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Biomedical subjects

C Y Kang

Publications and source records attributed to C Y Kang.

At least 91 records · Page 5Linked to original sources
PubMed1985

Frequent generation of new 3'-defective interfering particles of vesicular stomatitis virus.

We have isolated and partially characterized a number of different genome types of defective interfering (DI) particles newly generated by a highly heat-resistant strain of vesicular stomatitis virus in either Rat(B77) or Vero cells. Northern blot analyses revealed that many of these DI genomes contain N gene sequences and/or sequences of the NS, M, and G genes. One type contains NS sequences without any indication for the presence of either N, M, or G sequences. Another type of DI particle genomes did not contain any detectable sequences of N, NS, M, or G, but contain panhandle-type sequences and, thus, most likely resembles the 5'-panhandle-type DI particles. Unlike previously assumed, these data demonstrate that DI genomes which have the 3'-terminal N, NS, M, and G genes or portions of these genes conserved do frequently arise together with 5'-DI particle genomes after serial undiluted passages of the heat-resistant strain of vesicular stomatitis virus.

Animals↗
PubMed1985

Vesicular stomatitis virus-infected cells fuse when the intracellular pool of functional M protein is reduced in the presence of G protein.

Five highly cytolytic strains of both Indiana and New Jersey serotypes of vesicular stomatitis virus were shown to induce cell fusion in BHK-21 and R(B77) cells. Inhibition of protein synthesis after the eclipse period of viral replication is a prerequisite for vesicular stomatitis virus-induced cell fusion. Pulse-chase experiments showed that inhibition of protein synthesis would lead to a drastic reduction in the intracellular pool of M protein as compared with other proteins. A temperature-sensitive mutant defective in M protein function (G31) was the only mutant of the five complementation groups to spontaneously induce polykaryocytes at the nonpermissive temperature. Previously, G protein has been shown to play a role in vesicular stomatitis virus-induced cell fusion. These results suggest that the combination of the presence of G protein on the virus-infected cell surface and the absence of functional M protein or a reduced level of intracellular M protein promotes cell fusion. On the basis of this study, we propose that vesicular stomatitis virus infection can induce cell fusion when the functional M protein pool declines to a critical level while G protein remains on the cell surface.

Amino Acids↗
PubMed1985

Analysis of a TH1----TH2 helper cell circuit.

In the present study, the T15 idiotype-recognizing T helper cell circuit was dissected with respect to its homeostasis, interactive specificity, stability over time, and effects on B cell expression. Analysis of the TH1 cells by adoptive transfer experiments indicates their short-lived state of activity, during which TH2 cells are stimulated. TH1 cell activity was also directly monitored by the use of TNP-anti-T15 hybridoma antigens. It was found that TH1 cells are detected 1 wk after priming with PC-Hy, whereas TH2 cells become activated after 4 wk of priming. Comparative analysis of TH1 cells by using two different TNP-anti-T15 hybridoma antigens indicates a TH1 specificity for a shared idiotope. The stability over time of the TH1----TH2 circuit was demonstrated by comparing TH2 frequencies in young and old mice. Finally, we addressed the question of the function of the idiotype-recognizing T helper cells and showed that stimulation of T15-idiotype-specific TH2 cells can be correlated with a significant increase in the percentage of T15 idiotype in an anti-PC response. Collectively, these data describe an idiotype-specific T helper circuit as part of the network homeostasis of the immune system.

Age Factors↗
PubMed1984

Structural characterization of virion proteins and genomic RNA of human parainfluenza virus 3.

The virion proteins and genomic RNA of human parainfluenza virus 3 have been characterized. The virion contains seven major and two minor proteins. Three proteins of 195 X 10(3) molecular weight (195K), 87K, and 67K are associated with the nucleocapsid of the virion and have been designated L, P, and NP, respectively. Three proteins can be labeled with [14C]glucosamine and have molecular weights of 69K, 60K, and 46K. We have designated these proteins as HN, F0, and F1, respectively. HN protein has interchain disulfide bonds, but does not participate in disulfide bonding to form homomultimeric forms. F1 appears to be derived from a complex, F1,2, that has an electrophoretic mobility similar to that of F0 under nonreducing conditions. A protein of 35K is associated with the envelope components of the virion and aggregates under low-salt conditions; this protein has been designated M. The genome of human parainfluenza virus 3 is a linear RNA molecule with a molecular weight of approximately 4.6 X 10(6).

Capsid↗
PubMed1984

Positive serological evidence that Hantaan virus, the etiologic agent of hemorrhagic fever with renal syndrome, is endemic in Canada.

Hemorrhagic fever with renal syndrome is endemic in most parts of the world. The etiological agent in known as Hantaan virus. More than 2000 Canadian sera from all age groups and provinces were tested for the presence of antibody to this virus by the indirect immunofluorescent antibody technique. The frequency of seropositivity ranged from 0.3 to 4.0%, with the national average being 1.4%. Newfoundland and New Brunswick in the Atlantic region had the highest positivity, being higher than hyperendemic areas in Korea. The inland provinces of Ontario, Manitoba, and Alberta had only 0.5% positives to Hantaan virus. In contrast, approximately 1.5% of sera from Saskatchewan, Quebec, and British Columbia were positive. No correlation in positivity was found between geography or sex, but positivity did increase with age. The highest titres were found in the group aged 65 to 93 years.

Adult↗
PubMed1983

Reticuloendotheliosis virus-transformed cells contain infectious and noninfectious proviral sequences in different chromosomes.

The integration site of reticuloendotheliosis virus proviral DNA in the DNA from a cloned reticuloendotheliosis virus-transformed bone marrow cell line was studied. These reticuloendotheliosis virus-transformed bone marrow cells produce a replication-defective transforming virus (REV-T) and a nontransforming helper virus, designated reticuloendotheliosis-associated virus (REV-At). The DNA from this REV-T transformed bone marrow cell line was hybridized with 3H-labeled in vitro synthesized DNA complementary to the reticuloendotheliosis virus (RE) genome to show that these cells contain approximately five genome equivalents per haploid genome. These hybridization experiments did not distinguish between the transforming and nontransforming virus sequences in these cells. Metaphase chromosomes have been isolated from colcemid-treated bone marrow cells and separated into four different size classes on zonal gradients. Hybridization experiment with RE-specific cDNA indicated that all four size classes of chromosomes contain RE-specific sequences. To locate the infectious provirus DNA of the helper virus REV-At, transfection experiments were performed with DNA extracted from the chromosomes of each size class. Infectious REV-At provirus DNA was found principally in one size class. This size class contained the intermediate size macrochromosomes 5 through 11. These results suggest that REV-At proviral DNA must be integrated into a specific chromosome to produce infectious virus.

Animals↗
PubMed1982

Vesicular stomatitis virus can establish persistent infections in Syrian hamsters.

Persistent infections by vesicular stomatitis virus (VSV) of the Indiana serotype were readily established in adult Syrian hamsters following intraperitoneal injection of the virus. Plaque-forming virus, identified as VSV by serological and physical criteria, was isolated from brain homogenates of five hamsters that were tested 3 to 8 months after infection. Four of these animals had exhibited either transient or permanent paralysis, whereas the fifth appeared healthy, during the period of observation. At the time of sacrifice all hamsters had high titres of anti-VSV-neutralizing antibodies in their sera.

Animals↗
PubMed1982

Mediators of protection against lethal systemic vesicular stomatitis virus infection in hamsters: defective interfering particles, polyinosinate-polycytidylate, and interferon.

Homologous defective interfering (DI) particles protected adult Syrian hamsters against lethal systemic infection with vesicular stomatitis virus (VSV) serotype Indiana. The DI particles had to be biologically active, but did not have to be administered at the same inoculation site as the infectious virus. Serum and tissue levels of VSV postinoculation were significantly lower in DI-protected animals than in unprotected controls, suggesting that true autointerference was occurring. However, some aspects of protection also must be mediated through nonspecific mechanisms, since susceptible hamsters could be protected against VSV Indiana by coinjection with heterologous DI particles prepared from VSV serotype New Jersey or by simultaneous administration of polyinosinic acid-polycytidylic acid. By measuring serum levels of putative hamster interferon (type 1), we found that animals coinjected with VSV and DI particles or polyinosinic acid-polycytidylic acid produced significant levels of interferon. Since similarly high serum levels of interferon were measured in recipients of VSV alone (animals that eventually died from infection), there appeared to be no correlation between protection against lethal disease and induced levels of serum interferon. Instead, serum interferon levels correlated positively with amounts of VSV PFU found in serum and tissues of infected animals, the lowest levels being found in serum of animals protected with homologous DI particles. The data are consistent with the hypothesis that autointerference by DI particles as well as various host defense mechanisms (possibly including induction of interferon) participates in protecting hamsters against lethal VSV infection.

Animals↗
PubMed1981

Role of glycosylation in the H-2-restricted cytolysis of virus-infected cells.

The role of the oligosaccharide portions of cell surface glycoproteins in the susceptibility of virus-infected cells to H-2-restricted cytolysis was investigated by using the antibiotic tunicamycin (TM). TM inhibits the addition of sugars to the polypeptides of glycoproteins. TM treatment of P815 cells before and during infection with vesicular stomatitis virus (VSV) inhibited glycosylation of proteins and reduced by about 50% the lysis of infected P815 cells by VSV-immune, H-2-identical killer cells. In contrast, TM treatment had a modest inhibitory effect on cytolysis of P815 cells by alloimmune effector cells. TM treatment did not inhibit the surface expression of either H-2 or VSV glycoprotein. Thus, glycosylation of H-2 and/or viral glycoprotein is a prerequisite for the lysis of infected cells by H-2-identical, VSV-immune cytotoxic cells.

Animals↗
PubMed1981

Genetic analysis of resistance to lethal infections of vesicular stomatitis virus in Syrian hamsters.

Vesicular stomatitis virus (VSV), Indiana serotype, causes a lethal disease in adult Syrian hamsters. Susceptibility to low doses of VSV (10 to 100 plaque-forming units) was shown to be genetically determined by examining six inbred strains. Three strains, LSH, MHA, and CB, were found to be extremely susceptible, with more than 70% of the animals dying within 72 h after intraperitoneal injection. Two strains, MIT and UT2, were intermediately susceptible, with approximately 60% of VSV-infected animals surviving. One strain, UT1, was found to be highly resistant; however, resistance was not acquired until the 4th or 5th week of age, and 100% of VSV-infected neonatal hamsters died. Analyses of F1 hybrid and segregant backcross populations derived from the LSH and UT1 strains suggested that at least three independent genetic loci contribute to phenotypic resistance. One locus resides on the X chromosome; the others reside on autosomes. No obvious linkage to the hamster major histocompatibility complex was detected. F1 hybrids of two highly susceptible strains, CB and MHA, were more resistant than either parental strain, suggesting that alleles of unlinked genes in the susceptible strains interact to produce a partially resistant phenotype. These alleles probably are the cause of the resistance phenotype found in the random-bred LVG strain which shares a common heritage with the CB and MHA strains.

Animals↗
PubMed1981

Involvement of cells of hematopoietic origin in genetically determined resistance of Syrian hamsters to vesicular stomatitis virus.

Susceptibility of Syrian hamsters of the inbred LSH and MHA strains to injection of as few as 10 plaque-forming units of vesicular stomatitis virus (VSV) was shown to occur only after intraperitoneal and intrapleural injection and not after injection of VSV intravenously, intranasally, or in the footpads. Despite the fact that fewer LSH hamsters died when VSV was injected via the latter routes, the histopathology of the VSV-induced disease at early times after infection was identical irrespective of the route of virus administration. Histological examination of tissues at various times after administration of VSV by the various routes revealed that VSV exhibited tropism for lymphoreticular tissue, with the greatest amount of necrosis in the splenic periarteriolar lymphoid sheath. A similar pattern also was observed in VSV-infected tissues from genetically resistant UT1 hamsters. Infectivity titrations of various tissues at different times after intraperitoneal injection of VSV revealed that resistant UT1 hamsters began to clear virus from tissues between 40 and 48 h postinfection, whereas virus titers remained high in susceptible animals. Resistance of UT1 hamsters appeared to require an intact spleen since survival of splenectomized animals was less than that of sham-splenectomized UT1 controls. Sublethal whole-body irradiation was also able to reduce resistance of UT1 hamsters (survival was reduced from 100 to 50%). Bone marrow cells from resistant (UT1 X LSH) F1 females were transferred into lethally irradiated susceptible LSH hamsters, and hematopoietic chimeras were produced. After intraperitoneal injection of 100 plaque-forming units of VSV, all of the female chimeras survived, but only 33% of male chimeras survived. These data indicate that resistance to VSV in Syrian hamsters is mediated, at least partially, by cells of hematopoietic origin.

Animals↗
PubMed1981

Suppression of vesicular stomatitis virus defective intefering particle generation by a function(s) associated with human chromosome 16.

Human-mouse somatic cell hybrids were made between adenine phosphoribosyltransferase-deficient mouse L cells and a strain of human primary fibroblasts and selected in medium containing alanosine and adenine (J. A. Tischfield and F. H. Ruddle, Proc. Natl. Acad. Sci. U.S.A. 71:45-49, 1974). These hybrids were tested for the generation of defective interfering (DI) particles of vesicular stomatitis virus to determine whether or not a host gene controls the induction of DI particles. None of the seven independently arising hybrid clones tested generated detectable DI particles during 13 successive undiluted passages. In addition, the parental human cells also failed to generate DI particles. In contrast, the parental mouse cells generated a detectable level of DI particles during continuous passage. Thus, failure to generate DI particles appears to act in a dominant fashion in these hybrids. Human chromosome 16 and adenine phosphoribosyltransferase were present, as a direct consequence of the selection system, in all of the hybrid clones that failed to generate DI particles. It was the only human chromosome observed in the cells of every hybrid clone. This was verified by both isozyme and karyotype analyses. After hybrids were back-selected (with 2,6-diaminopurine) for loss of human adenine phosphoribosyltransferase and chromosome 16, they gained the ability to generate DI particles. Replication of DI particles already present in virus stocks, however, was normal in all of the hybrid clones and the parental human cells. This suggests that the induction, but not the replication, of DI particles is affected by the human genome and that a factor on human chromosome 16 seems to selectively suppress the mouse cell's ability to generate DI particles in the hybrids. These results support the idea that the induction of DI particles is controlled in part by host cell function(s), as suggested previously (C. Y. Kang and R. Allen, J. Virol. 25:202-206, 1978).

Animals↗