Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The open reading frame potentially encoding a 78 amino acid, 9101 Da hydrophobic protein (HP) and, mapping at the 3' end of the porcine transmissible gastroenteritis coronavirus (TGEV) genome, was shown to be expressed during virus replication. The cloned HP gene was placed in a plasmid under control of the T7 RNA polymerase promoter and in vitro translation of transcripts generated in vitro yielded a 9.1-kDa protein that was immunoprecipitable with porcine hyperimmune anti-TGEV serum. Antiserum raised in rabbits against a 31 amino acid synthetic polypeptide that represented the central hydrophilic region of HP specifically immunoprecipitated HP from TGEV-infected cells. HP was further shown to become associated with microsomal membranes during synthesis in vitro and was found to be closely associated with the endoplasmic reticulum and cell surface membranes in infected cells. The intracellular location of HP suggests that it may play a role in the membrane association of replication complexes or in virion assembly.
 ...
PMID:The 9-kDa hydrophobic protein encoded at the 3' end of the porcine transmissible gastroenteritis coronavirus genome is membrane-associated. 131 Jan 91

The Spike (S) protein from a virulent British field isolate of porcine transmissible gastroenteritis virus (TGEV) FS772/70 was constructed from cDNA and inserted into the vaccinia virus (VV) thymidine kinase gene locus under the control of the VV early/late gene P7.5k promoter. Recombinant S protein was synthesized as an endo-beta-N-acetylglucosaminidase H (Endo H)-sensitive glycoprotein with high mannose simple oligosaccharides (gp 190) that underwent post-translational modification to an Endo H-resistant glycoprotein with complex oligosaccharides (gp210). Immunofluorescence analysis demonstrated that the majority of recombinant S protein was retained at the Golgi but some S protein was expressed on the plasma membrane. Monoclonal antibodies (mAbs) raised against native S protein reacted with this recombinant S protein; also, mice infected with the recombinant vaccinia virus (rVV) expressing the S protein induced TGEV neutralizing antibodies. A truncated S protein (S delta) was also expressed in rVV-infected cells by introducing a deletion into the S protein cDNA that removed 292 amino acids from the C-terminus. The S delta protein (gp 170) was shown to be antigenically similar to TGEV S protein by immunofluorescence and immunoprecipitation tests but was retained in the endoplasmic reticulum and not expressed on the cell surface.
 ...
PMID:Intracellular processing of the porcine coronavirus transmissible gastroenteritis virus spike protein expressed by recombinant vaccinia virus. 185 Sep 27

A case of prolonged diarrhoea following Escherichia coli 0111 gastroenteritis is reported. Electron microscopy of the jejunal biopsy revealed effacement of the brush border and attachment of bacteria by pedestal formation. Specific activities of brush border enzymes showed marked depression of disaccharidases, zinc-resistant alpha-glucosidase, and alkaline phosphatase. In contrast, marker enzymes for basolateral membranes and endoplasmic reticulum were unaffected. The biochemical changes support the pathogenic mechanism suggested by ultrastructural studies previously reported.
 ...
PMID:Ultrastructural and biochemical changes in human jejunal mucosa associated with enteropathogenic Escherichia coli (0111) infection. 351 Dec 12

Protracted diarrhea is a clinical entity characterized by diarrhea lasting greater than 2 weeks, starting before 3 months of age, with severe nutritional aggravation and negative stool culture for enteropathogens. This report deals with the ultrastructural abnormalities found in the intestinal mucosa of children with protracted diarrhea. Forty children (mean age 5.1 months) were studied. They were submitted to the following tests of intestinal function: D-xylose, triglyceride tolerance, small bowel biopsy (light and electron microscope), sigmoidoscopy, and sweat test. D-Xylose absorption and triglyceride tolerance test in these patients were both significantly lower than controls. Ultrastructural analysis of the small bowel of 12 patients showed various degrees of alterations, mainly shortening of the microvilli, increased number of multivesicular bodies, and vacuolation of mitochondria and endoplasmic reticulum. These lesions were totally reversible after clinical and nutritional recovery as could be proven in two children. The most common cause of protracted diarrhea in these patients was secondary carbohydrate intolerance and dietary protein cow's milk and soy bean intolerance, which resulted in colitis or malabsorption as a consequence of intestinal mucosa injury due to acute gastroenteritis.
 ...
PMID:Protracted diarrhea in infancy: clinical aspects and ultrastructural analysis of the small intestine. 404 29

An electron microscopic study of intestinal epithelial cells of neonatal piglets infected with transmissible gastroenteritis (TGE) virus revealed a unique parasite-host cell interaction. Entry of the TGE virus into intestinal epithelial cells of newborn piglets is mediated through a network of cytoplasmic tubules of plasmalemma origin. the tubules, called microcanaliculi, are morphologically distinct from endoplasmic reticulum and Golgi. In uninfected animals similar tubules appear to be responsible for the indiscriminate uptake of large quantities of macromolecules from colostrum during the first few days of life.Thin-section profiles of plasmalemma invaginations resembled tubules or canals and frequently contained viral particles. TGE viral particles developed and accumulated within cytoplasmic vacuoles. Initially the vacuoles were continuous with the microcanaliculi formed by deep plasmalemma invagination. Mature viral particles were 60 to 85 mu in diameter with an electron dense doughnut-shaped nucleoid surrounded by a trilaminar membrane which resembled the vacuolar wall. Abundant evidence of viral effects was observed in absorbtive epithelial cells of the jejunum and ileum but not of the duodenum. The ability of absorbtive intestinal epithelial cells to form deep cytoplasmic tubular invaginations is temporally related to the pathogenesis of TGE and may explain in part why pigs usually are fatally affected by TGE only during the neonatal period.
 ...
PMID:Electron microscopy of intestinal epithelial cells of piglets infected with a transmissible gastroenteritis virus. 426 98

Light and electron microscopy findings in the jejunal mucosa of the normal feeder pig and feeder pigs infected with transmissible gastroenteritis (TGE) virus are reported. Villi in the mid jejunum of the normal feeder pig were elongated, finger shaped and covered with a layer of columnar absorptive cells with a well developed and regular brush border. Severe lesions of villous atrophy were present in all jejunal segments of feeder swine killed 96 hours post infection with TGE virus. Atrophic villi were covered by flat to cuboidal cells with a poorly developed brush border in some areas. In other segments, cells varied in appearance from sub-columnar to columnar type of near normal appearance. The ultrastructure of the jejunal absorptive cells in the normal feeder pig was found to be similar to that described for the jejunal cells of other adult mammals. There were no significant indications of high pinocytotic activity. The epithelial cells covering the atrophic villi of TGE infected pigs had a fine structure similar to that described for the crypt cells, ranging in appearance from very immature to moderately differentiated cells. Microvilli were very short, decreased markedly in number and irregular in arrangement. The terminal web was poorly developed. Strands of rough endoplasmic reticulum were markedly diminished and an increase in free ribosomes was noted. The significance of these observations in explaining pathogenesis of TGE in feeder pigs is discussed.
 ...
PMID:Transmissible gastroenteritis in feeder pigs: observations on the jejunal epithelium of normal feeder pigs and feeder pigs infected with TGE virus. 427 43

We studied the ultrastructure of the jejunal epithelium of six children suffering from acute episodes of gastroenteritis. Ultrastructural alterations of the jejunal mucosa occurred in practically all of the fragments analyzed, although the intensity of the abnormalities observed varied considerably. In most of the patients the alterations were confined to the microvilli, which appeared shortened and tufted in comparison with controls. These ultrastructural alterations are nonspecific and may represent a general response of the intestinal mucosa against different noxious agents. Severe alteration of the epithelial cells was observed in only one patient. In this case the cytoplasm contained multiple vacuoles that may correspond to dilated endoplasmic reticulum. It is hypothesized that the small intestinal lesions observed in these patients may allow penetration of food antigens, resulting in the appearance of food intolerance frequently described in children suffering from acute diarrhea.
 ...
PMID:Ultrastructural study of alterations in the small intestinal epithelium of children with acute diarrhea. 648 62

The prevailing hypothesis is that the intracellular site of budding of coronaviruses is determined by the localization of its membrane protein M (previously called E1). We tested this by analyzing the site of budding of four different coronaviruses in relation to the intracellular localization of their M proteins. Mouse hepatitis virus (MHV) and infectious bronchitis virus (IBV) grown in Sac(-) cells, and feline infectious peritonitis virus (FIPV) and transmissible gastroenteritis virus (TGEV) grown in CrFK cells, all budded exclusively into smooth-walled, tubulovesicular membranes located intermediately between the rough endoplasmic reticulum and Golgi complex, identical to the so-called budding compartment previously identified for MHV. Indirect immunofluorescence staining of the infected cells showed that all four M proteins accumulated in a perinuclear region. Immunogold microscopy localized MHV M and IBV M in the budding compartment; in addition, a dense labeling in the Golgi complex occurred, MHV M predominantly in trans-Golgi cisternae and trans-Golgi reticulum and IBV M mainly in the cis and medial Golgi cisternae. The corresponding M proteins of the four viruses, when independently expressed in a recombinant vaccinia virus system, also accumulated in the perinuclear area. Quantitative pulse-chase analysis of metabolically labeled cells showed that in each case the majority of the M glycoproteins carried oligosaccharide side chains with Golgi-specific modifications within 4 h after synthesis. Immunoelectron microscopy localized recombinant MHV M and IBV M to the same membranes as the respective proteins in coronavirus-infected cells, with the same cis-trans distribution over the Golgi complex. Our results demonstrate that some of the M proteins of the four viruses are transported beyond the budding compartment and are differentially retained by intrinsic retention signals; in addition to M, other viral and/or cellular factors are probably required to determine the site of budding.
 ...
PMID:Coronavirus M proteins accumulate in the Golgi complex beyond the site of virion budding. 808 90

The porcine aminopeptidase-N (pAPN) is the cellular receptor for the transmissible gastroenteritis virus (TGEV) due to the specific binding of the spike protein S to APN. In the present study, we performed both biological and biochemical experiments to analyze how the level of expression of a virus receptor can influence the viral protein biosynthesis and the virus production. We generated two swine testis cell clones overexpressing pAPN (ST-APN clones). These clones produced 10(4) less infectious virus than control ST cells. Plaque assays revealed a four-fold reduction of the diameter of the plaques in ST-APN cells compared to ST cells. Pulse-chase experiments revealed that S transport from the endoplasmic reticulum to the Golgi apparatus was not affected in ST-APN cells. Additionally, an anti-APN antibody was able to increase the virus released in the supernatant of ST-APN cells. Likewise, BHK clones expressing variable amounts of pAPN were shown to acquire TGEV susceptibility and to produce infectious particles as an inverse function of their level of pAPN expression. In contrast, MDCK clones expressing low or large amounts of pAPN failed to produce infectious particles. Taken together, these studies strongly suggest that overexpression of receptor, but also other(s) undetermined factor(s), can impair the production of viral particles.
 ...
PMID:Overexpression of TGEV cell receptor impairs the production of virus particles. 883 May 12

Rotaviruses are nonenveloped viruses that infect enterocytes of the small intestine and cause severe infantile gastroenteritis. It was previously thought that rotavirus exits cells by lysis, but this behavior does not match the local pathogenesis of the virus. In this study, we have investigated the release of the simian rotavirus strain (RRV) from the polarized intestinal Caco-2 cells. We found that RRV is released almost exclusively from the apical pole of Caco-2 cells before any cells lyse. Using confocal laser scanning microscopy and drugs that inhibit vesicular transport, we studied the RRV transport route from the endoplasmic reticulum (ER) to the apical side of intestinal cells. We demonstrated that RRV exits from the ER through a carbonyl cyanide m-chlorophenylhydrazone-sensitive vesicular transport. RRV staining was never found within the Golgi apparatus or lysosomes, suggesting that the RRV intracellular pathway does not involve these organelles. This finding was confirmed by treatment with monensin or NH4Cl, which do not affect release of RRV. Electron microscopic analysis revealed RRV containing small smooth vesicles in the apical area and free virions outside the cell in the brush border, consistent with a vesicular vectorial transport of virus. These results may provide, for the first time, a cellular explanation of the pathogenesis of rotavirus.
 ...
PMID:Rotavirus is released from the apical surface of cultured human intestinal cells through nonconventional vesicular transport that bypasses the Golgi apparatus. 934 79


1 2 3 4 Next >>