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Results for “Virus Replication”

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At least 1,477 records · Page 82Linked to original sources
PubMed1983

Genetic mapping of a mouse chromosomal locus required for mink cell focus-forming virus replication.

Mouse-hamster somatic cell hybrids were used to show that the recombinant mink cell focus-forming murine leukemia viruses and their ecotropic virus progenitors require different mouse chromosomes for replication. Mouse chromosome 1 was shown to carry the genetic information necessary for the replication of six different mink cell focus-forming isolates, and this gene, designated Rmc-1, was tentatively positioned at the distal end of the chromosome.

Animals↗
PubMedDate not supplied

Inhibition of influenza A virus replication by a kanamycin derivative.

We studied the antiviral activity and the mechanism of action of a new antiviral agent and kanamycin derivative, 1-N-eicosanoyl-3"-N-trifluoroacetyl kanamycin A (ETKA), against influenza A virus. From yield reduction assays with VERO cells, ETKA showed a significant antiviral activity with negligible cytotoxic effect. In the presence of 20 micrograms/ml of ETKA at which VERO cell growth was not inhibited, virus titer was suppressed to 11.2% of control, and at 100 micrograms/ml virus production was suppressed to more than 99%. ETKA markedly inhibited viral protein synthesis when cells were pretreated with the drug before infection, but there was no inhibition when the drug was added 15 min post-infection. ETKA did not inhibit virus adsorption and penetration. Nor did it affect the activity of viral RNA polymerase in vitro. We found that the drug had a direct inactivating effect on influenza A virus under acidic conditions. These results suggest that ETKA exerts its antiviral action mainly in the early stage, prior to uncoating by direct inactivation of the virus due to the acidic environment of the endocytic vesicle. Aerosol treatment with the drug protected mice against a lethal influenza A virus infection.

Animals↗
PubMed1984

Epstein-Barr virus replication in oropharyngeal epithelial cells.

Despite the well-established tropism of the Epstein-Barr virus (EBV) for human B lymphocytes, the cell type within the oropharynx capable of allowing EBV replication has never been conclusively identified. Using in situ cytohybridization, we demonstrated EBV DNA in oropharyngeal epithelial cells from 10 of 12 patients with infectious mononucleosis. In duplicates of specimens found to contain cell-associated EBV DNA, we detected EBV RNA in two of four samples, using a biotin-labeled EBV DNA probe, thereby confirming the intracellular location of the viral genome. In 20 of 28 throat washings analyzed, cytohybridization results and assays for cell-free infectious virus were in agreement. In seven of the eight remaining specimens, cytohybridization identified intracellular EBV DNA in the absence of detectable extracellular virus. We conclude that the oropharyngeal epithelial cell may be the target cell type that is productively infected in infectious mononucleosis.

Cell Line↗
PubMed1984

Cells from newborn rat brain established in primary tissue culture will support rubella virus replication.

We have initiated an in vitro study comparing the susceptibility of newborn and adult animals to rubella virus (RV) associated encephalitis. Glial cells from injured adult rat brain (RG cells) have been established in continuous culture and these cells were reported to restrict RV replication. When RG cells were infected, no infectious progeny virus particles were detected in tissue culture media and only five intracellular viral polypeptides could be detected using immune precipitation techniques (p75, p60, VP44, VP41, and VP19). Two polypeptides normally associated with a productive infection. VP24 and p30, could not be detected. In this report we have applied these techniques to an investigation of RV replication in newborn brain cells and have shown that relatively normal yields of all seven polypeptides found in RV-infected cells could be detected. These data indicate that some glia from newborn brain in primary culture are permissive for RV replication unlike the restricting RG cells and that this difference in restriction is critical in determining the outcome of their infection by RV.

Animals↗
PubMed1979

Site of Epstein-Barr virus replication in the oropharynx.

Cells and cell-free material in saliva, parotid secretions, and throat washings from patients with acute infectious mononucleosis and patients undergoing tonsillectomy were assayed for the presence of infectious Epstein-Barr (EBV) virus. The agent was invariably present in cell-free form in saliva; neither infectious virus nor viral antigens were found in the cells. Tonsillar lymphocytes from eight patients were also free of EBV. In 10 of 40 patients virus was recovered in secretions from parotid-gland orifices or ducts. These findings suggest that the salivary glands are the site of EBV production in the oropharynx.

Acute Disease↗
PubMed1983

Safety evaluation of nuclear polyhedrosis virus replication in pigs.

To evaluate the hygienic risk involved in using baculoviruses for insect pest control, safety studies are required. Pigs were chosen as representative test animals of commercial and agricultural importance. The tests were aimed at detecting virus propagation, immune reactions, and signs of acute infection (changes in body temperature and hematology profile, swelling of lymph nodes). Four of five animals inoculated with nuclear polyhedrosis virus showed a slight temperature rise at day 2 postinfection. After day 4 postinfection, no differences between infected animals and controls were observed. In the bioassay, virus activity could be recovered from fecal samples; however, no activity was found in organ extracts. The data did not indicate hygienic risks involved in the application of nuclear polyhedrosis virus, especially that from Mamestra brassicae, in biological pest control.

Animals↗
PubMed2006

Possible association of vigorous hepatitis B virus replication with the development of fulminant hepatitis.

A 49 year-old man was referred to our hospital for fear of developing fulminant hepatic failure. There had been an outbreak of fulminant hepatitis B in a dialysis clinic in the western part of Honshu, Japan, that resulted in four deaths among six patients. After the sixth patient contracted severe hepatitis, all patients in the unit were screened biweekly for hepatitis B surface antigen (HBsAg) to detect newly infected patients as soon as possible. Our patient was the seventh victim, and on the day he gave a positive result for HBsAg, his hepatitis B virus (HBV) DNA level had reached 1.1 x 10(11) copies/ml as assessed by real time polymerase chain reaction. Sequence analysis of the causal HBV revealed the presence of a mutation in the precore region (nt 1896), two mutations in the core promoter (nt 1762 and nt 1764), and some minor mutations in the P gene that were restricted to the upstream region. These mutations are indicative of a virus with a high replicative rate that cannot secrete HBeAg. Taken together, these findings indicate that it is very likely that the replicative ability of the causal virus was as vigorous as that of HBV in hepatitis B e antigen-positive asymptomatic carriers with markedly high viral titers. The present case report provides clinical evidence of a possible association between the rapid spread of highly replicative HBV before host immunological recognition and the development of fulminant hepatitis.

DNA, Viral↗