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Articles by Jose Luna-Munoz
Total Records ( 4 ) for Jose Luna-Munoz
  Viviana Falcon , Nelson Acosta-Rivero , Mineko Shibayama , Jose Luna-Munoz , Magdalena Miranda- Sanchez , Jorge Gavilondo , Maria-C de la Rosa , Ivón Menéndez , Bienvenido Gra , Waldo Garcia , Santiago Duenas-Carrera , Jose Silva , Glay Chinea , Maritza Gonzalez Bravo , Felix Alvarez , Juan Morales , Juan Kouri and Victor Tsutsumi
  Analysis of Hepatitis C Virus (HCV)-infected hepatocytes at the cellular level may contribute to elucidate the mechanisms of HCV pathogenesis. In this work, the presence of HCV components and pathological reactions in apoptotic hepatocytes from chronic HCV-infected patients were studied by electron microscopy and confocal microscopy. Eight samples of liver biopsies from patients with chronic hepatitis C were studied by laser scanning confocal microscopy, Transmission Electron Microscopy (TEM) and Immunoelectron Microscopy (IEM). Data provide evidence for apoptosis of hepatocytes from HCV-infected liver biopsies during chronic HCV infection. Confirmation of this process was based on the morphological data by TEM including cell shrinkage; chromatin condensation; formation of apoptotic bodies; phagocytosis by neighbouring cells; and the presence of DNA fragmentation by TUNEL assay and caspase 3 activation. Interestingly, Hepatitis C core protein (HCcAg) was specifically immunolabeled in the rough endoplasmic reticulum, mitochondria as well as in the nucleus of apoptotic hepatocytes. In addition, E1 was specifically immunostained in the cytoplasm and in the mitochondria of some hepatocytes. The presence of Crystalloid Bodies (CB) similar to those observed in recombinant P. pastoris expressing HCcAg was observed in the cytoplasm of some hepatocytes. Immunogold labelling showed that HCcAg co-localized with these CB. In addition, structures forming a paracristalline array and particles with a diameter of 50 nm appeared in the mitochondria of some apoptotic hepatocytes. Moreover, unstructured large aggregates containing HCcAg similar to those detected at late stages of HCcAg expression in recombinant P. pastoris cells were frequently observed in damaged hepatocytes. Of note, these aggregates were specifically immunostained with anti-HCcAg. Data suggest the possibility for a direct role of these HCV-related structures as well as HCcAg and E1 in apoptosis and pathogenicity.
  Viviana Falcon , Nelson Acosta-Rivero , Nelson Acosta-Rivero , Jose Luna-Munoz , Magdalena Miranda-Sanchez , Maria-C de la Rosa , Ivon Menendez , Bienvenido Gra , Santiago Duenas-Carrera , Waldo Garcia , Eduardo Vilar , Jose Silva , Deliana Lopez , Maritza Gonzalez-Bravo , Celia Fernandez-Ortega , Dionne Casillas , Juan Morales , Juan Kouri and Victor Tsutsumi
  In this study, we examined the expression of hepatitis C virus (HCV) components in hepatocytes and peripheral blood mononuclear cells (PBMC) from patients positive for anti-HCV antibodies and negative for serum HCV-RNA. The samples obtained from 25 randomly selected patients (13 of 25 patients showed no histological evidences of chronic hepatitis and had normal serum ALAT and GGTP levels) were studied by in situ Hybridization and Immunofluorescence assays. The findings show that HCV-RNA of both positive and negative polarity was carried in the hepatocytes of more than 80% of cases. The proportion of cells expressing the negative strand (mean ± SD, 10.25% ± 5.56%) was lower than those expressing positive strand (mean ± SD, 19.88% ± 9.19%) (p=0.0076; Student’s t test). In addition, reaction products suggestive of HCV core, E1 and E2 antigens within hepatocytes were also observed. Both hybridization and immunofluorescence signals were localized in the cytoplasm suggesting that this is the place of active HCV replication. On the other hand, the HCVRNA of positive polarity was detected in PBMC from 16 out of 17 samples analyzed (94%) while the HCV-RNA of negative polarity was detected in 82% of samples investigated. Positive hybridization signals were localized in the cytoplasm of PBMC. Interestingly, 12 out of 13 patients with clinical and histological resolution of hepatitis, contain HCV-RNA in either liver or PBMC. These results provide further evidences that the intermediate replicative form of the HCV genome can persist in hepatocytes and PBMC after apparently complete resolution of chronic hepatitis C.
  Viviana Falcon , Nelson Acosta-Rivero , Mineko Shibayama , Jose Luna-Munoz , Magdalena Miranda-Sanchez , Maria-C de la Rosa , Ivon Menendez , Waldo Garcia , Bienvenido Gra , Santiago Duenas-Carrera , Deliana Lopez , Maritza Gonzalez Bravo , Celia Fernandez-Ortega , Dionne Casillas , Juan Morales , Juan Kouri and Victor Tsutsumi
  Understanding the mechanism of Hepatitis C Virus (HCV) pathogenesis is an important part of HCV research. In this study, the presence of apoptosis in HCV-infected liver and Peripheral Blood Mononuclear Cells (PBMC) from patients positive for anti-HCV antibodies and negative for serum HCV-RNA was investigated. The samples obtained from 21 patients were studied by in situ Hybridization (ISH), Immunofluorescence, TUNEL reaction and caspase 3 activation assays. The findings show that both DNA fragmentation by TUNEL assay and activation of caspase 3 were detected in hepatocytes from patients histologically confirmed as bearing chronic hepatitis or with abnormal ALAT or GGTP as well as in patients with no histological evidences of chronic hepatitis and normalization of transaminases. Apoptotic cells were also detected in PBMC samples by the TUNEL assay. ISH analysis of liver biopsies and PBMC samples showed both positive and negative strands of the HCV genome localized in some cells showing nuclear characteristics of apoptosis such as chromatin margination, condensation and fragmentation. These typical morphological changes of apoptotic cell death were also observed in some hepatocytes showing reaction products suggestive of HCcAg. Data suggest that under certain conditions HCV induces apoptosis in the absence of liver injury. Induction of apoptosis in HCV-infected cells may interfere with viral replication, which may lead to undetectable levels of HCV-RNA in serum.
  Janneth Peralta-Ramirez , J. Manuel Hernandez , Rebeca Manning-Cela , Jose Luna-Munoz , Carlos Garcia-Tovar , Jean- Philippe Nougayrede , Eric Oswald and Fernando Navarro-Garcia
  Many pathogenic bacteria subvert normal host cell processes by delivering effector proteins which mimic eukaryotic functions directly into target cells. EspF is a multifunctional protein injected into host cells by attaching and effacing pathogens, but its mechanism of action is not understood completely. In silico analyses of EspF revealed two key motifs: proline-rich domains and PDZ domain binding motifs. Such functional domains may allow EspF to act as an actin nucleation-promoting factor by mimicking host proteins. In agreement with these predictions, we found that EspF from rabbit enteropathogenic Escherichia coli (E22) participates in the regulation of actin polymerization by binding to a complex of proteins at the tight junctions (TJ). EspF bound to actin and profilin throughout the course of infection. However, after 2 h of infection, EspF also bound to the neural Wiskott-Aldrich syndrome protein and to the Arp2/3, zonula occludens-1 (ZO-1), and ZO-2 proteins. Moreover, EspF caused occludin, claudin, ZO-1, and ZO-2 redistribution and loss of transepithelial electrical resistance, suggesting that actin sequestration by EspF may cause local actin depolymerization leading to EspF-induced TJ disruption. Furthermore, EspF caused recruitment of these TJ proteins into the pedestals. An E22 strain lacking EspF did not cause TJ disruption and pedestals were smaller than those induced by the wild-type strain. Additionally, the pedestals were located mainly in the TJ. The overexpression of EspF caused bigger pedestals located along the length of the cells. Thus, actin sequestration by EspF allows the recruitment of junctional proteins into the pedestals, leading to the maturation of actin pedestals and the disruption of paracellular permeability.
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