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H Ichimura

Publications and source records attributed to H Ichimura.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Occurrences of human papilloma virus DNA in cervical carcinomas].

Out of 16 cases involving a cervical carcinoma that were investigated by Southern blot hybridization, found were human papilloma virus (HPV) types 16 and 18 DNA sequences in 8 (50%) and in one (6.3%), respectively. Six out of the 8 HPV 16-positive specimens were from squamous cell carcinomas, one was from an adenocarcinoma, and the remaining specimen was from an argyrophil small cell carcinoma. In 7 out of 9 HPV-positive specimens, the viral sequences were integrated in the tumor cell genome, whereas in the remaining two they were not integrated and remained circular and/or oligomeric in form.

Adenocarcinoma↗
PubMed1989

[Antitumor effects of cisplatin, cyclophosphamide and interferon-gamma (gamma-IFN) against argyrophil small cell carcinoma of the uterine cervix heterotransplanted into nude mice].

We investigated antitumor effect of cis-diammine-dichloroplatinum (cisplatin or CDDP), cyclophosphamide (CY) and interferon-gamma (gamma-IFN) against argyrophil small cell carcinoma (ASCC) of the uterine cervix using heterotransplanted ASCC tumor (YIK-1) into nude mice, containing HPV 16 DNA in a multicopy integrated form. No tumor growth retardation was observed in the nude mice which received the single administration of CDDP 2 mg/kg, CY 10 mg/kg or gamma-IFN 1 x 10(7) U/kg. However, the combined administration of CDDP and CY, or CDDP, CY and gamma-IFN markedly inhibited the tumor growth. Moreover, with comparison about relative tumor volume between these two groups, the combination of CDDP, CY and gamma-IFN was more effective than that of CDDP and CY. These data suggest that the combination chemotherapy of CDDP, CY and/or gamma-IFN was effective for the suppression of tumor growth in argyrophil small cell carcinoma of the uterine cervix. Further study on the antitumor potentiation of various anti-cancer agent and the combination of them against ASCC is needed.

Adult↗
PubMed1988

Influence of hepatitis delta virus superinfection on the clearance of hepatitis B virus (HBV) markers in HBV carriers in Japan.

To elucidate the influence of hepatitis delta virus (HDV) superinfection on the clearance of hepatitis B virus (HBV) associated antigens in HBV carriers, we examined for antibody to hepatitis delta antigen (anti-HD) serial sera collected from 1,029 HBV carriers in Kure, Japan. Of the 242 HBV carriers with hepatitis B e antigen (HBeAg), 28 became seropositive for anti-HD, of whom 18 (64.3%) cleared HBeAg; 214 did not become seropositive for anti-HD, of whom 70 (32.7%) cleared HBeAg. Thus, HBeAg clearance was observed in a significantly higher proportion of HDV-superinfected carriers as compared with carriers without HDV infection (P less than 0.005). In the 56 HBV carriers who cleared hepatitis B surface antigen (HBsAg), anti-HD was detected in three cases with increased serum alanine aminotransferase activity preceding HBsAg clearance. The duration of anti-HD seropositive state was less than 5 years, and the titer of anti-HD was relatively low in every case. These data suggest that the HDV infection rate in Japan is higher than previously reported, that HDV superinfection can be one of the factors that induce the HBeAg clearance and HBsAg clearance in HBV carriers, and also that the most likely outcome of HDV superinfection in HBV carriers in Japan may be acute self-limited infection.

Adult↗
PubMed1988

Heterotransplantation of argyrophil small cell carcinoma of the uterine cervix integrating HPV16 DNA into nude mice.

Argyrophil small cell carcinoma of the uterine cervix (ASCC) containing human papillomavirus type 16 (HPV16) DNA has been successfully transplanted in nude mice for the first time, and we have designated the resultant cell line as YIK-1. Histology of YIK-1 was similar to that of the original tumor. The original and YIK-1 tumor cells contained argyrophil granules and neurosecretory granules in the cytoplasm, and were immunohistochemically stained positive for neuron-specific enolase, serotonin and chromogranin. Both tumors contained HPV16 DNA in a multiple-copy integrated form. Thus, YIK-1 maintains the characteristics of the original ASCC, and may therefore be useful as an animal system for experimental studies of ASCC.

Animals↗
PubMed1988

Isolation and comparative restriction endonuclease DNA fingerprinting of equine herpesvirus-1 from cattle.

Deoxyribonucleic acid fingerprinting analyses with 4 restriction endonucleases (EcoRI, BamHI, BglII, and HindIII) and serotest results have definitively indicated that 5 herpesviruses isolated from 1974 to 1986 from aborted bovine fetuses and from bovine tissues and nasal secretions were abortigenic subtypes of equine herpesvirus type 1 (EHV-1). The herpesviruses, designated BH1247, 3M20-3, G118, H1753, and 9BSV4, were neutralized by EHV-1-specific antiserum and could be propagated in cultures of either bovine or equine cells. Only minor differences in restriction endonuclease patterns were detected from the pattern of an Army 183 isolate of EHV-1 subtype 1 that had been passaged only in equine cells and from that of an attenuated EHV-1 subtype 1 (RQ) strain that had been passaged several hundred times in non-equine cells. The individual differences in the restriction endonuclease fragments of the 5 bovine isolates and the Army 183 and RQ strains mainly were attributable to alterations in the terminally repeated and the unique short nucleotide sequences of the EHV-1 genomes, which are known to be hot spots for deletions and tandem repeats. The BamHI restriction endonuclease pattern of the 1977 bovine isolate H1753 was identical to that of EHV-1 subtype-1 strains responsible for most of the virus abortions in vaccinated horses since 1981. Abortigenic EHV-1 strains have the ability to infect cattle and cause disease under natural conditions.

Abortion, Veterinary↗
PubMed1987

Prevalence of antibody to delta antigen among HBV carriers in Japan.

Of 280 hepatitis B virus (HBV) carriers in Kure, Hiroshima Prefecture, Japan, 14 (5.0%) were seropositive for antibody to delta antigen (anti-HD by radioimmunoassay. HBV carriers with chronic liver disease had a greater frequency of seropositivity of anti-HD than asymptomatic HBV carriers (7% vs. 0%, P less than 0.05). Among the various geographic regions of Kure, the east suburban area had a significantly higher prevalence of anti-HD when compared with all other regions combined (9.8% vs. 2.7%, P less than 0.025). It is suggested that hepatitis delta virus (HDV) infection exists in Japan and HDV may be an etiologic agent of chronic liver disease.

Carrier State↗
PubMed1987

Phosphorylation of nucleoside analogs by equine herpesvirus type 1 pyrimidine deoxyribonucleoside kinase.

Replication of equine herpesvirus type 1 (EHV-1) was sensitive to 9-(1,3-dihydroxy-2-propoxymethyl)guanine(DHPG) but relatively resistant to E-5-(2-bromovinyl)-2'-deoxyuridine (BVDU). Likewise, plaque formation by EHV-1 was inhibited by DHPG, but not by BVDU. Plaque formation by a thymidine kinase-negative (tk-) mutant of EHV-1 was not inhibited by DHPG. In order to investigate biochemical mechanisms determining the differential sensitivity of EHV-1 to these drugs, the EHV-1-encoded thymidine kinase enzyme activity (TK)1 was partially purified from EHV-1-infected cells and analyzed. The EHV-1-induced enzyme utilized both ATP and CTP as phosphate donors and differed in relative electrophoretic mobility from the TKs of mock-infected and HSV-1-infected cells. Phosphorylation of 3H-dThd by the EHV-1 TK was inhibited by AraT, IdUrd, BVDU, and DHPG. The EHV-1 TK phosphorylated 125I-dCyd and 3H-ACV. The results indicate that EHV-1 encodes a pyrimidine deoxyribonucleoside kinase with broad nucleoside substrate specificity. These observations suggest that the failure of BVDU to inhibit EHV-1 replication is not attributable to an inability of the EHV-1 TK to phosphorylate BVDU, but may result from the incapacity of the viral TK to convert BVDU monophosphate to the triphosphate or from lack of inhibitory effect of BVDU triphosphate on viral DNA polymerase reactions.

Acyclovir↗
PubMed1987

Differential metabolism of (E)-5-(2-iodovinyl)-2'-deoxyuridine (IVDU) by equine herpesvirus type 1- and herpes simplex virus-infected cells.

Thymidine kinase (TK) enzymes encoded by herpes simplex viruses types 1 and 2 (HSV-1, HSV-2), and equine herpesvirus type 1 (EHV-1) catalyze the phosphorylation of thymidine (dThd) and (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU). The replication of HSV-1 is sensitive to BVDU, but the replication of HSV-2 and EHV-1 is not. To investigate the differential sensitivity of the viruses to halogenated vinyldeoxyuridine drugs, the phosphorylation of 125I-labeled (E)-5-(2-iodovinyl)-2'-deoxyuridine (IVDU) was studied. Cytosol enzymes from cells infected by HSV-2 and EHV-1 phosphorylated [125I]IVDU to the monophosphate, IVDUMP, but did not convert IVDUMP to higher di- plus triphosphates (IVDUDP plus IVDUTP) forms. In contrast, enzymes from HSV-1-infected cells converted [125I]IVDU to radioactive IVDUMP and IVDUDP plus IVDUTP. Experiments with mixtures of EHV-1- and HSV-1-induced enzymes showed that the EHV-1 enzyme did not inhibit formation of the IVDUDP plus IVDUTP by the HSV-1 enzyme. With [125I]IVDU as substrate, the Km values for the EHV-1 and HSV-1 TKs were 1.82 and 0.34 microM, respectively, and the Ki (dThd) value for the EHV-1 TK was 0.35 microM. In vivo experiments showed that HSV-1-infected cells converted IVDU to the mono- and the di- plus triphosphate forms. In contrast, EHV-1-infected cells converted IVDU to the monophosphate to a lesser extent than did HSV-1-infected cells, and did not produce the di- plus triphosphates. Thus, inefficient phosphorylation of the monophosphates probably contributes to the insensitivity of EHV-1 replication to IVDU, as it does to the insensitivity of HSV-2 replication to this drug.

Animals↗
PubMed1987

Nucleotide sequence changes in thymidine kinase gene of herpes simplex virus type 2 clones from an isolate of a patient treated with acyclovir.

To identify the nucleotide changes that occur in drug-induced thymidine kinase (TK) mutants of herpes simplex virus type 2 (HSV-2), we compared the nucleotide sequences of the tk genes of two mutant HSV-2 clones isolated from a patient who had been treated with acyclovir [9-(2-hydroxyethoxymethyl)guanine; ACV] with the nucleotide sequence of the parental TK+ HSV-2(8703) strain isolated from the same patient. One of the mutants, TK-altered (TKA) HSV-2(9637), was ACV resistant but induced the incorporation of [14C]thymidine into the DNA of infected rabbit skin cells. The nucleotide sequence of the tk gene of mutant TKA HSV-2(9637) had a single change (G to A) at nucleotide 668, which would cause an arginine-to-histidine substitution at amino acid residue 223 of the TK polypeptide. The second ACV-resistant mutant, TK- HSV-2(8710), did not induce detectable incorporation of [14C]thymidine into the DNA of infected rabbit skin cells. This mutant exhibited a deletion of a single base at nucleotide 217 of its nucleotide sequence. This deletion would cause a frameshift mutation at amino acid residue 73 and chain termination at amino acid residue 86 of the TK polypeptide. The nucleotide sequence of TK+ HSV-2(8703) was the same as that of the laboratory strain, TK+ HSV-2(333). The nucleotide sequence of a bromodeoxyuridine-resistant TK- HSV-2(333) mutant of TK+ HSV-2(333) also exhibited a single-base deletion, but at nucleotide 439. This deletion would cause a frameshift mutation at amino acid residue 147 and chain termination at amino acid residue 182. The frameshift mutations of TK- HSV(8710) and TK- HSV-2(333), respectively, occurred in sequences in which C was repeated three times and G was repeated seven times. The results raise the possibility that TK- frameshift mutations of HSV-2 may be common.

Acyclovir↗
PubMed1987

Second-generation pseudorabies virus vaccine with deletions in thymidine kinase and glycoprotein genes.

A modified-live pseudorabies virus (PRV) vaccine, designated PRV(dlg92/d1tk), with deletions in the thymidine kinase (tk) and glycoprotein-gIII (g92) genes, was derived from the PRV (Bucharest [BUK]-d13) vaccine strain. The vaccine virus also contained a deletion in glycoprotein gI. Despite 3 deletions, PRV(dlg92/d1tk) replicated to high titers in cell culture from 30 C to 39.1 C. Enzyme assays and autoradiography revealed that PRV(dlg92/d1tk) did not induce a functional tk activity in infected tk- RAB(BU) cells (rabbit skin). Rabbit skin cells were infected with PRV(dlg92/d1tk), with vaccine strains derived from BUK or Bartha K strains of PRV or with the virulent Illinois (ILL), Indiana-Funkhauser (IND-F), and Aujeszky (Auj) strains of PRV and were labeled with [3H]mannose from 4 or 5 to 24 hours after infection to investigate whether these viruses induced the synthesis of glycoprotein gIII. Nonionic detergent extracts were prepared and immunoprecipitated with antisera from pigs vaccinated with tk(-)-PRV(BUK-d13) or tk+-Bartha K, pigs vaccinated with tk+-PRV(BUK) strains and then challenge exposed to tk+-PRV(IND-F), naturally infected domestic or feral pigs, and pigs vaccinated with tk-)-PRV(dlg92/d1tk). Mouse monoclonal antibodies against PRV glycoproteins gIII, gp50, and gII were also studied. After immunoprecipitation, labeled PRV-specific proteins were analyzed by sodium dodecylsulfate-polyacrylamide gel electrophoresis and autoradiography. The PRV glycoprotein-gII complex, but not glycoprotein gIII, was synthesized in PRV(dlg92/d1tk)-infected cells. Glycoprotein gII and gIII were made in cells infected with PRV vaccine strains BUK, Bartha K, and BUK-d13 and with virulent PRV strains ILL, IND-F, and Auj. Cells infected with PRV(dlg92/d1tk) and with PRV strains ILL, IND-F, Auj, Bartha K, BUK, and BUK-d13, excreted into the cell culture medium a highly sulfated glycoprotein gX of about 90 kilodaltons. Antibodies to glycoprotein gIII were not detected in the sera of pigs inoculated with PRV(dlg92/d1tk), but were found in all other swine sera.

Animals↗
PubMed1986

Induction of thymidine kinase activity by viruses with group B DNA genomes: bovine cytomegalovirus (bovine herpesvirus 4).

The bovine herpesvirus type 4 (BHV-4) group has a slow replication cycle, a narrow host range, and cytopathogenic effects characteristic of cytomegaloviruses (CMV), but a Group B genome structure similar to that of lymphotropic Herpesvirus saimiri (HVS). Reference BHV-4 strain DN599 and BHV-4 strains N124 and FHV-2 induced in the cytosol fraction of thymidine kinase-negative (TK-) rabbit skin (RAB-BU) cell mutants a novel TK activity. The BHV-4-induced thymidine kinase (TK) differed from the principal cytosol TK of mock-infected cells in PAGE mobility (Rm) under non-denaturing conditions and in the capacity to efficiently substitute CTP for ATP as a phosphate donor. The BHV-4 thymidine phosphorylating activity could also be distinguished from many common herpesvirus-induced TKs because it lacked iododeoxycytidine phosphorylating activity. Iododeoxyuridine, trifluorothymidine and bromovinyldeoxyuridine inhibited [3H]thymidine (0.01 mM) phosphorylation by the BHV-4 enzyme in a dose-dependent manner, but arabinosylthymine and 2'-fluoro-5-methyl-arabinosyluracil (FMAU) were poor inhibitors of [3H]thymidine phosphorylation, and acyclovir and (dihydroxy-2-propoxymethyl)guanine (DHPG) did not inhibit at all at 60 and 40 times the concentrations of [3H]thymidine, respectively.

Animals↗