Anti-human immunodeficiency virus type 1 activities of novel non-nucleoside reverse transcriptase inhibitors.
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Antiviral Agents↗
Biomedical subjects
M R Visser
Publications and source records attributed to M R Visser.
Enhancement of HIV-1 replication in peripheral blood mononuclear cells by Cryptococcus neoformans is monocyte-dependent but tumour necrosis factor-independent.
OBJECTIVE: To investigate the possible role of Cryptococcus neoformans in HIV-1 pathogenesis. DESIGN: An in vitro system was developed to study HIV-1 replication in freshly HIV-1-infected peripheral blood mononuclear cells (PBMC) incubated with whole azide-killed C. neoformans. METHODS: Human PBMC or peripheral blood lymphocytes were infected with lymphocytotropic HIV-1 and incubated with azide-killed encapsulated or non-encapsulated C. neoformans for 10 days. Viral replication was followed by HIV-1 p24 enzyme-linked immunosorbent assay and median tissue culture infective dose determination. Tumour necrosis factor (TNF) release by PBMC, induced by C. neoformans, was measured. Anti-TNF monoclonal antibodies or pentoxifylline were used to inhibit TNF bioactivity. RESULTS: Both encapsulated and non-encapsulated C. neoformans enhanced HIV-1 replication in PBMC but not in peripheral blood lymphocytes. C. neoformans induced TNF release by PBMC. Inhibition of TNF bioactivity did not block C. neoformans-enhanced HIV-1 replication in PBMC. CONCLUSIONS: C. neoformans can enhance HIV-1 replication in T cells only in the presence of monocytic cells. This enhancement is not dependent on encapsulation nor can it be attributed to TNF release.
Antibodies, Monoclonal↗
Infection of epithelial cell line HEp-2 with human immunodeficiency virus type 1 is CD4 dependent.
HEp-2 cells, human epithelial cells derived from a larynx carcinoma, were found to be highly susceptible to infection with HIV-1 stain IIIb and MN, but not to infection with the monotropic strain IIIBa-L or the clinical isolate HIV-1AT. HEp-2 cells infected with HIV-1 IIIb continuously secreted high levels of p24 antigen, while no cytopathic effects were observed. Although no CD4 antigen could be detected on the cells by flow cytometric analysis, CD4 mRNA was detected by reverse transcriptase PCR. Furthermore, infection could be blocked by anti-CD4 monoclonal antibody OKT4a indicating a CD4 mediated viral entry in HEp-2 cells. HEp-2 cells are commonly used in clinical virology for the culture of different viruses from clinical specimens. HEp-2 cells should therefore be handled with caution as they may potentially become infected with HIV.
Antibodies, Monoclonal↗
Binding of HIV-1 to human follicular dendritic cells.
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Blood Physiological Phenomena↗
Safety and efficacy of lomefloxacin versus norfloxacin in the treatment of complicated urinary tract infections.
Seventy patients with complicated urinary tract infections were treated with either lomefloxacin (400 mg once daily) or norfloxacin (400 mg twice daily) for 10 to 14 days. A total of 19 (86%) of 22 patients treated with lomefloxacin and 20 (74%) of 27 patients treated with norfloxacin were cured, as defined by a negative culture five to nine days after completion of therapy (p = 0.09). After four to six weeks, the figures were 56% for lomefloxacin and 48% for norfloxacin. Adverse effects in the lomefloxacin group were observed on 20 occasions in 12 patients (one stopped treatment) compared to nine occasions in five patients treated with norfloxacin (difference not significant).
Adolescent↗
Non-radioactive PCR method for quantification of HIV-infected peripheral blood mononuclear cells in HIV-positive subjects.
A nested PCR method for quantification of HIV-infected peripheral blood mononuclear cells (PBMC) which does not use radioactivity nor plasmids is described. Quantification was achieved by means of limiting dilutions and an ACH2 cell standard. The method was used to study 23 HIV-infected patients. A significant correlation was seen between the stage of HIV disease, as classified by CDC criteria, and the number of infected PBMC. Although the CD4+ cell count also correlated well with the stage of HIV disease, there was only weak correlation between the result obtained by the PCR method and the CD4+ cell count.
Base Sequence↗
An outbreak of Serratia marcescens traced to a contaminated bronchoscope.
An outbreak of colonization and infection with Serratia marcescens in a surgical Intensive Care Unit is described. A case-control study pointed to a bronchoscope as the source of the epidemic strain, and cultures of washing effluent of the incriminated bronchoscope yielded S. marcescens. Discontinuation of the use of the instrument and the implementation of recommendations for future use of bronchoscopes ended the outbreak.
Adolescent↗
A decade of experience with selective decontamination of the digestive tract as prophylaxis for infections in patients in the intensive care unit: what have we learned?
Infection is a frequent and often life-threatening complication in patients treated in intensive care units. Many regimens have been developed to prevent infections in these patients. Recently, a new method of prophylaxis was introduced: selective decontamination of the digestive tract. This paper reviews the results of studies on selective decontamination of the digestive tract with oral, nonabsorbable antimicrobial agents. Most studies showed a positive effect of selective decontamination; a significant decrease in the incidence of nosocomial pneumonia among patients receiving agents for selective decontamination was observed. However, the great differences among the various studies in the incidence of infections among control patients make it difficult to compare the results. The use of antimicrobial agents for selective decontamination had no effect on mortality and in some studies even led to the emergence of resistant microorganisms. The lack of recent data on the incidence, pathogenesis, and epidemiology of infections in patients in intensive care units makes it difficult to recommend routine use of selective decontamination for these patients.
Anti-Bacterial Agents↗
Down-regulation of human immunodeficiency virus type (HIV-1) production after stimulation of monocyte-derived macrophages infected with HIV-1.
Macrophages infected with human immunodeficiency virus (HIV) can be stimulated as a result of secondary infections. The effect of stimulation of HIV-1-infected monocyte-derived macrophages on HIV-1 production by these cells was studied. Exposure of macrophages to phorbol 12-myristate 13-acetate or to opsonized Escherichia coli, Staphylococcus aureus, or zymosan resulted in a decrease in HIV production. HIV production was inversely related to the degree of stimulation, measured as lucigenin-enhanced chemoluminescence. The production of reactive oxygen intermediates, however, did not seem to be the direct cause of the diminished HIV production, since oxygen-radical scavengers did not prevent the decrease in HIV production. Furthermore, oxygen-radical scavengers did not affect HIV production by nonstimulated macrophages. These results indicate that activation signals have an opposite effect and reactive oxygen intermediates have no effect on HIV production in macrophages compared with the effect described in T cells.
Acetylcysteine↗
Phagocytic function of monocyte-derived macrophages is not affected by human immunodeficiency virus type 1 infection.
The immunopathogenesis of human immunodeficiency virus (HIV) infection is characterized by the failure to control opportunistic infections. Here, the direct effect of HIV on macrophage phagocytic function was studied. HIV-1-infected monocyte-derived macrophages expressed as many Fc gamma and complement receptors as did control macrophages. The function of these receptors was not affected by HIV-1 infection since binding and internalization of opsonized Escherichia coli and Staphylococcus aureus were not impaired. Production of reactive oxygen species induced by stimulation of the HIV-1-infected macrophages with opsonized E. coli, zymosan, or PMA was intact. HIV-1-infected macrophages killed opsonized E. coli and Candida albicans as effectively as did control macrophages. These results, therefore, do not support the hypothesis that HIV-1 infection of macrophages causes phagocytic dysfunction and suggest that HIV-induced abnormalities outside the mononuclear phagocyte system may lead to the inability to control opportunistic pathogens.
Antigens, Surface↗
Changes in adherence of respiratory pathogens to HEp-2 cells induced by subinhibitory concentrations of sparfloxacin, ciprofloxacin, and trimethoprim.
Preincubation with subinhibitory concentrations of sparfloxacin, ciprofloxacin, and trimethoprim decreased the adherence of the respiratory pathogens Klebsiella pneumoniae, Haemophilus influenzae, and Moraxella (Branhamella) catarrhalis to human larynx carcinoma HEp-2 cells. Subinhibitory concentrations of sparfloxacin did not change the adherence of Pseudomonas aeruginosa or Streptococcus pneumoniae 15.62, but adhesion of S. pneumoniae 15.42 was significantly enhanced by subinhibitory antimicrobial concentrations.
Anti-Infective Agents↗
Herpes simplex virus and atherosclerosis.
This paper presents a brief overview of our current understanding of the relationship between herpes simplex virus (HSV) and atherogenesis. In the search for a viral trigger of atherosclerosis, several investigators reported the detection of herpes simplex virus in some, but not all atherosclerotic lesions. HSV infections are very common, not only in atherosclerotic patients but also in the general population, making epidemiological studies difficult to interpret. Different mechanisms by which HSV may contribute to atherogenesis have been described. In vascular cells, HSV infection leads to lipid accumulation. HSV infection of endothelial cells attracts leukocytes with subsequent inflammatory damage; it activates procoagulant changes on endothelium with increased thrombin generation and platelet adhesion, and changes its interaction with extracellular matrix proteins. Future studies should delineate whether these mechanisms are operative in the pathogenesis of atherosclerosis.
Arteriosclerosis↗
Comparison of the autoSCAN-W/A and Vitek Automicrobic systems for identification and susceptibility testing of bacteria.
The identification and susceptibility testing of bacteria by the autoSCAN-W/A rapid panels and Vitek Automicrobic systems were compared. A total of 291 clinical isolates, including 207 members of the Enterobacteriaceae, 41 nonfermentative gram-negative bacilli, 31 Staphylococcus aureus strains and 12 Enterococcus faecalis strains, were tested. autoSCAN-W/A and Vitek correctly identified 93% and 94% respectively of the Enterobacteriaceae, the identification in an additional 2% and 5% of strains respectively being reported as correct with a low probability. autoSCAN-W/A reported all identification results within 2 h after inoculation, whereas Vitek reported the identification results for the majority of gram-negative bacilli between 4 h and 6 h after inoculation. autoSCAN-W/A and Vitek reported 81% and 74% of MIC results respectively after 3-6 h incubation. The rates of very major susceptibility errors were 0.4% and 0.4% for autoSCAN-W/A and Vitek respectively, the rates of major errors 0.4% and 1% respectively, and the rates of minor errors 4% and 3% respectively. Six of 30 Pseudomonas aeruginosa strains failed to grow sufficiently for susceptibility testing in the autoSCAN-W/A system, and four Xanthomonas maltophilia strains had insufficient growth for susceptibility testing in both systems. The majority of results of susceptibility testing of nonfermentative gram-negative bacilli were reported more than 6 h after inoculation. Both systems were reliable and easy to operate, and gave accurate results for common clinical isolates.
Bacteria↗
Antibodies and complement enhance binding and uptake of HIV-1 by human monocytes.
OBJECTIVE: To characterize antibody- and complement-mediated binding and uptake of HIV-1 by human monocytes. DESIGN: The first step in the infection of the monocyte by HIV-1 is binding of the virus to the susceptible cell. Procedures were designed to assess the influence of anti-HIV-1 antibodies and complement on this binding, and to study the process of internalization following binding. METHODS: Human monocytes were incubated with fluorescein-labelled purified HTLV-IIIB virions and human sera with high-titre anti-HIV-1 antibodies and/or complement. Binding and uptake of virus by the monocytes was measured as fluorescence per cell by flow cytometry. RESULTS: Binding of purified HIV-1 to monocytes was increased by complement and, to a lesser extent, by anti-HIV-1 antibodies. Uptake of HIV-1 bound to the monocyte appeared to be mediated by antibodies and was increased further by the presence of complement. Complement alone, however, resulted in the uptake of only a small part of the bound virus. CONCLUSIONS: Complement significantly increases the binding of HIV-1 to human monocytes, and a combination of antibodies and complement efficiently mediates uptake of HIV-1 by monocytes.
Antibodies, Monoclonal↗
Antibody mediated enhancement of HIV-1 infection of an EBV transformed B cell line is CD4 dependent.
Low levels of anti-viral antibodies may facilitate virus infection of Fc-receptor bearing cells. For human immunodeficiency virus (HIV) it has been reported that antibodies can enhance infection of phagocytic cells. We show that HIV-1 can infect an Epstein-Barr virus transformed B cell line and that low levels of anti-HIV antibodies enhance infection. The enhanced infection was characterized by an increase in viral DNA and increased HIV p24 protein production. Detection of cell surface antigen expression of CD4, the receptor for HIV, Fc-receptor type II for IgG, but not of type I and III could be demonstrated by immunofluorescence cytometry. The enhancement was abrogated when infection was performed in presence of a monoclonal antibody directed against CD4. Based on these results we conclude that antibody mediated enhancement of HIV-1 infection can also occur in non-phagocytic cells in a CD4 dependent manner and that IgG Fc-receptors other than types I or III are involved in this process.
B-Lymphocytes↗
Double-blind randomized study comparing the efficacies and safeties of a short (3-day) course of azithromycin and a 5-day course of amoxicillin in patients with acute exacerbations of chronic bronchitis.
The efficacies and safeties of a three-dose regimen of azithromycin (500 mg once daily for 3 days) and a 15-dose regimen of amoxicillin (500 mg three times daily for 5 days) were compared in a double-blind manner in patients with an acute exacerbation of chronic bronchitis. A total of 92% of patients suffered a type 1 exacerbation. Treatment success, defined as cure or major improvement, was achieved in all patients in the azithromycin group by day 5, compared with 23 (92%) of 25 patients in the amoxicillin group. On day 12, these data were 24 of 25 (96%) in the azithromycin group and 20 of 25 (80%) in the amoxicillin group (results were not significantly different). Several pathogens were isolated (MIC ranges [micrograms per milliliter] in parentheses): Haemophilus influenzae or Haemophilus parainfluenzae was isolated 23 times (azithromycin, less than or equal to 0.06 to 32; amoxicillin, 0.12 to 2); Streptococcus pneumoniae was isolated from 11 patients (azithromcyin, less than or equal to 0.06 greater than 256; amoxicillin, less than or equal to 0.06 to 0.25); Moraxella (Branhamella) catarrhalis was isolated from eight patients (azithromycin, less than or equal to 0.06; amoxicillin, less than or equal to 0.06 to 16); and other members of the family Enterobacteriaceae were isolated from eight patients. One patient treated with azithromycin had Legionella pneumophila pneumonia, and another in that group had a significant rise in titer of antibody against influenza A virus. One patient treated with amoxicillin also had a significant rise in titer of antibody against influenza A virus. Microbiological response rates were comparable. One patient who received azithromycin developed abnormal liver function. Two patients treated with amoxicillin developed abnormal liver functions, one developed exanthema, and one treatment was stopped because of nausea. It is concluded that a three-dose (3-day) regimen of azithromycin is as effective clinically and microbiologically as a 15-dose (5-day) regimen of amoxicillin in the treatment of acute exacerbations of chronic bronchitis.
Aged↗
Infectious disease therapy in the 1990s. Where are we heading?
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Animals↗
Intracerebral Nocardia asteroides abscess treated by neurosurgical aspiration and combined therapy with sulfadiazine and cefotaxime.
We present a patient with a Nocardia brain abscess who failed to respond to repeated neurosurgical aspiration in combination with sulfadiazine therapy but improved after additional treatment with cefotaxime.
Adult↗