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Biomedical subjects

R Yanagihara

Publications and source records attributed to R Yanagihara.

At least 145 records · Page 8Linked to original sources
PubMed1988

Leakey virus: a new hantavirus isolated from Mus musculus in the United States.

A hantavirus, designated Leakey virus, was isolated from a Mus musculus captured in Real County, Texas, U.S.A. in August 1986. Virus-specific fluorescence was first detected 13 days after inoculation of Vero-E6 cells with spleen tissue from the seropositive M. musculus. Ultrastructurally, the new isolate resembled other hantaviruses. Leakey virus induced a fatal meningoencephalitis in infant Fischer rats, with viral antigen detectable in brain, lung, liver, kidney and spleen. Serum dilution, plaque reduction neutralization tests indicated that Leakey virus was antigenically distinct from Hantaan, Seoul, Puumala and Prospect Hill viruses, and therefore constitutes a new serotype.

Animals↗
PubMed1988

Tubulovesicular structures in experimental Creutzfeldt-Jakob disease and scrapie.

Tubulovesicular structures, measuring 20-50 nm in diameter, were found in dilated neuronal processes in brains from mice infected with the Fujisaki strain of Creutzfeldt-Jakob disease virus. These particles were similar to those observed in brains from hamsters infected with scrapie. These structures are consistently present in naturally occurring and experimentally induced spongiform encephalopathies, irrespective of the host species or virus strain. Their role in pathogenesis is undetermined.

Animals↗
PubMed1987

Serological survey of Prospect Hill virus infection in indigenous wild rodents in the USA.

We found serological evidence of infection with Prospect Hill virus, a Hantaan-like virus isolated from meadow voles (Microtus pennsylvanicus), in microtine and cricetid rodents trapped in Maryland, West Virginia, Minnesota and California, USA. Fluorescent antibodies were detected in sera from M. pennsylvanicus (74/277), M. californicus (39/185), Clethrionomys gapperi (5/51), Peromyscus maniculatus (4/22) and P. truei (1/11). Sera from seropositive P. maniculatus contained neutralizing antibodies against Prospect Hill virus, confirming that infection with Prospect Hill virus or antigenically related viruses is not restricted to microtine rodents in the USA. Despite the widespread distribution of Prospect Hill virus in indigenous rodents, the recent demonstration that American mammalogists are only rarely infected supports the view that the overall risk of Prospect Hill virus infection in man is low.

Animals↗
PubMed1987

Intra-blood-brain barrier synthesis of human immunodeficiency virus antigen and antibody in humans and chimpanzees.

The presence of human immunodeficiency virus (HIV) antigens in cerebrospinal fluid (CSF) was associated with progressive encephalopathy in adult and pediatric patients with acquired immunodeficiency syndrome (AIDS). HIV antigen was detected in CSF from 6 of 7 AIDS patients with progressive encephalopathy. By contrast, HIV antigen, whether free or complexed, was detected in CSF from only 1 of 18 HIV antibody seropositive patients without progressive encephalopathy and from 0 of 8 experimentally infected chimpanzees without clinical signs. Intra-blood-brain barrier synthesis of HIV-specific antibody was demonstrated in the majority of patients with AIDS (9/12) or at risk for AIDS (8/13) as well as in the experimentally infected chimpanzees, indicating HIV-specific B-cell reactivity in the brain without apparent neurological signs. In 6 of 11 patients with HIV infection, antibodies synthesized in the central nervous system were directed against HIV envelope proteins. Active viral expression appears to be necessary for both the immunodeficiency and progressive encephalopathy associated with HIV infection.

AIDS-Related Complex↗
PubMed1987

Morphology and morphogenesis of viruses of hemorrhagic fever with renal syndrome. II. Inclusion bodies--ultrastructural markers of hantavirus-infected cells.

Three distinctive types of viral inclusion bodies were identified in hantavirus-infected cells by thin-section electron microscopy. The inclusion bodies, designated granular, granulofilamentous, and filamentous, were intracytoplasmic and closely associated with the rough endoplasmic reticulum and Golgi cisternae. Virus specificity of the inclusions was verified by immune colloidal gold and immunoperoxidase labeling. The inclusion bodies were a common morphological marker for 13 strains of hantaviruses studied, irrespective of their origin.

Animals↗
PubMed1986

Pathogenesis of experimental Hantaan virus infection in laboratory rats.

Weanling Fischer rats inoculated intramuscularly with Hantaan virus (strain 76-118) developed subclinical infections characterized by transient viremia and shedding of virus in saliva, persistence of virus in lung, pancreas, spleen and liver, and development of fluorescent and neutralizing antibodies in serum with immune complex deposition in lung. Viremia and virus shedding in saliva occurred 10 to 13 days after inoculation. Horizontal intracage transmission of infection occurred between 35 and 63 days post-inoculation, long after disappearance of virus in oropharyngeal secretions and blood. Multiple attempts to demonstrate infectious virus in feces and urine during this period were unsuccessful. The inability to detect virus in urine samples of experimentally infected rats may have resulted from intermittent or low-titered viruria. This contrasts sharply with the prolonged high-titered viruria reported in striped field mice (Apodemus agrarius) infected with Hantaan virus, suggesting differences in the mode(s) of virus transmission in nature.

Animals↗
PubMed1986

Collagenase activity in skin fibroblasts of patients with amyotrophic lateral sclerosis.

In the current study we have measured collagenase activity released from skin explants and fibroblasts of patients with both Guam-type and sporadic amyotrophic lateral sclerosis and controls. The rationale for such a study derives from work reported more than 20 years ago demonstrating abnormalities in skin collagen metabolism in patients with the disease. We were not able to find significant differences in collagenase activity when fibroblasts were compared relative to the total protein secreted. This is explained, in part, by our finding of an increase in total protein released from fibroblasts of the amyotrophic lateral sclerosis patient group. Increased collagenase release did occur when activity was expressed per number of cells plated but was not statistically significant. In addition, increased release followed a 3-day lag period in skin organ culture. These results suggest that collagenase and other enzymes known to activate collagenase, such as plasminogen activator, capable of degrading extracellular matrix components might be responsible for the increased collagenolytic activity previously observed in amyotrophic lateral sclerosis patients' skin. Further evaluation of extracellular-acting degradative enzymes from skin, muscle, nerve and central nervous system may be important to follow-up such leads in understanding the pathogenesis of this enigmatic and fatal disorder.

Amyotrophic Lateral Sclerosis↗
PubMed1986

Amyotrophic lateral sclerosis and parkinsonism-dementia on Guam: a 30-year evaluation of clinical and neuropathologic trends.

We reviewed the records of 279 Guamanian Chamorro patients with amyotrophic lateral sclerosis (ALS) and 293 patients with parkinsonism-dementia (PD), who had onset of symptoms between 1950 and 1979, to determine if there were changes in the clinical and neuropathologic features that might clarify the declining incidence rates in the past decade. There were no major temporal changes in the frequencies of physical findings or histopathologic features, but in the past three decades, an increase in age at onset was observed for both ALS and PD. There was also a shorter duration of illness in ALS and a longer duration in PD. Good correlation was found between the clinical and pathologic findings for both ALS and PD throughout this period.

Amyotrophic Lateral Sclerosis↗
PubMed1985

Differential susceptibility and resistance of immunocompetent and immunodeficient mice to fatal Hantaan virus infection.

Susceptibility and resistance to fatal Hantaan virus meningoencephalitis were studied in immunocompetent (nu/+) and congenitally T-cell deficient (nu/nu) CD-1 mice of different ages. Susceptibility of nu/+ mice to fatal infection was age-dependent, as evidenced by 100 percent mortality in mice inoculated intracerebrally with Hantaan virus (strain 76-118) during the first week of life, 60 percent mortality in mice inoculated at 9 days of age, and no disease or death in mice inoculated at 14 to 42 days of age. Deaths occurred significantly earlier in nu/+ mice inoculated at 5 and 7 days of age than in nu/+ mice less than 24 hours old. Nu/nu littermates of the same age did not exhibit a similar inverse relationship between age and survival times. Moreover, nu/nu mice 14 days or older remained susceptible, albeit with delayed onset of illness and time of death. Virus titers in brain tissues of nu/+ mice inoculated at 7 days and of nu/nu mice inoculated at 7, 9 and 14 days of age were nearly identical. In older nu/+ mice, peak virus titers were comparatively lower, but they did not seem to be influenced by the magnitude of the neutralizing antibody response. The more rapidly fatal course in nu/+ mice inoculated at a week of age than at birth, and the differential resistance between weanling nu/+ and nu/nu mice to Hantaan virus meningoencephalitis suggest that cell-mediated immunity may be responsible for both enhancement of disease and recovery from infection.

Age Factors↗
PubMed1985

Immune spleen cell-mediated protection against fatal Hantaan virus infection in infant mice.

To clarify the basis of the age-dependent susceptibility of infant mice to fatal meningoencephalitis caused by Hantaan virus, we investigated the ability of spleen cells from immune and nonimmune weanling BALB/c mice to confer protection to syngeneic infant mice. Intraperitoneal transfer of 10 X 10(7), 5 X 10(7), 2.5 X 10(7), and 1.2 X 10(7) immune spleen cells to infant mice 24 hr after intracerebral challenge with 100 50% lethal doses of Hantaan virus (strain 76-118) resulted in 100%, 70%, 64%, and 30% protection, respectively. Even as late as 48 hr after virus challenge, transfer of 10 X 10(7) immune spleen cells conferred complete protection. In contrast, nonimmune spleen cells offered no protection, even when cells were transferred 48 hr before virus challenge. The protective capacity of immune spleen cells was abolished following treatment with antibody to theta antigen and guinea pig complement, but was preserved after the depletion of B cells, a result suggesting that T cells play a crucial role in the resistance of mice to fatal Hantaan virus infection.

Aging↗
PubMed1985

Serotypic classification of hantaviruses by indirect immunofluorescent antibody and plaque reduction neutralization tests.

Antisera prepared against 16 strains of hantaviruses isolated from patients with hemorrhagic fever with renal syndrome (HFRS) or from rodents captured in HFRS-endemic and nonendemic regions were titrated against Hantaan virus strain 76-118, Puumala virus strain Sotkamo, and Prospect Hill virus strain Prospect Hill-I by using the indirect immunofluorescent antibody and plaque reduction neutralization tests. Isolates fell into one of four distinct groups or serotypes. Serotype 1 included Apodemus-derived strains, serotype 2 included Rattus-derived strains, serotype 3 included Clethrionomys-derived strains, and serotype 4 included Microtus-derived strains. Serotypic classification of hantavirus infections was possible for humans and rodents in widely varied geographical areas, but in a few instances, sera from patients with HFRS did not conform to any of the four serotypes, suggesting the existence of as yet unidentified serotypes. A definitive serological classification of hantaviruses must await analysis of additional virus isolates.

Animals↗
PubMed1985

Propagation of nephropathia epidemica virus in Mongolian gerbils.

Nephropathia epidemica virus, the etiological agent of hemorrhagic fever with renal syndrome in Scandinavia, was serially propagated in Mongolian gerbils (Meriones unguiculatus). Intracerebrally inoculated suckling gerbils developed subclinical infections, with viral antigen found in lung, brain, liver and spleen. The distribution of viral antigen was similar to that seen in experimentally infected bank voles (Clethrionomys glareolus), the principal wild rodent reservoir of nephropathia epidemica virus. This model provides a readily available animal host for the study of experimental nephropathia epidemica virus infection.

Animals↗
PubMed1985

Experimental infection with Puumala virus, the etiologic agent of nephropathia epidemica, in bank voles (Clethrionomys glareolus).

Subclinical chronic infections characterized by transient viremia, prolonged virus shedding in oropharyngeal secretions and feces, and virus persistence in tissues (particularly lung) developed in laboratory-bred weanling bank voles (Clethrionomys glareolus) inoculated intramuscularly with Puumala virus (strain Hällnäs), the etiologic agent of nephropathia epidemica. Viral antigen, as evidence by granular fluorescence, was detected in the lungs, liver, spleen, pancreas, salivary glands, and small intestine. Infectious virus was found in the lungs from 14 to 270 days postinoculation, and feces and urine collected 35 to 130 days postinoculation were regularly and sporadically infectious, respectively. Horizontal transmission coincided with virus shedding in oropharyngeal secretions. Suckling voles also developed asymptomatic persistent infections after intracerebral inoculation, and histopathological changes were absent despite widespread infection. Our data resemble findings in Apodemus agrarius experimentally infected with Hantaan virus, the prototype virus of hemorrhagic fever with renal syndrome, suggesting that the mechanisms of maintenance and transmission of Puumala and Hantaan viruses are similar in their respective wild-rodent hosts.

Animals↗
PubMed1985

Disappearance of high-incidence amyotrophic lateral sclerosis and parkinsonism-dementia on Guam.

The high incidence rates of amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD) occurring among the Chamorros of Guam have declined to rates only slightly higher than those observed in the continental United States. This decline has occurred principally among males, especially those born after 1920 and living in areas where calcium and magnesium levels are low in soil and water. The male-to-female ratio among affected patients now approaches unity, compared with ratios of 2 to 1 for ALS and 3 to 1 for PD three decades ago. These changes are consistent with the hypothesis that the previously high incidence resulted from defects in mineral metabolism and secondary hyperparathyroidism, provoked by nutritional deficiencies of calcium and magnesium, with resultant deposition of calcium and aluminum in neurons.

Adult↗