversion of RTPs with gingival overgrowth from CsA to tacrolimus may provide an effective management strategy for this clinical problem.

Cyclosporin associated gingival overgrowth in renal transplant recipients.

OBJECTIVES: To investigate the prevalence and severity of gingival overgrowth in a group of renal transplant recipients treated in one centre in Northern Ireland. STUDY DESIGN: A consecutive group of patients who had had a renal transplant for at least 6 months and were attending the Renal Unit in Belfast City Hospital took part in the study. These were divided into a group of 84 subjects treated with cyclosporin since their transplant who were compared with a control group of 36 transplant recipients who had never received cyclosporin. Each subject had a periodontal examination and completed a questionnaire. The severity of gingival overgrowth was scored from plaster models. OUTCOME MEASURES: Clinically significant gingival overgrowth was equated with a score of > or = 30 using the index developed by Seymour et al (1985). RESULTS: 41 (49%) of the cyclosporin group had clinically significant gingival overgrowth compared with none of the controls. A significantly higher proportion of males had overgrowth than females. There were significant correlations between age at transplant, plaque, bleeding, pocketing and the severity of gingival overgrowth. Many patients with clinically significant gingival overgrowth were apparently unconcerned about this condition. CONCLUSIONS: It is concluded that gingival overgrowth is a significant problem for renal transplant patients treated with cyclosporin, particularly if they are also treated with a calcium channel blocker. None of the factors measured, in isolation, explained the variable expression of gingival overgrowth in those at risk.

The host range and interference properties of two closely related feline leukemia variants suggest that they use distinct receptors.

The proviral clones 61E and 61C represent two closely related variants of feline leukemia virus (FeLV) that exhibit significant differences in their biological and pathogenic properties. The major pathogenic determinant has been mapped to the extracellular envelope glycoprotein (Env-SU), but the mechanism by which envelope differences influence pathogenesis is not well understood. Moreover, it is unclear whether these viruses infect the same target cells and/or enter cells using the same receptor. In the present study, we exploited a recently developed single cycle infection assay to examine the host range and interference properties of 61E and 61C FeLVs and found that these two FeLV variants differ significantly in their host ranges and receptor usages. FeLV-61C was found to be an ecotropic virus; the entry of viruses bearing a 61C envelope protein (Env-SU) into cell lines was limited to feline T-cells and feline fibroblasts. In contrast, the host range of 61E includes, in addition to all feline cells examined, some canine, murine, and human cell lines. Feline fibroblast and feline T-cells that expressed 61E envelope were resistant to infection with a virus bearing a 61E Env-SU, whereas these same cells were susceptible to infection by an otherwise similar virus pseudotyped with the 61C Env-SU. This pattern of interference was observed in cells expressing 61E envelope alone, in the absence of other FeLV gene products, demonstrating that interference was mediated specifically by Env-SU. Fibroblast cells chronically infected with a 61C virus were partially resistant to infection with a virus having a 61C Env-SU, but were not resistant to infection by a virus having a 61E Env-SU. On the basis of the current understanding of virus-receptor interactions, the lack of interference between 61E and 61C under conditions where there is significant homologous interference, combined with the differences in their host cell range, leads us to conclude that 61E and 61C use two distinct primary cellular receptors for entry.

Three distinct envelope domains, variably present in subgroup B feline leukemia virus recombinants, mediate Pit1 and Pit2 receptor recognition.

Subgroup B feline leukemia viruses (FeLV-Bs) evolve from subgroup A FeLV (FeLV-A) by recombining with portions of endogenous FeLV envelope sequences in the cat genome. The replication properties of FeLV-B are distinct from those of FeLV-A; FeLV-B infects many nonfeline cell lines and recognizes the human Pit1 (HuPit1) receptor, whereas FeLV-A infects primarily feline cells, using a distinct but as yet undefined receptor. Here, we demonstrate that some FeLV-Bs can also use human Pit2 (HuPit2) and hamster Pit2 (HaPit2) for entry. By making viruses that contain chimeric surface (SU) envelope proteins from FeLV-A and FeLV-B, and testing their infectivity, we have defined genetic determinants that confer host range and specific receptor recognition. HuPit1 receptor recognition determinants localize to the N-terminal region of the FeLV-B SU, amino acids 83 to 116, encompassing the N-terminal portion of variable region A (VRA). While this 34-amino-acid domain of the FeLV-B VRA is sufficient for infection of some cells (feline, canine, and human), amino acids 146 to 249 of FeLV-B, which include variable region B (VRB), were required for efficient infection in other cell types (hamster, bovine, and rat). Chimeras encoding FeLV-B VRA and VRB also infected cells expressing HaPit2 and HuPit2 receptors more efficiently than chimeras encoding only the VRA of FeLV-B, suggesting that VRB provides a secondary determinant that is both cell and receptor specific. However, viruses containing additional FeLV-B sequences in the C terminus of SU could not recognize HuPit2, implying that there is a determinant beyond VRB that negatively affects HuPit2 interactions. Thus, Pit2 recognition may drive selection for the generation of specific FeLV-B recombinants, offering an explanation for the two major classes of FeLV-B that have been observed in vivo. Furthermore, the finding that some FeLV-Bs can use both Pit1 and Pit2 may explain previous observations that FeLV-B and GALV, which primarily uses Pit1, display nonreciprocal interference on many cell types.

Isolation of a novel subgroup B feline leukemia virus from a cat infected with FeLV-A.

Proviruses were cloned directly from a cat that developed neurological disorders approximately 28 months after inoculation with a molecularly cloned, minimally pathogenic subgroup A feline leukemia virus (FeLV-A). In addition to FeLV-A proviruses that were nearly identical to the inoculated virus, we detected a subgroup B-like variant in brain, bone marrow, and lymph node that apparently had acquired the major portion of its extracellular envelope gene (gp70) from endogenous FeLV-related sequences. A similar recombinant was also detected, by PCR, at low levels in bone marrow from an early time postinfection (2.5 months). A full-length proviral variant with this recombinant structure cloned from brain tissue encoded a replication-defective virus. A chimera encoding the 5' gag-pol portion of FeLV-A and the 3' env-LTR portion of the defective brain-derived clone was replication-competent and had the extended host range properties of FeLV-B.