Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human embryonic lung (HEL) cells infected with human cytomegalovirus (HCMV) restricted the replication of herpes simplex virus type 1 (HSV-1). A delay in HSV replication of 15 h as well as a consistent, almost 3 log inhibition of HSV replication in HCMV-infected cell cultures harvested 24 to 72 h after superinfection were observed compared with controls infected with HSV alone. Treatment of HCMV-infected HEL cells with cycloheximide (100 micrograms/ml) for 3 or 24 h, conditions known to result in accumulation of HCMV immediate-early and early mRNA, was demonstrated effective in blocking HCMV protein synthesis, as shown by immunoprecipitation with HCMV antibody-positive polyvalent serum. Cycloheximide treatment of HCMV-infected HEL cells and removal of the cycloheximide block before superinfection inhibited HSV-1 replication more efficiently than non-drug-treated superinfected controls. HCMV DNA-negative temperature-sensitive mutants restricted HSV as efficiently as wild-type HCMV suggesting that immediate-early and/or early events which occur before viral DNA synthesis are sufficient for inhibition of HSV. Inhibition of HSV-1 in HCMV-infected HEL cells was unaffected by elevated temperature (40.5 degrees C). However, prior UV irradiation of HCMV removed the block to HSV replication, demonstrating the requirement for an active HCMV genome. HSV-2 replication was similarly inhibited in HCMV-infected HEL cells. However, replication of adenovirus, another DNA virus, was not restricted in these cells under the same conditions. Superinfection of HCMV-infected HEL cells with HSV-1 labeled with [3H]thymidine provided evidence that the labeled virus could penetrate to the nucleus of cells after superinfection. Evidence for penetration of superinfecting HSV into HCMV-infected cells was also provided by blot hybridization of HSV DNA synthesized in cells infected with HSV alone versus superinfected cell cultures at 0 and 48 h after superinfection. In addition, superinfection with vesicular stomatitis virus ruled out a role for interferon in restriction of HSV replication in this system.
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PMID:A human cytomegalovirus function inhibits replication of herpes simplex virus. 282 46

Vero cells were infected with the ts-045 strain of vesicular stomatitis virus, and the cells were incubated at 39 degrees C to accumulate the mutant G glycoprotein in the ER as a misfolded aggregate. Cycloheximide was added to the culture medium 3.5 h after infection to prevent further protein synthesis, and the temperature was lowered to 10, 15, or 31 degrees C. At these temperatures, the mutant G glycoprotein correctly folds and oligomerizes. Immunofluorescence light microscopy showed that the G glycoprotein was exported to the Golgi complex at 31 degrees C and to the intermediate compartment (IC) at 15 degrees C, but no export was observed at 10 degrees C. However, incubations at 10 degrees C followed by shift to 15 or 31 degrees C resulted in the normal transfer of the glycoprotein to the IC and the Golgi, respectively. Immunoelectron microscopical analysis confirmed all these results, but showed also that the glycoprotein was frequently clustered in the ER at 10 degrees C. Conventional electron microscopy showed that the morphology of the ER, IC, and Golgi complex remained essentially unchanged at all temperatures. The only significant difference detectable in cells incubated at 10 degrees C was the increased number of partially coated ER protrusions, longer than those detected at higher temperatures. These results demonstrate that the transport toward the Golgi complex of G glycoprotein can be arrested at a step preceding the entry into the IC, thus suggesting that ER and IC are separate stations in the exocytic pathway.
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PMID:Morphological analysis of the transfer of VSV ts-045 G glycoprotein from the endoplasmic reticulum to the intermediate compartment in vero cells. 883 70