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Biomedical subjects

T Morishima

Publications and source records attributed to T Morishima.

At least 127 records · Page 7Linked to original sources
PubMed1992

Prophylactic oral acyclovir in outbreaks of primary herpes simplex virus type 1 infection in a closed community.

Oral acyclovir was given prophylactically to 37 children in the early stages of three outbreaks of herpes simplex virus type 1 (HSV-1) infection and the results were compared with those in untreated control subjects in two other outbreaks. The rates of seroconversion to HSV were significantly reduced in children treated with acyclovir compared with control subjects (91% vs 27%, P less than .001). The incidence of symptomatic disease was also significantly reduced (82% vs 0%, P less than .001). In some children receiving prophylactic acyclovir, anti-HSV antibody titers did not rise despite the presence of replicative HSV on throat swabs just before the start of treatment. Restriction endonuclease analysis of isolated HSV-DNA confirmed that one strain was responsible for the five outbreaks. No resistance to acyclovir was detected during the study, and no adverse effects of treatment were noted. In conclusion, short-term prophylactic acyclovir may limit the spread and reduce clinical manifestations of HSV infections in closed communities, although this use should be restricted to communities where severe symptoms are observed.

Acyclovir↗
PubMed1992

Human herpesvirus-6 DNA in cerebrospinal fluid of a child with exanthem subitum and meningoencephalitis.

The involvement of human herpesvirus-6 (HHV-6) and herpes simplex virus infections was evaluated virologically and serologically in a 13-month-old girl with meningoencephalitic illness occurring in the pre-eruptive stage of exanthem subitum. An isolation of HHV-6 from blood and seroconversion to the virus confirmed the primary infection with the virus. HHV-6 gene sequences were detected in cerebrospinal fluid of acute stage of the disease by polymerase chain reaction. There was no evidence of herpes simplex virus infection in blood and cerebrospinal fluid. The patient recovered from the disease without any sequelae, although abnormal electroencephalography and cerebral computed tomography findings were observed temporally in the acute stage of the disease. These findings strongly suggest that HHV-6 invades the central nervous system and causes meningoencephalitis.

Antibodies, Viral↗
PubMed1992

Relapse of herpes simplex encephalitis in children.

The polymerase chain reaction method was used to diagnose herpes simplex encephalitis in children. Initial samples of cerebrospinal fluid from 15 patients with herpes simplex encephalitis were all positive for the herpes simplex virus DNA by polymerase chain reaction assay. In terms of early diagnosis, polymerase chain reaction assay became positive significantly earlier than the detection of intrathecally produced anti-herpes simplex virus antibody using the enzyme-linked immunosorbent assay (4.4 vs 8.9 days after onset; P less than .01). Serial examinations showed that the presence of virus DNA in cerebrospinal fluid continued for 3 to 18 days after the neurologic onset (mean 10.1 days). Four of the 15 patients had a relapse of encephalitis after completing acyclovir therapy. The mean duration of initial acyclovir therapy in the recurrent group was significantly shorter than that in the nonrecurrent group. In recurring cases, herpes simplex virus DNA reappeared temporarily in the cerebrospinal fluid of two patients. These results show that polymerase chain reaction assay is a useful diagnostic tool for the early and noninvasive diagnosis of herpes simplex encephalitis in children. Results also suggest that a comparatively short duration of acyclovir therapy may be related to a relapse of herpes simplex encephalitis in some children.

Acyclovir↗
PubMed1992

Spitz naevus of the toe.

A 68-year-old Japanese woman presented with a brownish macule, containing two papules, on her left fourth toe. Histological examination revealed an intradermal epithelioid cell tumour with irregularly shaped, bizarre giant cells. In the upper portion of the tumour, the epithelioid cells contained abundant melanin. A low amount of 5-S-cysteinyldopa and a diploid DNA distribution histographic pattern were helpful in differentiating the lesion from malignant melanoma. This location of a Spitz naevus is exceptional.

Aged↗
PubMed1991

Serum hepatitis C virus sequences in posttransfusion non-A, non-B hepatitis.

We investigated 17 patients (12 males and 5 females, ages 2 to 57 years old) with posttransfusion non-A, non-B hepatitis to determine relationships between clinical courses and hepatitis C virus (HCV) markers. The patients were grouped according to time course of abnormal serum alanine aminotransferase (ALT) levels into three categories (chronic biochemical disease, biochemically resolved chronic disease, and acute disease). Latest serum samples (1.3 to 10.8 years after blood transfusion) were used to detect antibodies against C100-3 antigen (anti-HCV) by enzyme-linked immunosorbent assay and HCV sequences by polymerase chain reaction (PCR) assay. Of the 17 patients, 13 patients (76.5%) were anti-HCV positive and 8 patients (47.1%), including one anti-HCV negative case, were positive for HCV RNA. In total, 14 patients (82.4%) were positive for either HCV markers. With respect to clinical course, HCV RNA was detected in six of eight patients (75%) with chronic biochemical disease, and in two of five patients (40%) with biochemically resolved chronic disease. HCV RNA was not detectable in convalescent sera from four patients with acute disease. These results show that there is a relationship between clinical status and HCV viremia, but that normal liver function tests do not always represent the clearance of the virus. Viremia in two patients with normal ALT level suggests that hepatitis is not only caused by viral cytopathic effects, but also by immunologic reactions against virus-infected cells. Thus, PCR is useful in determining the persistence of HCV infection as well as to diagnose anti-HCV negative HCV infection.

Adolescent↗
PubMed1991

Detection of viral DNA in neonatal herpes simplex virus infections: frequent and prolonged presence in serum and cerebrospinal fluid.

Polymerase chain reaction (PCR) assay was used to detect herpes simplex virus (HSV) DNA in mouth, skin, sera, or cerebrospinal fluid (CSF) from seven neonates with HSV infection. In a culture-negative patient, the diagnosis was confirmed by detection of HSV DNA. Serial examinations revealed that HSV DNA remained in the serum and/or CSF from several patients for 1-2 weeks after the beginning of treatment. Next, the results of PCR assay in neonatal HSV infections were compared with those in older children with herpes simplex encephalitis (HSE). HSV DNA was detected in CSF from four neonates with central nervous system involvement and in CSF from all nine children with HSE. Sera were positive for HSV DNA in five of seven neonates, including two cases of localized infections, but in none of the children with HSE. These results suggest that HSV may be spread principally via viremia in neonates. PCR assay could be useful for the confirmative diagnosis of neonatal HSV infections, especially in culture-negative cases.

Base Sequence↗
PubMed1991

The pathogenicity of ribonucleotide reductase-null mutants of herpes simplex virus type 1 in mice.

The pathogenicity of ribonucleotide reductase (RR)-null mutants (hrR3 and ICP6 delta) of herpes simplex virus (HSV) type 1 was studied after intracerebral and corneal inoculation in newborn and adult ICR mice. ICP6 delta failed to replicate in brains of mice greater than or equal to 8 days old but exhibited significant virulence for newborn mice as a result of viral replication in the brains. The RR- and a thymidine kinase (TK)-deficient mutant of HSV-1 strain KOS could grow in eye tissues of adult ICR mice. Viral DNA of hrR3 was detected in brain tissues of intracerebrally infected mice or in the trigeminal ganglia of corneally infected mice greater than or equal to 50 days after infection, and infectious hrR3 could be recovered from these tissues by superinfection of the mice with wild-type HSV-2. These observations indicate that pathogenicity of RR- mutants in mice is highly dependent on the physiologic state of tissues infected and that RR- mutants have the ability to establish latency in nervous system tissues of mice by either the peripheral or intracerebral route. It was also demonstrated that the inability of the RR- mutants to invade the central nervous system was efficiently complemented by simultaneous infection with another defective virus, the TK- mutant of KOS.

Animals↗
PubMed1991

Detection of varicella-zoster virus (VZV) DNA in clinical samples from patients with VZV by the polymerase chain reaction.

A polymerase chain reaction system for the detection of varicella-zoster virus was established. Of 25 nucleotides, 4 oligonucleotide pairs (regions of thymidine kinase, thymidylate synthetase, glycoprotein I, and immediate early gene) were synthesized. The first three oligonucleotide pairs could be used as primers on the basis of specific DNA amplification. Varicella-zoster virus DNA was amplified by this polymerase chain reaction system in 20 of 20 vesicle samples, 5 of 6 crusts, and 12 of 13 throat swabs collected from patients with clinical varicella.

Base Sequence↗
PubMed1991

Detection of pre-C and core region mutants of hepatitis B virus in chronic hepatitis B virus carriers.

We analyzed the pre-C and core region of hepatitis B virus (HBV) DNA by a polymerase chain reaction in 22 chronic carriers. In 9 hepatitis B e antigen-positive asymptomatic carriers, a single DNA band was detected at the expected size, whereas additional shorter DNA bands were observed in 7 out of 11 patients with chronic hepatitis. The smaller-sized DNAs from one chronic hepatitis patient had various lengths of deletions spanning from 105 to 183 bp in the middle of the core gene, and all deletions included common nucleotide sequences. All of the smaller-sized DNAs from the other patients proved to be variant core genes. They were deleted in similar regions by Southern analysis using oligonucleotide probes. A follow-up study revealed that four out of seven chronic hepatitis patients with a short core gene seroconverted to antibody to hepatitis B e antigen, but those with only a "wild type" did not. In another set of sequence studies, clones isolated from two chronic carriers displayed heterogeneity of the pre-C and core gene which was more often present in sera with normal alanine aminotransferase levels than with abnormal levels. These results suggest that mutant HBV alters the host immune response, and may modulate the clinical course of HBV infection. An alternative possibility is that chronic hepatitis selects for mutant forms.

Adolescent↗
PubMed1991

Quantitative determination of hepatic glucose uptake using an innovative approach: effect of strict glycemic regulation and exercise in diabetic subjects.

For perfect glycemic control in diabetics, therapeutic modalities which enhance impaired hepatic glucose uptake seen in diabetics should be utilized. In animal experiments, we demonstrated that factors promoting hepatic glucose uptake are the glucose gradient between the central nervous system and the hepato-portal system, portal hyperinsulinemia and normal premeal glycemia. Therefore, we investigated both the effects of intensified insulin therapy and a single bout of exercise on hepatic glucose uptake by euglycemic hyperinsulinemic clamp combined with oral glucose loading. In 56 out of 77 patients, perfect glycemic normalization was established with mean regular insulin doses of 10, 7, 7 U at breakfast, lunch and dinner, respectively. The ratio of splanchnic glucose disposal to the amount of ingested glucose increased significantly from 19.0 to 42.1%. A single bout of exercise enhanced hepatic glucose uptake from 23.4 to 50.5%. Both strict glycemic regulation and exercise enhance hepatic glucose uptake significantly in non-obese diabetic patients.

Diabetes Mellitus, Type 2↗
PubMed1991

Clinical manifestations of primary herpes simplex virus type 1 infection in a closed community.

The clinical features and the molecular epidemiology of primary herpes simplex virus type 1 (HSV-1) infection among children younger than 3 years of age were investigated in day-care nursery. Serial sera were assayed for anti-HSV-1 glycoprotein B antibody by enzyme-linked immunosorbent assay. Serologic examinations revealed 55 cases of primary HSV infection during the observation period. Fifty-one of them (93%) had typical herpetic gingivostomatitis, showing a high rate of clinically overt infection. Four outbreaks of herpetic gingivostomatitis were observed during the observation period. Forty-one children were infected with HSV-1 in the outbreaks. The rates of infection in the susceptible children were 81%, 73%, 78%, and 100%, respectively, in the four outbreaks. Restriction endonuclease analysis of DNA of isolated HSV revealed that only one strain of HSV-1 had been transmitted among children for a long period.

Age Factors↗
PubMed1990

Inhibitory effect of herpes simplex virus infection to target cells on recognition of minor histocompatibility antigens by cytotoxic T lymphocytes.

Target cell lysis by CTL specific for minor histocompatibility Ag (minor HA), which were generated in (C3H/He x BALB/c)F1 mice immunized with A/J mouse spleen cells, was dramatically reduced by infection of HSV to Neuro-2a (A/J mouse origin) cells as target. The reduction was apparent at 5 h after infection of HSV to target cells, when many viral proteins were produced in the cells. Conversely, MHC-restricted HSV-specific CTL-mediated cell lysis increased time dependently. Using an RNA virus, vesicular stomatitis virus, significant reduction of minor specific CTL-mediated target cell lysis was also found. During the time when this reduction of target cell lysis by HSV occurred, the surface expression of class I H-2Dd molecules was maintained, and anti-H-2a allo-MHC-specific CTL lysed HSV-infected Neuro-2a cells as strongly as uninfected Neuro-2a cells. When HSV-infected or uninfected Neuro-2a cells were treated with Brefeldin A that selectively blocks transportation of newly synthesized proteins out of endoplasmic reticulum, both HSV- and minor HA-specific CTL-mediated cell lyses were blocked. These observations demonstrated that minor HA are continuously synthesized and associated with class I molecules at pre-Golgi and transported via trans Golgi system with quick turnover, and that newly synthesized HSV Ag, which are also associated with class I molecules and transported via the same system, should take the place of intrinsic minor HA and be presented on the surface of the cells to be recognized by MHC-restricted CTL.

Animals↗