Hepatitis C virus core protein up-regulates anergy-related genes and a new set of genes, which affects T cell homeostasis.

Hepatitis C virus (HCV) infection is the main cause for chronic hepatitis, leading to cirrhosis and hepatic carcinoma. Virally induced immune dysfunction has been called as the cause for viral persistence. Previous results demonstrate that CD4 Jurkat cells stably expressing the HCV core protein show an increased activation of NFAT transcription factor and an impaired IL-2 promoter activity, affecting intracellular signaling pathways in a manner that mimics clonal anergy. We had shown previously that NFAT activates a transcriptional program, ensuing in immunological tolerance. In the present work, we have engineered lentiviral vectors expressing the HCV core to analyze the events, which unfold in the initial phase of HCV core-induced anergy. We show that genes initially described to be up-regulated by ionomycin-induced anergy in mice are also up-regulated in humans, not only by ionomycin but also by HCV core expression. We also show that HCV core is sufficient to cause NFAT nuclear translocation and a slow-down in cell-cycle progression, and using whole genome microarrays, we identify novel genes up-regulated in Jurkat cells expressing HCV core. The relevance of our results is highlighted by the presence of HCV in CD4 T cells from HCV chronically infected patients.

Lidocaína endovenosa como coadyuvante en el tratamiento inicial de la neuralgia postherpética. Bases fisiopatológicas del uso de anestésicos locales en el tratamiento del dolor neuropático / Endovenous lidocaine as co-adjuvant in the initial treatment of post-herpetic neuralgia. Physiopathological basis of the use of local anesthetics for the treatment of neuropathic pain

Introducción:La neuralgia postherpética es el cuadro álgico que permanecetras desaparecer las vesículas del episodio agudodel herpes zóster, habiendo pasado un periodo mínimo detiempo de 8-12 semanas. Hasta un 50% de los pacientescon edad superior a 70 años, lo desarrollará tras el episodio agudo de herpes zóster. Sus bases fisiopatológicas nohan sido aclaradas, por lo que su prevención es difícil y sutratamiento sintomático.Material y métodos:Se estudiaron 100 pacientes incluidos de forma aleatoriaen uno de los grupos diseñados (n = 25): grupo A1, pacientesmenores de 70 años, tratados con gabapentina adosis crecientes; grupo A2, pacientes mayores de 70 años,tratados con gabapentina a dosis crecientes; grupo B1, pacientesmenores de 70 años tratados con gabapentina y lidocaínaendovenosa; grupo B2, pacientes mayores de 70años tratados con gabapentina y lidocaína endovenosa. Seevaluó el dolor referido por el paciente en cuatro momentosa lo largo de las cuatro primeras semanas.Resultados:Se observaron diferencias estadísticamente significativas,p < 0,05, en las medias de EVA referido por los pacientes,presentando una EVA menor los grupos tratadoscon lidocaína endovenosa y pacientes menores de 70 añosen ambos grupos.Conclusiones:El tratamiento de la neuralgia postherpética es un tratamientosintomático. Los anestésicos locales han sido utilizadoscon éxito en algunos tipos de dolor neuropático. Lalidocaína endovenosa puede ser útil como coadyuvante enel periodo inicial del tratamiento de la neuralgia posthetpética,al reducir significativamente la EVA referida por lospacientes. Los pacientes de edad avanzada respondieronpeor al uso de lidocaína, aunque presentaron medias deEVA inferiores a los pacientes a los que no se administró lidocaína

Introduction:Post-herpetic neuralgia is the algic condition that remainswhen the vesicles of an acute episode of herpeszoster have disappeared after a minimum period of 8-12weeks. Up to 50% of patients older than 70 years will developthis condition after an acute episode of herpes zoster.Its physiopathological basis is still unclear, so its preventionis difficult and its treatment is aimed to symptoms.Materials and methods:One hundred patients were randomized to one of thestudy groups (n = 25): group A1, patients 70 years of age treated with gabapentin and endovenouslidocaine; group B2, patients > 70 years of agetreated with gabapentin and endovenous lidocaine. Painreported by the patient was assessed at four time pointsduring the first four weeks.Results:Statistically significant differences were observed (p <0,05) in the mean VAS scores reported by the patients,with a lower VAS score within the groups treated with endovenouslidocaine and in patients < 70 years of age inboth groups.Conclusions:The treatment of post-herpetic neuralgia is aimed tosymptoms. Local anesthetics have been successfully usedfor some types of neuropathic pain. Endovenous lidocainecan be useful as co-adjuvant during the initial treatment ofpost-herpetic neuralgia, since it significantly reduces theVAS score reported by patients. Aged patients had a poorerresponse to the use of lidocaine, as well as lower meanVAS scores, compared to patients that did not received lidocaine

Mujer de 65 años con ensanchamiento mediastínico / A 65-year-old woman with mediastinal enlargement

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[Determination of insulin, leptin and neuropeptide y by radioimmunoanalysis in patients with morbid obesity and anorexia nervosa after therapeutic intervention]. / Determinación por radioinmunoanálisis de insulina, leptina y neuropéptido Y en pacientes con obesidad mórbida y anorexia nerviosa después de intervención terapéutica.

The present study was conducted in order to analyze the relationship existing between leptin, insulin and neuropeptide Y (NPY) levels in massive weight loss and weight recovery. Twenty-three patients with severe obesity, 23 patients with anorexia nervosa and 28 healthy control subjects were studied. Patients with severe obesity underwent a vertical banded gastroplasty followed by an 800 kcal/day diet during 16 weeks, with evaluation taking place before (Body mass index, BMI, 52,1 8 Kg/m2) and after the drastic weight loss (BMI 39,2 6,2 Kg/m2). Patients with anorexia nervosa were treated with nutritional therapy exclusively during 16 weeks, and they were evaluated in the low weight situation (BMI 15,3 1,7 Kg/m2) and after weight recovery (BMI 18,9 2,8 Kg/m2). Normal subjects had a normal BMI from 20 to 27 (average 21,8 2 Kg/m2). BMI, percentage of body fat, and serum levels of leptin, insulin, and NPY, were determined in each patient and normal subjects. In severe obese patients serum leptin and insulin decreased significantly after drastic weight reduction (leptin: from 48,8 19,2 to 24,3 9,8 ng/ml; insulin: from 26,2 10,8 to 18 6 U/ml). In patients with anorexia nervosa serum leptin mean levels were significantly higher after weight recovery (3,7 1,9 vs 9,2 5,1 ng/ml). In subjects with morbid obesity NPY levels decreased after weight loss below those of control group (43,5 16,1 vs 57,3 12,8 pmol/l). On the other hand, patients with anorexia nervosa had NPY levels superior to those of control group. In subjects with anorexia, NPY levels decreased after weight recovery (69,1 16,7 a 59,1 20,3 pmol/l). In the whole population, Leptin and NPY plasma levels were correlated with body fat percentage. Leptin was positively correlated with BMI and body fat percentage in obese and anorectic subjects after weight loss or recovery, respectively. NPY was inversely correlated with body fat percentage in controls and obese subjects before treatment. These data reveal that the concentration of serum leptin and NPY correlates significantly with the total adiposity in subjects with a wide weight range and caloric intake. Leptin plasma levels are proportional to fat stores in patients with severe obesity and anorexia nervosa after drastic weight loss or recovery, respectively. NPY serum levels are negatively correlated with de total body fat in normal weight subjects and obese patients in their initial weight.

Enteropathogenic Escherichia coli virulence factor bundle-forming pilus has a binding specificity for phosphatidylethanolamine.

The bundle-forming pilus (BFP) of enteropathogenic Escherichia coli (EPEC), an established virulence factor encoded on the EPEC adherence factor (EAF) plasmid, has been implicated in the formation of bacterial autoaggregates and in the localized adherence of EPEC to cultured epithelial cells. While understanding of the pathogenic mechanism of this organism is rapidly improving, a receptor ligand for BFP has not yet been identified. We now report, using both solid-phase and liposome binding assays, that BFP expression correlates with phosphatidylethanolamine (PE) binding. In a thin-layer chromatogram overlay assay, specific recognition of PE was documented for BFP-expressing strains, including E2348/69, a wild-type EPEC clinical isolate, as well as a laboratory strain, HB101, transformed with a bfp-carrying plasmid. Strains which did not express BFP did not bind PE, including a bfpA disruptional mutant of E2348/69, EAF plasmid-cured E2348/69, and HB101. E2348/69 also aggregated PE-containing liposomes but not phosphatidylcholine- or phosphatidylserine-containing liposomes, while BFP-negative strains did not produce aggregates with any tested liposomes. Purified BFP preparations bound commercial PE standards as well as a PE-containing band within lipid extracts from human epithelial cells and from E2348/69. Our results therefore indicate a specific interaction between BFP and PE and suggest that PE may serve as a BFP receptor for bacterial autoaggregation and may promote localized adherence to host cells, both of which contribute to bacterial pathogenesis.

Quorum sensing is a global regulatory mechanism in enterohemorrhagic Escherichia coli O157:H7.

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is responsible for outbreaks of bloody diarrhea and hemolytic-uremic syndrome in many countries. EHEC virulence mechanisms include the production of Shiga toxins (Stx) and formation of attaching and effacing (AE) lesions on intestinal epithelial cells. We recently reported that genes involved in the formation of the AE lesion were regulated by quorum sensing through autoinducer-2, which is synthesized by the product of the luxS gene. In this study we hybridized an E. coli gene array with cDNA synthesized from RNA that was extracted from EHEC strain 86-24 and its isogenic luxS mutant. We observed that 404 genes were regulated by luxS at least fivefold, which comprises approximately 10% of the array genes; 235 of these genes were up-regulated and 169 were down-regulated in the wild-type strain compared to in the luxS mutant. Down-regulated genes included several involved in cell division, as well as ribosomal and tRNA genes. Consistent with this pattern of gene expression, the luxS mutant grows faster than the wild-type strain (generation times of 37.5 and 60 min, respectively, in Dulbecco modified Eagle medium). Up-regulated genes included several involved in the expression and assembly of flagella, motility, and chemotaxis. Using operon::lacZ fusions to class I, II, and III flagellar genes, we were able to confirm this transcriptional regulation. We also observed fewer flagella by Western blotting and electron microscopy and decreased motility halos in semisolid agar in the luxS mutant. The average swimming speeds for the wild-type strain and the luxS mutant are 12.5 and 6.6 microm/s, respectively. We also observed an increase in the production of Stx due to quorum sensing. Genes encoding Stx, which are transcribed along with lambda-like phage genes, are induced by an SOS response, and genes involved in the SOS response were also regulated by quorum sensing. These results indicate that quorum sensing is a global regulatory mechanism for basic physiological functions of E. coli as well as for virulence factors.

Community-acquired bacterial pneumonia in human immunodeficiency virus-infected patients: validation of severity criteria. The Grupo Andaluz para el Estudio de las Enfermedades Infecciosas.

Severity criteria for community-acquired pneumonia (CAP) have always excluded patients with human immunodeficiency virus (HIV) infection. A 1-yr, multicenter, prospective observational study of HIV-infected patients with bacterial CAP was done to validate the criteria used in the American Thoracic Society (ATS) guidelines for CAP, and to determine the prognosis-associated factors in the HIV-infected population with bacterial CAP. Overall, 355 cases were included, with an attributable mortality of 9.3%. Patients who met the ATS criteria had a longer hospital stay (p = 0.01), longer duration of fever (p < 0.001), and higher attributable mortality (13.1% versus 3.5%, p = 0.02) than those who did not. Three factors were independently related to mortality: CD4(+) cell count < 100/microl, radiologic progression of disease, and shock. Pleural effusion, cavities, and/or multilobar infiltrates at admission were independently associated with radiologic progression. A prognostic rule based on the five criteria of shock, CD4(+) cell count < 100/microl, pleural effusion, cavities, and multilobar infiltrates had a high negative predictive value for mortality (97.1%). The attributable mortality for severe pneumonia was 11.3%, as compared with 1.3% for nonsevere disease (p = 0.008). The ATS severity criteria are valid in HIV-infected patients with bacterial CAP. Our study provides the basis for identification of patients who may require hospitalization determined by clinical judgment and the five clinical criteria of shock, a CD4(+) cell count < 100/microl, pleural effusion, cavities, and multilobar involvement. These prognostic factors should be validated in independent cohort studies.

[Plasma levels of insulin and leptin in patients with morbid obesity and anorexia nervosa after weight loss or gain, respectively]. / Niveles plasmáticos de insulina y leptina en pacientes con obesidad mórbida y anorexia nerviosa después de pérdida o ganancia de peso, respectivamente.

The present study was conducted in order to analyze the relationship existing between leptin and insulin levels in massive weight loss and weight recovery. Thirteen patients with severe obesity, 14 patients with anorexia nervosa and 13 healthy control subjects were studied. The patients with severe obesity underwent a vertical banded gastroplasty followed by an 800 kcal/day diet for 12 weeks. They were evaluated prior to (body mass index [BMI] 51.2 +/- 8.8 Kg/m2) and after drastic weight loss (BMI 40.6 +/- 6.7 Kg/m2). Patients with anorexia nervosa were treated exclusively with nutritional therapy during 12 weeks, and they were evaluated at their lowest weight status (BMI 16.2 +/- 2.2 Kg/m2) and after weight recovery (BMI 17.9 +/- 2.3 Kg/m2). The BMI of the normal subjects was in the normal range of 20 to 27 Kg/m2 (average 22.8 +/- 2.6 Kg/m2). BMI, percentage of body fat, waist circumference, and serum levels of leptin, insulin, and C-peptide were determined in each patient and normal subject. In severely obese patients, serum leptin and insulin decreased significantly after drastic weight reduction (leptin: from 51.8 +/- 22.3 to 23.7 +/- 10.2 ng/ml; insulin: from 27.1 +/- 13.3 to 17.2 +/- 7.2 mU/ml). In patients with anorexia nervosa, the mean serum leptin levels were significantly higher after weight recovery (5.5 +/- 3.2 vs 7.6 +/- 6 ng/ml). Serum leptin in the severe obesity group correlated positively with BMI, percentage body fat and waist circumference before and after weight loss. In those patients suffering from anorexia nervosa, serum leptin correlated positively with the BMI, percentage of body fat, and waist circumference in the low weight state and after weight recovery. In addition, their serum insulin correlated with BMI and waist circumference after weight recovery. These data reveal that serum leptin concentration correlates significantly with the BMI and body fat content 1) in subjects with a range of weight and caloric intake, 2) in obese patients after drastic weight loss; 3) in anorexic patients after weight gain; and that hyper- or normoinsulinemia do not seem to have any influence on the leptin changes caused by weight loss or gain.

The locus of enterocyte effacement (LEE)-encoded regulator controls expression of both LEE- and non-LEE-encoded virulence factors in enteropathogenic and enterohemorrhagic Escherichia coli.

Regulation of virulence gene expression in enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) is incompletely understood. In EPEC, the plasmid-encoded regulator Per is required for maximal expression of proteins encoded on the locus of enterocyte effacement (LEE), and a LEE-encoded regulator (Ler) is part of the Per-mediated regulatory cascade upregulating the LEE2, LEE3, and LEE4 promoters. We now report that Ler is essential for the expression of multiple LEE-located genes in both EPEC and EHEC, including those encoding the type III secretion pathway, the secreted Esp proteins, Tir, and intimin. Ler is therefore central to the process of attaching and effacing (AE) lesion formation. Ler also regulates the expression of LEE-located genes not required for AE-lesion formation, including rorf2, orf10, rorf10, orf19, and espF, indicating that Ler regulates additional virulence properties. In addition, Ler regulates the expression of proteins encoded outside the LEE that are not essential for AE lesion formation, including TagA in EHEC and EspC in EPEC. delta ler mutants of both EPEC and EHEC show altered adherence to epithelial cells and express novel fimbriae. Ler is therefore a global regulator of virulence gene expression in EPEC and EHEC.

Recognition of enteropathogenic Escherichia coli virulence determinants by human colostrum and serum antibodies.

Human colostra and sera collected from Mexican mothers and their children at birth and 6 months thereafter were studied for the presence of antibodies against the bundle-forming pilus and several chromosomal virulence gene products (intimin and secreted proteins EspA and EspB) of enteropathogenic Escherichia coli (EPEC). Among 21 colostrum samples studied, 76, 71.5, 57, and 47% of them contained immunoglobulin A (IgA) antibodies against EspA, intimin, EspB, and BfpA, respectively. Interestingly, there was a difference in IgG response to EPEC antigens between the sera from neonates and sera from the same children 6 months later. While the number of neonates reacting to Esps and intimin diminished when they reached 6 months of age, those reacting with BfpA increased from 9 to 71%. Intimin from an enterohemorrhagic E. coli strain was also recognized by most of the samples reacting with EPEC intimin. These data suggest that Bfp and Esps elicit an antibody response during the early days of life of neonates and support the value of breast-feeding in areas of the world where bacterial diarrheal infections are endemic.

Human antibody response to longus type IV pilus and study of its prevalence among enterotoxigenic Escherichia coli in Bangladesh by using monoclonal antibodies.

Mouse monoclonal antibodies (MAbs) were derived against longus (CS20), a type IV pilus expressed by human enterotoxigenic Escherichia coli (ETEC). One MAb (ICA39) detected longus in 56 (8.5%) of 662 ETEC isolates obtained from a routine surveillance of diarrheal stools from children and adults. Five patients with diarrhea from whom longus-positive ETEC were isolated were also recruited. Of these 61 isolates, 50 were positive for other colonization factors (CFs; 61% for CFA/II and 21% for CFA/I), and 11 were negative for any of the other 8 CFs that were tested. They were either positive for the heat-stable enterotoxin (ST; n=29) or for the heat-labile enterotoxin (LT) and ST (n=32). All longus-positive ETEC were confirmed by polymerase chain reaction to harbor lngA, the longus structural pilin gene. Sera and/or fecal extracts from the patients reacted with the 22-kDa pilin polypeptide in immunoblots and ELISA. These studies show that longus is prevalent among ETEC in Bangladesh and that longus gives rise to IgA antibody responses in patients.

Clinical parameters (body mass index and age) are the best predictors for the need of insulin therapy during the first 18 months of diabetes mellitus in young adult patients.

To address the question whether there are simple clinical predictors of need for insulin in the first 18 months of treatment of diabetes presenting in young adult subjects, a prospective study of 24 patients with diabetes mellitus (age: 18-40 years) was designed. At diagnosis of diabetes, age, sex, body mass index (BMI), glycemia, ketonuria, C-peptide, insulin autoantibodies, islet cell antibodies and glutamic acid decarboxylase antibodies were recorded before starting any treatment. At the end of the follow-up (18 +/- 4 months), they were divided into two groups according to their need for insulin therapy: group 1 (n=15; 62%), who needed insulin therapy, and group 2 (n=9; 38%), who did not. Each marker was related to actual need for therapy necessity. Multivariate analysis showed that BMI and age were the variables with greatest predictive value regarding need for insulin. These data reveal that the need for insulin therapy in young adult diabetic patients may be supported by the clinical criteria of age and BMI, which are both easily and quickly determined.

Opiáceos orales de liberación retardada: tramadol versus dihidrocodeína en dolor tumoral crónico por cáncer de próstata / Extended-release oral opiates: tramadol versus dihydrocodeine in chronic tumor pain associated to prostate cancer

Objetivos: Comparar la eficacia y tolerancia de tramadol y dihidrocodeína, ambos en comprimidos de liberación retardada (LR), en pacientes con dolor crónico, no neurológico, por cáncer de próstata con invasión extracapsular y metástasis óseas .Material y métodos: Ensayo clínico a triple ciego y cruzado, en fase IV. Se dividen aleatoriamente 32 pacientes con cáncer de próstata y metástasis óseas, tratados previamente con antiinflamatorios no esteroideos (escalón I de la OMS) o en asociación con codeína (escalón II de la OMS), en dos grupos de 16. En el grupo 1 se administra tramadol LR 100 mg cada 12 horas los 14 primeros días y dihidrocodeína LR 90 mg cada 12 horas los siguientes 14 días. En el grupo 2: viceversa. Si el dolor no se controla con estas dosis se duplica la dosis de opiáceo. Fármacos coadyuvantes: naproxeno 500 mg cada 12 horas y amitriptilina 25 mg al acostarse. Profilaxis de náuseas y vómitos con 5 gotas de haloperidol (0,1 mg/gota) cada 8 horas, durante los 4 primeros días de la toma de cada uno de los opiáceos. Prevención de estreñimiento con lactulosa. Control cada 7 d ías, con un total de 5 consultas, la segunda y la cuarta f u e ron telefónicas, cambiando de opiáceo en la tercera consulta. Se evalúa el dolor según escalas: verbal simple, verbal numérica, frecuencia del dolor, incapacidad por dolor y calidad del sueño. Asimismo se interroga sobre el tipo de vida del paciente y su grado de satisfacción con cada tratamiento. La calidad de la terapia analgésica se valora en relación al conjunto de las escalas citadas. Se recogen los efectos secundarios. Se excluyen los pacientes que durante el desarrollo del estudio requieren pasar a escalón III de la OMS, siendo ocupado su lugar por otro paciente. El análisis estadístico se realizó con el programa SPSS, considerando significativa una p<0,05.Resultados: Ambos analgésicos redujeron la intensidad del dolor, según escala numérica, a menos de 3 desde cifras medias iniciales de 7,09, con resultados favorables a tramadol LR.Lo mismo ocurrió con la calidad de la terapia analgésica.Presentaron náuseas y vómitos 21,6 por ciento, somnolencia: 28,1 por ciento, ambos sin diferencias significativas. El estreñimiento fue significativamente mayor con dihidrocodeína LR (56,3 por ciento), frente al 25 por ciento con tramadol LR. Dos pacientes en el grupo 1 y tres en el grupo 2 necesitaron duplicar la dosis tras la primera semana. Abandonaron el estudio 4 pacientes que precisaron del escalón III de la OMS.Conclusiones: Tramadol LR y dihidrocodeína LR fueron eficaces en el control del dolor tumoral crónico por cáncer de próstata con metástasis óseas en escalón II de la OMS. Los resultados sobre control del dolor fueron ligeramente mejores con tramadol LR. La incidencia de efectos secundarios fue menor con tramadol LR, especialmente en estreñimiento (AU)

Identification of enterotoxigenic Escherichia coli harboring longus type IV pilus gene by DNA amplification.

DNA amplification of lngA, the structural gene of longus type IV pilus produced by human enterotoxigenic Escherichia coli (ETEC) was achieved by the use of specific oligonucleotide primers designed from the nucleotide sequence of lngA. A 630-bp fragment representing the entire lngA gene was amplified in eight prototype strains previously characterized as longus positive. Five ETEC strains producing colonization factor antigen III (CFA III) (also a type IV pilus) were also positive by PCR, confirming the DNA homology between CFA III and longus. None of the non-ETEC and non-E. coli enteropathogens studied showed the 0.63-kbp amplicon. The procedure thus detected only ETEC strains harboring type IV pili genes with or without other colonization factors. Except for five lngA PCR-positive, probe-positive strains, all lngA PCR-positive strains produced the pilin as demonstrated by immunoblotting. To test the amplification procedure in a clinical setting, a collection of 264 fresh clinical E. coli strains isolated from 88 Mexican children with diarrhea was screened by PCR. Among 82 ETEC isolates found, 30 (36.5%) were lngA PCR-positive. Twenty-seven percent of the children shed ETEC that possessed lngA. In parallel with DNA probes or PCR protocols to detect enterotoxin genes, the lngA PCR method may prove useful for detection of ETEC harboring type IV pilus genes in epidemiological studies.

Haemophilus influenzae pneumonia in human immunodeficiency virus-infected patients. The Grupo Andaluz para el Estudio de las Enfermedades Infecciosas.

Although Haemophilus influenzae is a common etiologic agent of pneumonia in patients infected with human immunodeficiency virus (HIV), the characteristics of this pneumonia have not been adequately assessed. We have prospectively studied features of H. influenzae pneumonia in 26 consecutive HIV-infected inpatients. Most of these patients were severely immunosuppressed; 73.1% had a CD4+ cell count <100/microL. A subacute clinical presentation was observed in 27% of the patients and was associated with a higher degree of immunosuppression (P=.04). Bilateral lung infiltrates were noted radiographically in 57.7% of the cases. The mortality attributable to H. influenzae pneumonia was 11.5%. Thus, pneumonia caused by H. influenzae affects mainly patients with advanced HIV disease, and since its clinical and radiological features may be diverse, this etiology should be considered when pneumonia occurs in patients with advanced HIV infection. The mortality rate associated with H. influenzae pneumonia is not higher than that occurring in the general population.

Relationship of hepatitis C viremia to HIV state and to infection by specific hepatitis C genotypes.

AIMS/BACKGROUND: This study was undertaken to examine the relationship of hepatitis C (HCV) viremia to human immunodeficiency virus (HIV) infection and to investigate the evidence of infection by specific hepatitis C genotypes. PATIENTS AND METHODS: The analysis of HCV viremia was performed by reverse transcription-polymerase chain reaction in serum samples from 186 patients' selected by their positivity for anti-HCV antibodies. All samples were tested for HIV infection. In those patients with sera positivity for HCV RNA, isolates were genotyped by line probe assay. In those patients whose sera were negative for HCV RNA, antibodies specific for genotypes implicated in past HCV infection were detected by ELISA. RESULTS: HCV RNA was detected in 117 patients with anti-HCV antibodies (62.9%). There was no statistically significant association between HCV RNA and HIV positivity (Odds ratio, O.R.: 1.75, Confidence interval 95%, C.I.: 0.92-3.33, p = 0.095). A positive association was demonstrated between infection by HCV genotype 3 and HCV viremia (O.R.: 10.67, C.I.: 1.51-458.05, p = 0.015) in HIV-infected patients, as well as between infection by HCV genotype 1 and HCV viremia (O.R.: 4.71, C.I.: 1.65-13.75, p = 0.002) in HIV-non infected individuals. In both groups, a negative association was observed between past HCV infection by multiple genotypes and HCV viremia (HIV-infected patients, O.R.: 0.10, C.I.: 0.00-1.11, p = 0.033. HIV-non infected patients, O.R.: 0.05, C.I.: 0.00-0.41, p = 0.001). CONCLUSIONS: Infection by specific HCV genotypes (type 3 in HIV-infected patients and by type 1 in HIV-non infected ones) implies a higher risk of HCV viremia, whereas multiple HCV types infection is negatively associated with this probability. HIV coinfection does not influence the probability of HCV viremia.

Modulation of hepatic and intestinal glutathione S-transferases and other antioxidant enzymes by dietary lipids in streptozotocin diabetic rats.

Antioxidant enzymes in liver and small intestine were investigated using control and streptozotocin diabetic rats fed diets with 5% olive, sunflower or fish oil for five weeks. In liver, Glutathione Peroxidase and Superoxide Dismutase decreased and in intestine Glutathione-S-transferase (GST) increased by diabetes. In isolated jejunum and ileum, this increase in GST activity was due to an increase in GST-alpha and -mu isoenzymes in jejunum and GST-alpha, mu and -pi in ileum. Since GST plays an important role in protecting tissues from oxidative damage, our results highlight the role of the intestine against free radicals in physiological or pathological situations.

Virulence properties of atypical EPEC strains.

Virulence properties of 31 atypical enteropathogenic Escherichia coli (EPEC) strains isolated from cases of diarrhoea were examined. All except two strains adhered to HEp-2 cells in a localised adherence-like (LAL) pattern. With the exception of two strains, all were fluorescent actin staining (FAS) positive. Gentamicin HEp-2 invasion assay studies showed that all strains were invasive. Transmission electron microscopy of infected HEp-2 cells showed the characteristic attaching and effacing lesion and invasion of the cultured cells. Of the nine strains that hybridised with a DNA probe for alpha-haemolysin, five were haemolytic within 3 h of incubation, while the remaining strains were haemolytic only after incubation for 24 h. Three strains produced enterohaemolysin on blood agar. None of the 31 strains of E. coli induced fluid accumulation in the rabbit intestinal loop assay or displayed cytotoxic effects in HeLa and Vero cells. All the strains belonging to serotypes O26:H11, O26:H- and 0119:H2 expressed intimin beta, whereas all the strains from serotype O55:H7 expressed intimin gamma. The strains belonging to serogroup O111 expressed a non-typable intimin. The participation of intimin in LAL was supported by adhesion inhibition experiments in which antibodies to intimin significantly reduced the level of LAL.