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PubMed1989

Transient and persistent sodium currents in normal and denervated mammalian skeletal muscle.

1. Transient and persistent tetrodotoxin-sensitive sodium currents were recorded in response to depolarizing voltage pulses in voltage clamped segments of rat extensor digitorum longus muscle fibres at 20-25 degrees C in a triple Vaseline gap. 2. Appreciable persistent sodium current but little or no transient current was seen in response to depolarizations of up to 15 mV from a holding potential of -100 mV. 3. The maximum amplitude of both transient and persistent sodium currents occurred with depolarizations to -40 mV: the average peak amplitude of the transient current in fibres with a holding potential of -90 mV was -0.22 +/- 0.03 mA/microF (mean +/- 1 S.E.M., seven fibres) and the average amplitude of the persistent current was -0.94 +/- 0.10 microA/microF (mean +/- 1 S.E.M., twelve fibres). With a holding potential of -100 mV, the average amplitudes of the transient and persistent currents were -0.46 +/- 0.10 mA/microF (four fibres) and -1.4 +/- 0.22 microA/microF (five fibres), respectively. 4. The average maximum persistent sodium conductance in seven fibres held at -90 mV was 0.13 +/- 0.0078 microS and the potential for half-maximum conductance was -53 +/- 0.74 mV (mean +/- 1 S.E.M.). 5. When the transient sodium current was completely inactivated with 100 ms conditioning depolarizations to potentials more positive than -50 to -60 mV, there was little inactivation of the persistent current. 6. In six denervated fibres, the average amplitudes of the transient and persistent sodium currents generated by pulses to -40 mV from a holding potential of -90 mV were -0.11 +/- 0.01 mA/microF and -0.88 +/- 0.12 microA/microF, respectively (mean +/- 1 S.E.M.). It was concluded that there was a decrease in transient current but not persistent current amplitude following denervation and that the persistent current in denervated fibres with an increased input resistance could give rise to the spontaneous action potentials responsible for fibrillation.

Animals↗
PubMed2005

Synovial Chlamydia trachomatis up regulates expression of a panel of genes similar to that transcribed by Mycobacterium tuberculosis during persistent infection.

BACKGROUND: Synovial tissues in patients with Chlamydia associated arthritis are persistently infected by C trachomatis, an organism for which genetic manipulation is not possible. M tuberculosis also engages in persistent infection, and because this bacterium is genetically tractable many groups have been able to define transcriptional characteristics of mycobacterial growth and persistence. OBJECTIVE: To investigate whether the pattern of gene expression underlying chlamydial persistence is similar to that underlying mycobacterial persistence. METHODS: 194 genes in M tuberculosis that are transcriptionally up regulated to support in vivo growth and persistence of that organism have previously been identified. Each of those genes was compared with the C trachomatis genome to identify orthologues. Expression of selected chlamydial orthologues so identified was assessed by real time RT-PCR in an in vitro model of chlamydial persistence and synovial tissues from patients who were PCR positive for C trachomatis at that site. RESULTS: 67 C trachomatis genes were identified as being orthologous to mycobacterial persistence related genes, representing 35% of the genes tested. The chlamydial orthologues fell into similar metabolic and other categories as those in M tuberculosis. Expression of a majority of selected chlamydial orthologues was strongly up regulated in an in vitro model of chlamydial persistence and in synovial tissues of relevant patients, compared with their expression during active infection. CONCLUSIONS: These observations provide new insight into the molecular genetic basis underlying chlamydial persistence, and indicate that this information can be obtained, in some instances, by extrapolating observations made in other biological systems and/or organisms.

Arthritis, Reactive↗
PubMed1999

High conductance sustained single-channel activity responsible for the low-threshold persistent Na(+) current in entorhinal cortex neurons.

Stellate cells from entorhinal cortex (EC) layer II express both a transient Na(+) current (I(Na)) and a low-threshold persistent Na(+) current (I(NaP)) that helps to generate intrinsic theta-like oscillatory activity. We have used single-channel patch-clamp recording to investigate the Na(+) channels responsible for I(NaP) in EC stellate cells. Macropatch (more than six channels) recordings showed high levels of transient Na(+) channel activity, consisting of brief openings near the beginning of depolarizing pulses, and lower levels of persistent Na(+) channel activity, characterized by prolonged openings throughout 500 msec long depolarizations. The persistent activity contributed a noninactivating component to averaged macropatch recordings that was comparable with whole-cell I(NaP) in both voltage dependence of activation (10 mV negative to the transient current) and amplitude (1% of the transient current at -20 mV). In 14 oligochannel (less than six channels) patches, the ratio of transient to persistent channel activity varied from patch to patch, with 10 patches exhibiting exclusively transient openings and one patch showing exclusively persistent openings. In two patches containing only a single persistent channel, prolonged openings were observed in >50% of test depolarizations. Moreover, persistent openings had a significantly higher single-channel conductance (19.7 pS) than transient openings (15.6 pS). We conclude that this stable high-conductance persistent channel activity is responsible for I(NaP) in EC stellate cells. This persistent channel behavior is more enduring and has a higher conductance than the infrequent and short-lived transitions to persistent gating modes that have been described previously in brain neurons.

Animals↗
PubMed2005

[Persistence of IgM anti-HAV in prolonged form of HAV-infection].

UNLABELLED: Persistence of IGM anti-HAV antibody in sera of patients with acute HAV-infection can be followed up to 55 weeks. Available literature does not provide significant information on persistence of IgM anti-HAV antibody in prolonged form of disease. In multi-centric prospective study of the HAV infection prolonged form we have examined persistence of IgM anti-HAV in 30 patients with acute form of disease and 60 patients with prolonged form of disease. The aim of work was to examine length of IgM anti-HAV persistence in sera of patients with prolonged form of disease in relation to sex, length of persistence of sera aminotranspherasis activities and circulating immune complexes and length of secretion of Ag-HAV in stool. MATERIAL AND METHODS: IgM anti-HAV, IgG anti-HAV, HBV and HCV markers were determined with ELISA method. Circulating immune complexes were determined with fotometer in the sediment of poliethilenglicol on 480 nm wavelength. Antigen-HAV in stool was prescribe through a method of reversed immunoelectroosmophoresis. Results of examination have shown that the persistence of IgM anti-HAV in sera of patients suffering from acute and prolonged form of disease was first of all continued and than discontinued. In male patients the IgM anti-HAV persistence significantly longer (p < 0.05) in prolonged phase, while in female patients the same goes for acute phase of disease. In prolonged HAV-infection persistence of IgM anti-HAV antibody is three times longer that in acute infection. IgM anti-HAV maintained in sera of patients three times longer than the persistence of sera aminotranspherasis activities and secretion of Ag-HAV in stool, which is proportional to the persistence of circulating immune complexes in sera of patients with acute and prolonged HAV-infection.

Acute Disease↗
PubMed2005

Estimating medication persistency using administrative claims data.

OBJECTIVES: To review the definitions and methods for measuring medication persistency, and to propose a uniform definition of and calculation for persistency using pharmacy claims data. STUDY DESIGN: Literature review. METHODS: A MEDLINE search (1966 to present) was performed to identify articles detailing a definition or method of persistency measurement based on automated pharmacy data. Articles were screened for relevance by title and abstract. References from identified articles were used to expand the search results. RESULTS: The concept behind medication persistency measurement is to capture the amount of time that an individual remains on chronic drug therapy. The methods to calculate medication persistency can be classified into 1 of 3 categories: (1) Persistency as a function of the medication possession ratio; (2) persistency as a function of medication availability at a fixed point in time; and (3) persistency as a function of the gaps between refills. CONCLUSIONS: The common goal of all persistency measures should be to reflect the continuity of medication usage and to capture the timeliness and the frequency of refilling. The measurement of persistency as a function of the gaps between refills provides the best assessment of refill compliance across a variety of medication and disease states and lends itself to the well-established measurements of survival analysis.

Drug Prescriptions↗
PubMedDate not supplied

The role of persistent anticardiolipin antibody as risk factor of ischemic stroke.

AIM: To determine the role of persistent ACA and hyperviscosity as risk factor of ischemic stroke. METHODS: A study was conducted on 76 subjects whose age 40 to 70 years. Subjects consisted of 38 patients of post ischemic stroke and 38 controls with diagnosis other than stroke. Fresh blood samples were taken and mixed with EDTA for viscosity examination and serum for ACA IgM and IgG examination. The laboratory examination for persistent ACA IgM and IgG used ELISA method, while viscosity analysis was using viscometer. Statistic analysis used chi-square and multivariate analysis with logistic regression. RESULTS: In this study we found persistent ACA IgG in 25% of case group , and 2.63% in control group. Multivariate analysis showed persistent ACA IgG as risk factor for ischemic stroke with p < 0.05 and OR 14.11 (CI 95%:1.64;121.11). We found persistent ACA IgM in 2.78% of case group and 5.26% in control group. High blood viscosity was found in 15.79% case group and 10.53% in a control group. Statistical analysis showed no significant difference of viscosity (p = 0.740) and persistent ACA IgM (p = 1.000) between case and control group. CONCLUSION: study showed that persistent ACA IgG in stroke ischemic was higher than in control subjects. Blood viscosity examination and persistent ACA IgM did not show significant difference. While persistent ACA IgG with OR 14.11 (CI: 1.64; 121.11) was the risk factor for ischemic stroke. Blood viscosity and persistent ACA IgM were not risk factors for ischemic stroke.

Adult↗
PubMed1989

Descriptive epidemiology of persistent diarrhoea among young children in rural northern India.

In order to determine the descriptive epidemiology of persistent diarrhoea in rural northern India, a cohort of 963 children aged 0-71 months was followed prospectively for 12 months through weekly household visits. The incidence of persistent diarrhoea was 6.3 per 100 child-years among those aged 0-71 months, and was highest (31 per 100 child-years) among those aged 0-11 months. There were no significant sex-related differences in the incidence of the disease, and the overall seasonal distribution of acute and persistent diarrhoea was similar. The persistence of diarrhoeal symptoms was significantly correlated with a higher initial mean stool frequency (P less than 0.01) and passage of gross blood with stools (P less than 0.001). Persistent diarrhoea was an important problem among children during the first 2 years of life. Established enteric pathogens were isolated during the initial illness in 46.4% of persistent and 55.4% of acute episodes. Pathogens isolated during persistent episodes included enterotoxigenic Escherichia coli (ETEC 9.3%), Salmonella spp. (4.7%), as well as campylobacter (4.7%), Shigella spp. (2.3%), Entamoeba histolytica (2.3%), and rotavirus (2.3%). Similar proportions of these pathogens were isolated also during episodes of acute diarrhoea. Multiple pathogens were isolated in 7% of the persistent and 5% of the acute episodes. E. coli that manifested aggregative adherence (EAEC-A) was more common (34.9% versus 12.3%) in persistent than acute episodes (P less than 0.01), and initial faecal excretion of EAEC-A was significantly associated with the persistence of a diarrhoeal episode.

Child↗
PubMed1996

Assessment of myocardial viability in persistent defects on thallium-201 SPECT after reinjection using gradient-echo MRI.

This prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (+/-SD) was 11.5 +/- 2.7 mm and 5.8 +/- 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 +/- 3.4 mm and 3.7 +/- 3.1 mm in 31 with reversible lesions, 11.3 +/- 2.8 mm and 3.3 +/- 1.9 mm in 10 with mild persistent defects, 9.2 +/- 2.9 mm and 3.2 +/- 2.2 mm in 15 with moderate persistent defects, 5.8 +/- 1.7 mm and 1.3 +/- 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p < 0.0005) and systolic wall thickening (p < 0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.

Adult↗
PubMedDate not supplied

[Increased intestinal permeability to 51 Cr-EDTA among children with persistent diarrhea].

Persistent diarrhea, a condition highly prevalent in developing countries, causes different morphological and functional alterations of the mucosa of the small intestine, including increased permeability to different test molecules. In the present study we investigate for the first time the intestinal permeability to 51Cr-EDTA of Brazilian children with persistent diarrhea. The test of 51Cr-EDTA absorption was performed in 13 control children and in 14 children with persistent diarrhea by offering 50 microCi of the test substance by the oral route, with later detection of radioactivity excreted in 24-hour urine. There was a statistically significant difference between the control group (median = 1.26; range = 0.20-3.31%) and the group with persistent diarrhea (median = 4.68; range = 1.40-10.29%). Using the minimum and maximum values detected in the control group as the normal reference standard for the test of urinary 51Cr-EDTA absorption, we observed that 61.5% of the patients with persistent diarrhea showed altered results. Among the patients with persistent diarrhea, 51Cr-EDTA excretion was significantly higher in the group fed a protein hydrolysate diet and/or total parenteral nutrition than in the group that did not receive this diet. In four patients with persistent diarrhea, the test was performed after clinical recovery, with a fall in the excretion levels in all cases. On the basis of these data, we may conclude that: 1) in persistent diarrhea there must be alteration of intestinal permeability that might permit an increased entry of local alimentary antigens, with subsequent sensitization and allergic enteropathy, contributing to the perpetuation of the diarrhea, malabsorption and malnutrition cycle; 2) the 51Cr-EDTA test may be useful as an indicator of severity in persistent diarrhea; 3) alteration of intestinal permeability is a secondary phenomenon in persistent diarrhea, with normalization occurring after reconstruction of the intestinal barrier.

Absorption↗
PubMed1994

Persistent and recurrent neovascularization after laser photocoagulation for subfoveal choroidal neovascularization of age-related macular degeneration. Macular Photocoagulation Study Group.

OBJECTIVE: To determine the incidence and visual impact of and risk factors for persistent and recurrent neovascularization after laser photocoagulation of subfoveal choroidal neovascularization (CNV) in patients with age-related macular degeneration. DESIGN, PATIENTS, AND METHODS: The records of 189 eyes in the Subfoveal New CNV Study and 100 eyes in the Subfoveal Recurrent CNV Study assigned to laser photocoagulation were examined. Persistent CNV (detected within 6 weeks of treatment) and recurrent CNV (detected after 6 weeks) were defined angiographically by fluorescein leakage from the periphery of the treatment scar. Incidence was estimated using survival analysis methods. RESULTS: In both studies, persistent CNV was observed in approximately 13% of the eyes, and recurrent CNV was estimated to have developed by 3 years in an additional 35% of the eyes. In the New CNV Study, by 3 years, 36% of the eyes with persistent CNV had lost 6 or more lines of visual acuity as had 19% of the eyes with recurrent CNV and 27% of the eyes without persistence or recurrence. The presence of neovascular maculopathy in the fellow eye was associated with an increased risk for persistence or recurrence in the study eye. In the New CNV Study, partial coverage of the lesion with heavy laser treatment and/or runoff was associated with increased risk for persistence; less extensive natural scarring of the lesion at study entry was associated with increased risk for recurrence. CONCLUSIONS: Close to half of the eyes treated for subfoveal CNV have persistent or recurrent CNV within 3 years. There is a strong association between neovascular maculopathy in the fellow eye and the inability of laser photocoagulation to permanently obliterate signs of CNV from the study eye. Within these two studies, there was little additional damage to visual function resulting from persistent or recurrent neovascularization. There appears to be no reason to deviate from the protocol goal of covering the entire neovascular complex when treating eyes with subfoveal CNV.

Aged↗
PubMed1991

Characterization of the induction of persistent I-A expression by macrophages from Bcgr mice.

Peritoneal macrophages from mice that are resistant to Mycobacterium bovis (strain BCG) [Gros et al., J. Immunol. 127,2417, 1981] can be induced to express persistently or transiently major histocompatibility complex (MHC) class II glycoproteins. The induction of persistent expression is dependent on the dose of recombinant interferon-gamma (rIFN-gamma). High doses of rIFN-gamma (100 U) induce persistent Ia expression, whereas lower doses induce only transient Ia expression. Once induced, the persistent expression of Ia does not require its continued synthesis. We show that the expression of Ia by macrophages that transiently express MHC class II glycoproteins is reduced by the addition of cycloheximide or monensin, whereas Ia expression by macrophages that persistently express Ia is not affected. The differential sensitivity of Ia expression to cycloheximide was used to study the induction of persistence that is linked to the Bcg gene. Macrophages were primed with low doses of rIFN-gamma in order to induce transient, cycloheximide-sensitive Ia expression. The cells were then treated with high doses of rIFN-gamma in order to induce persistent, cycloheximide-resistant Ia expression. We found that the induction of persistent Ia expression requires at least 3 hr of exposure to rIFN-gamma. Furthermore, the addition of rIFN-gamma to primed macrophages is followed by a short burst of protein synthesis that is independent of the production of new mRNA. The rapidity with which persistent Ia expression is induced is consistent with the rapid onset of innate resistance to Mycobacterium following injection of BCG.

Animals↗
PubMed1993

Persistent infection with human parainfluenza virus 3 in CV-1 cells: analysis of the role of defective interfering particles.

Persistent infection of cultured cells with human parainfluenza virus type 3 (HPF3), established following infection at high multiplicity, has been associated with the presence of one or more viral defective-interfering (DI) particles in addition to standard viral genomes. We recently showed that persistent infection can also be established after low multiplicity infection, a condition not generally associated with amplification of DI particles. The association of DI particle genomes with persistent infection was therefore studied after infection with low multiplicity. Persistently infected cell cultures were established after low multiplicity infection with HPF3 in the presence of exogenous bacterial neuraminidase, and viral nucleocapsid RNA was analyzed for the presence of DI genomes at each passage after infection. In addition, the timing of DI particle appearance was assessed after infection with high multiplicity, a condition known to favor the amplification of DI particles. DI particles genomes did not appear until at least seven passages of persistently infected cell cultures, after either low or high multiplicity infection. Our data suggest that DI particles are not required for establishment of persistent infection of CV-1 cells by HPF3 and that DI particles are not generated early in infection. Despite reports of the association of paramyxovirus DI particles with persistent infection in culture, the role of these particles in HPF3 persistence is unknown; our findings offer insight into the complex interplay of viral and host factors in persistent infection.

Blotting, Northern↗
PubMed2003

Mechanism of reduction of virus release and cell-cell fusion in persistent canine distemper virus infection.

Canine distemper virus (CDV), a mobillivirus related to measles virus causes a chronic progressive demyelinating disease, associated with persistence of the virus in the central nervous system (CNS). CNS persistence of morbilliviruses has been associated with cell-to-cell spread, thereby limiting immune detection. The mechanism of cell-to-cell spread remains uncertain. In the present study we studied viral spread comparing a cytolytic (non-persistent) and a persistent CDV strain in cell cultures. Cytolytic CDV spread in a compact concentric manner with extensive cell fusion and destruction of the monolayer. Persistent CDV exhibited a heterogeneous cell-to-cell pattern of spread without cell fusion and 100-fold reduction of infectious viral titers in supernatants as compared to the cytolytic strain. Ultrastructurally, low infectious titers correlated with limited budding of persistent CDV as compared to the cytolytic strain, which shed large numbers of viral particles. The pattern of heterogeneous cell-to-cell viral spread can be explained by low production of infectious viral particles in only few areas of the cell membrane. In this way persistent CDV only spreads to a small proportion of the cells surrounding an infected one. Our studies suggest that both cell-to-cell spread and limited production of infectious virus are related to reduced expression of fusogenic complexes in the cell membrane. Such complexes consist of a synergistic configuration of the attachment (H) and fusion (F) proteins on the cell surface. F und H proteins exhibited a marked degree of colocalization in cytolytic CDV infection but not in persistent CDV as seen by confocal laser microscopy. In addition, analysis of CDV F protein expression using vaccinia constructs of both strains revealed an additional large fraction of uncleaved fusion protein in the persistent strain. This suggests that the paucity of active fusion complexes is due to restricted intracellular processing of the viral fusion protein.

Animals↗
PubMed1985

The persistent defect on exercise thallium imaging and its fate after myocardial revascularization: does it represent scar or ischemia?

Persistent defects on serial thallium scans are commonly thought to represent fibrosis or scar. However, such a pattern may also represent severe ischemia. To better understand persistent defects, exercise thallium and resting gated blood pool scans were reviewed in 52 patients pre and post coronary angioplasty for single-vessel left anterior descending (LAD) coronary artery disease, and the fate of persistent defects after successful revascularization was determined. Persistent and transient defects were defined from the average scores of three observers. Ten patients with 16 myocardial segments with persistent defects were compared to another 11 patients with 20 myocardial segments with transient defects. After angioplasty (PTCA), 75% of the regions that had persistent defects and 85% of the regions that had transient defects were normal by visual assessment. In the persistent defect group, only regional wall motion on the resting gated blood pool scan pre PTCA helped to distinguish those segments that would or would not revert to normal. We conclude that regions of persistent defect on thallium scan often revert to normal after PTCA (75%), suggesting that persistent defects may represent hypoperfusion of viable myocardium, and should not preclude consideration of an intervention.

Adult↗
PubMed1984

Persistent infection with influenza A virus: evolution of virus mutants.

A persistent infection (persistent infection I) of baby hamster kidney (BHK) cells with the WSN (H1N1) strain of influenza A virus was established using a virus stock which contained a high proportion of defective-interfering (DI) particles. Virus recovered from passage 92 (388 days) of persistent infection I was used to establish a second persistent infection (persistent infection II) in BHK cells. A number of phenotypic changes were identified in the virus isolated during the first 50 passages of persistent infection I (early pi virus). These included a decrease in the size of plaques, the appearance of temperature-sensitive mutants, and a decreased ability of amplified pi virus to agglutinate chicken erythrocytes. The decreased ability to cause hemagglutination was associated with a 20- to 30-fold increase in viral neuraminidase activity. Virus isolated after passage 63 of persistent infection I could not be amplified in eggs or in a number of cell lines. Although very little infectious virus was produced when cells were infected with these late pi viruses, cytopathology frequently occurred and an unusual pattern of viral protein synthesis was observed. The NP protein was the predominant protein synthesized, while the synthesis of M protein was drastically reduced relative to its synthesis in cells infected with parental WSN virus. The HA, NS1, and NS2 proteins were not detected; however, a virus-specific protein which migrates faster than NS2 was observed. Virus recovered from persistent infection II interfered with the replication of parental WSN virus in a mixed infection. The pattern of protein synthesis in such mixed infections resembled that in cells singly infected with late pi virus. DI particles did not appear to play a significant role either in the maintenance of the persistent infection, in the expression of the pi protein synthesis phenotype, or in the pi virus-mediated interference.

Animals↗
PubMed1992

Visual persistence of figures defined by relative motion.

In order to measure visual persistence of figures that were solely defined by relative motion (motion-defined figures or motion figures), random-dot kinematograms were used to form stimulus figures in the two-frame, missing element task introduced by Di Lollo, V. (1977 Nature, 257, 241-243). Experiment 1 showed that motion-defined figures persisted for about 130 msec after the termination of the stimulus presentation (i.e. after the dots stopped moving). This was similar to but several tens of milliseconds longer than the visual persistence of figures which were defined by a luminance difference (luminance-defined figures or luminance figures) in the same random-dot pattern. Since motion detectors are not found in the retina or lateral geniculate in primates, our results strongly suggest that visual persistence is not only a retinal phenomenon but also a cortical one. Experiment 2 investigated the possible influence of motion aftereffects on the visual persistence of motion figures. The results showed that coherent movement of the dots over the whole display after the stimulus offset did not reduce the visual persistence of motion figures, suggesting that the source of this persistence is not a motion aftereffect. In Experiment 3, visual persistence for the motion-defined figures was shown to be longer than that for luminance-defined figures independently of the contrast of the stimulus figure as long as the stimuli could be seen clearly enough. This suggests that different mechanisms are involved in the visual persistence of motion-defined and luminance-defined figures.

Afterimage↗
PubMed1991

The major site of murine K papovavirus persistence and reactivation is the renal tubular epithelium.

K virus, a murine papovavirus, produces a lethal pneumonia in newborn mice. Animals surviving acute illness develop a persistent infection which reactivates under conditions of immunosuppression. The present study was conducted to identify the cell populations which support persistent K virus infection and to determine the cell populations in which this persistent infection is reactivated during immunosuppression. Mice inoculated by the oral route with 100 50% newborn mouse lethal doses (LD50) of K virus at 14 days of age were followed over a period of 7 months. The distribution of infection was studied by virus assay, immunohistochemistry, and in situ nucleic acid hybridization methods. Viral replication during the acute phase of infection was confined to pulmonary and systemic vascular endothelial cells, as well as to scattered, apparently lymphoid cells within spleens. Beginning 2 months after inoculation, however, specific hybridization for K virus nucleic acids was detected in rare renal tubular epithelial cells, and by 6 months after inoculation renal tubular epithelial cells represented the major site of viral persistence. Positive cells were frequently present in groups of two or more, and a minority of positive cells also expressed viral capsid (V) antigen. Immunosuppression with cyclophosphamide resulted in reactivation of infection, with highest titers of virus being detected in kidneys and with increased numbers of renal tubular epithelial cells expressing viral capsid antigen. Capsid antigen was also detected in rare endothelial cells in kidneys, livers and lungs of these immunosuppressed mice. Although K virus behaves as an endotheliotrope during acute infection, the major site of K virus persistence and reactivation, the renal tubular epithelial cell, is similar to that involved during persistent infection by polyoma virus in mice, SV40 virus in monkeys, and BK and JC viruses in man. The observation that persistently infected renal tubular epithelial cells occur in groups of two or more and occasionally express capsid antigen suggests that virus may persist as a productive infection which is confined by antiviral antibody but maintains itself by cell-to-cell-spread. The present study represents the first instance in which the cell populations which support infection by a member of the polyomavirus subgroup in its natural host have been defined during acute, persistent, and reactivated infection.

Animals↗
PubMed2007

Persistent atrial fibrillation is associated with appropriate shocks and heart failure in patients with left ventricular dysfunction treated with an implantable cardioverter defibrillator.

AIM: The objective of this study was to investigate whether persistent atrial fibrillation (AF) and new-onset AF are associated with appropriate shocks, cardiovascular mortality, chronic heart failure (CHF), and inappropriate shocks in implantable cardioverter defibrillator (ICD) patients with left ventricular dysfunction. METHODS: We included 290 consecutive ICD patients with a documented left ventricular ejection fraction < or = 0.35 and compared outcomes between patients without AF (n = 207), those with persistent AF (n = 64), and those with new-onset AF (n = 19). RESULTS: The patients with persistent AF were older, more frequently had valve disease and cardiac surgery, and less frequently had coronary artery disease as compared with the patients without AF. Patients with persistent AF had a higher New York Heart Association class, however, left ventricular ejection fraction rates between these 2 groups were comparable (0.28 +/- 0.07 vs 0.29 +/- 0.08, P = not significant). No difference was found between patients with new-onset AF and those without AF. During follow-up (2.6 +/- 1.9 years), more patients with persistent AF received appropriate ICD shocks as compared with those without AF (24 [38%] vs 49 [24%], P = .04). Deterioration of CHF occurred more often in patients with persistent AF (19 [30%], P = .001) and those with new-onset AF (9 [47%], P < .001) as compared with patients without AF (31 [14%]). Multivariate analysis revealed that patients with persistent AF had an increased risk for appropriate ICD shocks (adjusted hazard ratio [HR] 1.9, 95% CI 1.2-3.2, P = .009). Persistent AF (adjusted HR 2.1, 95% CI 1.1-3.9, P = .03) and new-onset AF (adjusted HR 2.5, 95% CI 1.1-5.7, P = .02) were found to be independent risk indicators of CHF deterioration. CONCLUSIONS: In ICD patients with left ventricular dysfunction, persistent AF is associated with appropriate ICD shocks and deterioration of CHF. New-onset AF is related to deterioration of CHF.

Aged↗