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Biomedical subjects

K Miyamura

Publications and source records attributed to K Miyamura.

160 records · Page 9Linked to original sources
PubMed1978

Growth characteristics of acute hemorrhagic conjunctivitis virus in monkey kidney cells. III. Viral RNA synthesis at permissive and nonpermissive temperatures.

Monkey kidney cells infected with the J 670/71 strain of acute hemorrhagic conjunctivitis (AHC) virus in the presence of actinomycin D synthesized two species of viral RNA. One species had properties similar to the virion RNA, sedimented in a sucrose gradient with a sedimentation coefficient of 34S, and was sensitive to RNase. The other species sedimented at 18S and was resistant to RNase. The inability of AHC virus to replicate at 39 degrees was attributed to a lack of virus-specific RNA synthesis in infected cells.

Animals↗
PubMed1977

Virological and serological studies of neurological complications of acute hemorrhagic conjunctivitis in Thailand.

An extensive outbreak of acute hemorrhagic conjunctivitis (AHC) occurred from September to December 1974 in Thailand. At least 29 patients with polio-like motor paralysis that complicated AHC were hospitalized in Bangkok. Paired or triplicate samples of serum from 16 patients were tested for neutralizing antibody to enterovirus type 70 (EV70). A significant rise in titer of antibody was found for two patients, and the other 14 had neutralizing antibody titers ranging from 1:8 to 1:512 without an increasf larger than or equal to 1:16, a level which is considered to be diagnostically significant. Neutralizing antibody to EV70 was detected in 19S fractions of nine sera examined, but neutralizing antibody to three types of poliovirus was confined to 7S fractions. EV70 was isolated from one of seven stool specimens collected on day 37 after the onset of AHC and none of 10 samples of cerebrospinal fluid. These results and additional clinical and epidemiologic findings gave further support to the hypothesis that EV70 infection can cause polio-like motor paralysis as a complication of AHC.

Antibodies, Viral↗
PubMed1976

Growth characteristics of acute hemorrhagic conjunctivitis (AHC) virus in monkey kidney cells. II. Temperature sensitivity of the isolates obtained at various epidemic areas.

Acute hemorrhagic conjunctivitis (AHC) virus strains isolated in eight different areas during epidemics of AHC were tested for the reproductive capacity at 33, 37 and 39 degrees. All of the 25 strains tested grew better at 33 degrees but restrictively at 39 degrees. The degree of temperature sensitivity varied slightly from one strain to the other, but generally exceeded that of attenuated poliovirus type 1, strain LSc2ab. Temperature-resistant clones were selected by repeated passages of originally temperature-sensitive prototype strains at supraoptimal temperature. The importance of using a low temperature (32-34 degrees) for isolation of virus from external tissues of the body and for subsequent passages has been emphasized. It was suggested that the relatively low temperature of the conjunctiva has played a role in perpetuating temperature sensitivity of this virus.

Animals↗
PubMed1975

Serologic characterization and sero-epidemiologic studies on acute hemorrhagic conjunctivitis (AHC) virus.

Serologic and sero-epidemiologic characteristics of AHC virus infection were studied by neutralization test (NT). Four-fold or greater virus neutralizing (VN) antibody response was demonstrated to the Japanese isolate of AHC virus (the J 670/71 strain) in 77.3% and 66.7% of paired sera from clinical AHC patients in Japan (1971-1973) and Tunisia (1973). The four patients from Indonesia studied in 1972 showed similar antibody response. Cross-neutralization tests of AHC virus isolated in Japan (1971), Taiwan (1971), Hong Kong (1971), Thailand (1972), Indonesia (1972), Singapore (1972), Morocco (1971) and England (1971) with three kinds of antisera prepared against Japanese, Hong Kong and Moroccan AHC virus isolates indicated their antigenic identity. However, isolates from Sinapore in 1970 (Singapore 70 virus) were not neutralized with the AHC virus antisera mentioned above: Singapore 70 virus constitutes another antigenic type, to which, however, no VN antibody rise was found in paired patients' sera from Japan, Tunisia and Indonesia. Thus, no serologic evidence supporting an etiologic role of this virus group in the development of AHC was found. Although cross-tests using monospecific antisera suggested some cross-relation between AHC and both echovirus type 4 (E4) and coxsackie A (CA), type 19, no serologic relationship between AHC and these viruses was found. Sera from healthy individuals collected before and after AHC outbreaks were tested for VN antibody against AHC virus in Japan and two epidemic foci, Ghana and Indonesia. Before the epidemic, 80 to 90% of the people lacked antibody in the three countries, but 39.7% and 45.2% of inhabitants posessed VN antibody of 1:8 or over in Ghana and Indonesia after the outbreak. In Japan, however, only a slight increase was found in VN antibody prevalence afterwards. Serologic study showed that 41.5% of horse sera were VN positive at dilutions of 1:8 or more; many cattle sera also had a low VN titer but few cynomologus monkey sera had VN activity.

Acute Disease↗
PubMedDate not supplied

A study of the evolution of coxsackievirus A24 variant in Ghana by viral RNA fingerprinting analysis.

An epidemic of acute haemorrhagic conjunctivitis (AHC) caused by coxsackievirus A24 variant (CA24v) was reported in Accra, Ghana in May 1987. We studied 7 of the viral strains collected from May to November, 1987, by RNA genome fingerprinting. Pairwise comparisons of the oligonucleotide maps showed that genetic similarity among them ranged from between 60.0 to 84.7%. Using base sequence variations deduced from genetic similarity among the isolates, isolation time of the strains and the rate of nucleotide substitution (estimated in a previous paper, Miyamura et al., 1990), we calculated divergence times and constructed a phylogenetic tree. This tree indicated that all the 7 strains had diverged from each other from 11 to 26 months before the AHC epidemic in Accra. CA24v may have been introduced into the country or the neighbouring area, at least, more than two years earlier, i.e. in the early half of 1985.

Adult↗
PubMedDate not supplied

Epidemiology of rubella and congenital rubella infection in Japan.

During the last two decades, the Japanese mainland experienced three rubella epidemics; the first occurred in the latter half of 1960, the second in 1975-1977, and the third in 1981-1982. A retrospective study done after the first outbreak identified 49 newborns with congenital rubella syndrome (CRS). In contrast, the Ryukyu Islands were swept by a rubella epidemic in 1964-1965, and 408 babies with CRS were born, giving an incidence of 20 per 1,000 births. When the 1975-1977 epidemic hit the mainland, a notification system had been established, and two million cases of rubella were reported. In a retrospective survey, only 39 babies with CRS were found. The number of babies with CRS on the mainland was fewer than that observed on the Ryukyu Islands, and clinical illness appeared milder for these two populations than had previously been experienced. These observations seem to support a hypothesis that the teratogenicity of circulating rubella virus is lower in Japan than in the United States.

Abortion, Induced↗
PubMedDate not supplied

Beta 0-thalassemia due to a nonsense mutation at beta 90 (GAG----TAG) in human hemoglobin gene.

We studied a patient with severe anemia and jaundice who exhibited a high hemoglobin A1 (HbA1) level secondary to an increase in HbF despite normal glucose tolerance. The red blood cells showed anisocytosis, poikilocytosis and polychromasia; target cells, Howell-Jolly bodies, Heints bodies and punctate basophilia were observed. No defect or reduction in activity was observed in 19 red cell enzymes. A family history of similar anemia in the patient's daughter and cousins on the mother's side indicated an involvement of genetic factors. Gene cloning and DNA analysis showed that the condition is a new type of beta 0-thalassemia caused by a nonsense mutation (GAG----TAG) in codon 90 of the beta-globin gene.

Adult↗