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K Yoshiike

Publications and source records attributed to K Yoshiike.

At least 55 records · Page 3Linked to original sources
PubMed1986

Evolutionary changes of transcriptional control region in a minute-plaque viable deletion mutant of BK virus.

Two plaque morphology BK virus (BKV) mutants (pm526 and pm527) rescued from a hamster pineocytoma cell line Pc13 were characterized and compared with a similarly rescued and previously characterized mutant (pm522), its derivatives (tr530, tr531, and tr532), and the wild type (501) for their biological activities and for the structures of their transcriptional control regions. The two mutants grew somewhat more slowly in human embryonic kidney cells but transformed rat 3Y1 cells more efficiently than did the wild-type BKV. BKV pm526 formed minute plaques and had the shortest transcriptional control region, having only one 68-base-pair element, which is triplicated in the wild-type BKV. BKV pm526 was unstable during repeated replication in human embryonic kidney cells and yielded large-plaque viruses with longer HindIII C segments encompassing the BKV DNA replication origin. Comparison of nucleotide sequences of the transcriptional control regions among the mutants and the wild type showed that pm526 is a parent virus, from which all the other mutants had evolved, and that the evolutionary changes of the plaque size, from minute to small to large, were due to duplications of a certain segment containing the adenovirus E1A enhancer core or the simian virus 40 enhancer core found in the BKV 68-base-pair element. The activities to enhance early transcription, as measured by the ability to direct the synthesis of chloramphenicol acetyltransferase, approximately paralleled the plaque size. The duplication containing the adenovirus E1A enhancer core did not affect the transforming capacity of the parent virus, but the duplication including the simian virus 40 enhancer core significantly lowered the transforming capacity for rat cells.

Animals↗
PubMed1986

Mutation in the VP-1 gene is responsible for the extended host range of a monkey B-lymphotropic papovavirus mutant capable of growing in T-lymphoblastoid cells.

Monkey B-lymphotropic papovavirus (LPV) replicates only in B-lymphoblastoid cells, whereas the LPV mutant 76 (LPV-76) can grow in either B- or T-lymphoblastoid cells. The nucleotide sequence of the wild-type LPV PstI B segment was compared with that of LPV-76 PstI-B, within which the mutation responsible for the extended host range had been located. The VP-1 coding region of LPV-76 was found to have mutations, single-base substitutions causing three amino acid substitutions.

Animals↗
PubMed1986

Monkey B-lymphotropic papovavirus genome: the entire DNA sequence and variable regions.

DNA from monkey B-lymphotropic papovavirus (LPV) adapted to growth in human B-lymphoblastoid cell line BJA-B consisted of three classes of molecules of 5.1, 5.0, and 4.9 kilobases (kb), and the entire DNA sequence of 5.1-kb molecule was determined. The three types of LPV DNA yielded infectious virus upon transfection to BJA-B cells. Comparison of the structures among these clones and clone K38 sequenced by Pawlita et al. (1985) suggests that the transcriptional control region, the small-T antigen gene, and the VP-1 gene are variable in the LPV genome, and that the 5.0-kb LPV resembles the parent virus, from which all the others had evolved by duplication and deletion during passages in BJA-B cells, probably for adaptation to better growth in human cells.

Animals↗
PubMed1985

DNA rearrangement in the control region for early transcription in a human polyomavirus JC host range mutant capable of growing in human embryonic kidney cells.

A human polyomavirus JC virus (JCV) host range mutant (JC-HEK) can grow in human embryonic kidney cells, whereas the brain cell-tropic wild-type JCV strain (Mad-1) cannot; JC-HEK contains two complementing defective DNAs, JC-HEK-A and JC-HEK-B. We determined the nucleotide sequence of the putative transcriptional control region of JC-HEK-A DNA that can induce T-antigen synthesis in human embryonic kidney cells and compared it with the sequence of JCV Mad-1 DNA. The JC-HEK-A control region was found to have a complex DNA rearrangement, namely, a partial local duplication of a noncoding region generating two extra replication origins and translocation of segments from the large-T-antigen gene (415 base pairs) and the VP-1 gene (78 base pairs). In the rearranged segment, JC-HEK-A had seven sets of the sequence 5'TGGA(T)A(T)A(T)3', which is found in the simian virus 40 enhancer core, whereas JCV Mad-1 had only one set in its control region. JC-HEK-A also had a 5'TGGAAGTGTAA3' sequence resembling the adenovirus early region 1A enhancer core sequence 5'AGGAAGTGAA3'. Because the viral enhancer is host discriminatory and because another human polyomavirus, BK virus, that grows well in human embryonic kidney cells has these signals in its control region, it is likely that some of the newly acquired signals in JC-HEK play an important role in the altered host range of JCV.

Base Sequence↗
PubMed1985

Decreasing the number of 68-base-pair tandem repeats in the BK virus transcriptional control region reduces plaque size and enhances transforming capacity.

Wild-type BK virus, which has three 68-base-pair (bp) elements tandemly repeated in its transcriptional control region, forms clear, large plaques in human embryonic kidney cell cultures but rarely transforms hamster or rat cells. From this BK virus DNA, deletion mutants with fewer than three 68-bp elements were constructed and characterized. The mutant DNA with two 68-bp elements formed small, turbid plaques in human cell cultures and transformed rat 3Y1 cells inefficiently. The mutant DNA with one 68-bp element formed minute, turbid plaques in human cell cultures and transformed rat cells efficiently.

Animals↗
PubMed1985

Human papillomavirus DNA in female condylomata.

We have studied the presence and state of human papillomavirus (HPV) genomes in condylomata acuminata of the vulva, vagina, and cervix and in flat condylomas of the cervix from Japanese females by DNA hybridization with HPV 6 and 11 DNAs. Unintegrated HPV 6-related DNA (HPV 6 or 11 DNA) was detected in 55 out of 60 condylomata acuminata and in 1 out of 4 flat condylomas under stringent hybridization conditions. The HPV DNAs were identified as HPV 6 DNA in 29 condylomata acuminata (20 vulvar, 3 vaginal, and 6 cervical samples) and 1 flat condyloma and as HPV 11 DNA in 6 condylomata acuminata (6 vulvar samples). The data indicate close association of HPV types 6 and 11 with condylomata.

Adolescent↗
PubMed1985

Occurrence of human papillomavirus types 16 and 18 DNA in cervical carcinomas from Japan: age of patients and histological type of carcinomas.

We have detected by DNA hybridization human papillomavirus (HPV) types 16 and 18 DNA sequences in 19 and 3, respectively, out of 56 cervical carcinomas from Japan. Eighteen out of 19 HPV 16-positive specimens were from squamous cell carcinomas, whereas the three HPV 18-positive specimens were from a squamous cell carcinoma (1/50), an adenosquamous carcinoma (1/3), and an adenocarcinoma (1/3). The occurrence of HPV 16 DNA decreased in patients over 60 years old (less than or equal to 60 years, 15/34 (44%); 60 years less than, 4/22 (18%)) (P less than 0.05).

Adenocarcinoma↗
PubMed1984

Expression of viral early functions in rat 3Y1 cells infected with human papovavirus BK.

A plaque morphology mutant (pm-522) of BK virus (BKV) with a small deletion at map unit 0.72 can readily transform rat 3Y1 cells, but wild-type BKV (wt-501) cannot. We examined the expression of the viral early functions in BKV (wt-501 or pm-522)-infected 3Y1 cells within a 2-week period after infection, before foci of transformed cells became detectable, to know how the difference between the two BKVs occurs. After a high-multiplicity infection, comparable amounts of free viral DNA (forms I and II) were found by Southern blotting analyses to persist in the nuclei of the cells infected with wt and pm BKVs. Whereas the proportion of T antigen-positive cells, as revealed by the indirect immunofluorescence method with complement, remained at a level of 60% in pm BKV infection, the level of T antigen-positive cells in wt BKV infection decreased from the initial 45% to 1% on day 9. The results obtained by the immunoprecipitation analyses of radiolabeled proteins from the infected cells were consistent with the immunofluorescence data. Viral early mRNA was detectable on day 2 and increased on day 9 in pm BKV infection, but in wt BKV infection, the low level of early mRNA detected on day 2 disappeared on day 9. Cell DNA synthesis and cell growth were enhanced more in pm BKV infection than in wt BKV infection. The low level of viral DNA synthesis that occurred in the infected rat cells was more prominent in pm BKV infection than in wt BKV infection. These data indicate that the expression of viral early functions continued much longer in pm BKV-infected rat cells than in wt BKV-infected rat cells, where the expression was probably repressed soon after infection. Continued T antigen production directed by the unintegrated viral genomes appears to be required for efficient transformation of rat cells by BKV.

Antigens, Viral, Tumor↗
PubMed1984

Monkey B-lymphotropic papovavirus DNA: nucleotide sequence of the region around the origin of replication.

We have determined the nucleotide sequence of the HindIII-B DNA segment of African green monkey B-lymphotropic papovavirus (LPV), which shows a highly restricted host range and whose genome is a 5.1-kilobase-long circular DNA. The segment, consisting of 1,123 base pairs, contained the origin of DNA replication, the putative control region for early transcription, and the region probably coding for the amino-terminal portion of T antigens. The symmetrical region at the center of replication origin, 5'-GAGGC CA GGGGCCCC TA GCCTC-3' (on the L strand), has diverged in the central portion from the corresponding regions of primate polyomaviruses simian virus 40, BK virus, and JC virus, but resembles that of mouse polyomavirus. The structure of the control region upstream of the replication origin was unique to LPV and contained several repeated sequences, the longest of which were two 60-base-pair tandem repeats. The amino-terminal region common to LPV small T and large T antigens showed some homology (41%) in the deduced amino acid sequence to that of both simian virus 40 and the mouse polyomavirus. Like other polyomaviruses, the probable carboxyl-terminal region unique to LPV small T antigen contained two sets of the Cys-x-Cys-x-x-Cys structure. These data show that, despite the unique structures in the control region, LPV is evolutionally related to the mouse polyomavirus and to simian virus 40.

Amino Acid Sequence↗
PubMed1984

DNA rearrangement affecting expression of the BK virus transforming gene.

BK virus mutant pm-522, forming small turbid plaques on human cells, can transform rat or hamster cells much more efficiently than the wild-type BK virus (wt-501) does. We compared the nucleotide sequence of wt-501 HindIII C segment with that of pm-522 HindIII-C, which contains the mutation responsible for the altered plaque type and transforming capacity. The difference between the two BK viruses was the local DNA rearrangement (deletions and duplications) that had occurred in the putative control region for early transcription in pm-522 DNA. Whereas wt-501 had three sets of 68-base pair repeats (the central set had a deletion of 18 base pairs) in this region, pm-522 had one set of 68-base-pair units and two sets of shorter 37-base-pair repeats. Three BK virus mutants, forming clear large plaques like those of wt-501 but capable of transforming rat cells, were derived from the recombinant virus carrying the HindIII C segment of pm-522. These mutants had further duplications of short segments originating from the pm-522 sequence in the putative early control region.

Animals↗
PubMed1984

[DNA rearrangement affecting expression of the early genes in papovaviruses].

We characterized a plaque-morphology mutant of human papovavirus BK (pm-522), which can transform rat 3Y1 cells much more efficiently than a wild type (wt-501) does. Unintegrated pm-522 genomes appeared to be continuously transcribed, to direct synthesis of large T antigen, and to cause abortive transformation of the infected rat cells during the first two-week period before foci of the stably transformed cells develop. Despite the initial transcription and T antigen production, wt-501 genomes ceased being transcribed soon. T antigen, together with a yet unidentified factor from rat cells, may suppress transcription of the wt early genome. The difference in control of early transcription of the free viral genomes in rat cells could account for the difference in transforming capacity between wt-501 and pm-522. Some of the three small deletions clustering in the probable transcriptional control region were found to be responsible for the plaque morphology and high-transforming capacity of pm-522. Comparison of nucleotide sequences between the two viruses indicated that pm-522 was probably generated from wt-501 through deletion followed by two small local duplications in the area containing 68-base-pair repeats characteristic of BK virus.

Animals↗
PubMed1983

High-titer SV40 replication in human fibroblast cell lines derived from patients with Wiskott-Aldrich syndrome.

Human fibroblast cell lines established from skin biopsies of patients with Wiskott-Aldrich syndrome (WAS), a sex-linked immunodeficiency disorder, were found to have unusually high sensitivity to SV40 infection. When examined by immunofluorescence, two of the cell lines showed almost 100% positive staining for tumor and viral antigens 4 days after infection, while the third cell line showed 75% positive cells for both antigens. Marked cytopathic changes were seen in infected cultures and viral yields of 10(8) pfu/ml were obtained. After six serial passages in WAS cells, the viral DNA was examined by restriction endonuclease analysis and found to have HindIII cleavage pattern similar to that of DNA from SV40 grown in monkey cells.

Antigens, Viral↗
PubMed1983

Genomic structure of human polyoma virus JC: nucleotide sequence of the region containing replication origin and small-T-antigen gene.

The nucleotide sequence of the region of human polyoma virus JC DNA between 0.5 and 0.7 map units from a unique EcoRI cleavage site was determined and compared with those of the corresponding regions of another human polyoma virus, BK, and simian virus 40 DNAs. Within this region consisting of 945 base pairs, we located the origin of DNA replication near 0.7 map units, the entire coding region for small T antigen, and the splice junctions for large-T-antigen mRNA. The deduced amino acid sequences for small T antigen and the part of large T antigen markedly resembled those of polyoma virus BK and simian virus 40. The results strongly suggest that polyoma virus JC has the same organization of early genome as polyoma virus BK and simian virus 40 on the physical map, with the EcoRI site as a reference point.

Amino Acid Sequence↗
PubMed1983

Alignment of the genome of monkey B-lymphotropic papovavirus to the genomes of simian virus 40 and BK virus.

We located the origin of DNA replication of African green monkey B-lymphotropic papovavirus DNA by analyzing pulse-labeled form I DNA. With the replication origin used as a reference point, the B-lymphotropic papovavirus genome was aligned with the genomes of simian virus 40 and BK virus from DNA homology between specific fragments hybridized under low-stringency conditions. From the results of these experiments, it was possible to deduce the correlation between the physical and functional maps of the B-lymphotropic papovavirus genome.

BK Virus↗
PubMed1982

Two defective DNAs of human polyomavirus JC adapted to growth in human embryonic kidney cells.

Human polyomavirus JC (JCV) adapted to growth in human embryonic kidney (HEK) cells contains two or more species of shorter-length viral DNA even after two cycles of plaque purification in HEK cells. We have molecularly cloned JCV DNA from one plaque isolate and determined the physical map of its DNA. Using gel electrophoresis and electron microscopy, we found that the cloned DNA consisted of two classes of JCV DNA. One class of DNA had a deletion of 30% (between 0.7 and 1.0 map units from the EcoRI site) and an insertion of 1% at the same site in the late region. The other had a deletion of 35% (0.18 to 0.53 map units) and an insertion of 12% at the same site in the early region of the JCV genome. Both DNAs had added sequences near the origin of DNA replication. From their structure, the two DNAs appear to complement each other. These results indicate that the HEK-adapted JCV may be replicating by complementation between two defective mutants.

Cell Line↗
PubMed1982

Biological and biochemical studies of African green monkey lymphotropic papovavirus.

The growth of African green monkey lymphotropic papovavirus (LPV) in human lymphoblastoid cell line BJA-B was found to be slow and inefficient due to the accumulation of defective particles. An analysis of molecularly cloned LPV DNAs showed that 3 of 19 clones had DNAs that were longer (5.1 kilobases) than the DNAs of the other clones. The 5.1-kilobase DNA was infectious for BJA-B cells, whereas the shorter (4.8-kilobase) molecules were defective. Unlike the wild-type virus, stocks of LPV made from cloned, infectious DNAs were homogeneous and had higher titers. Using stocks of nondefective LPV, we investigated other biological properties. LPV replication in another human B-lymphoblastoid cell line was observed. The virus did not cause tumors when it was inoculated into newborn hamsters. Serological surveys of human and nonhuman primate sera indicated that virtually all primates, including humans, show evidence of infection by viruses antigenically related to LPV.

Animals↗
PubMed1982

Change of DNA near the origin of replication enhances the transforming capacity of human papovavirus BK.

A turbid-plaque-forming mutant (pm522) of human papovavirus BK, which has a small deletion at about 0.7 map unit and grows somewhat more slowly in human cells than does wild-type BK virus, transformed hamster and rat cells in culture much more efficiently than did wild-type virus. Another plaque morphology mutant, pm525, forming turbid plaques larger than those of pm522 also had a high transforming capacity. The similar difference in transforming capability between wild-type and plaque morphology viruses was observed with DNAs extracted from virions. Recombinant viruses were constructed from the wild-type DNA fragment lacking HindIII-C (0.62 to 0.73 map unit) and pm522 HindIII-C (including the origin of replication) by the molecular cloning method. Characterization of the recombinants showed that the change near the origin of DNA replication was responsible both for the altered plaque morphology and for the enhanced transforming capacity of the BK virus mutant.

Animals↗