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S M Matsui

Publications and source records attributed to S M Matsui.

29 records · Page 2Linked to original sources
PubMed1992

Astroviruses and caliciviruses: emerging enteric pathogens.

Acute, infectious gastroenteritis is an extremely common disease that contributes significantly to morbidity and mortality worldwide. In the United States, it is the second most frequent illness encountered in families. While this illness generally runs a self-limited course, it may be temporarily incapacitating and impact substantially on numbers of days lost from work or school. At present, 30-40% of infectious gastroenteritis cases in the United States are attributable to viral agents, while 20-30% are due to bacteria and parasites. These estimates are almost certainly low, since the cause of gastroenteritis is not discernible in approximately 40% of the cases, and gastroenteritis may be caused by viruses or other pathogens that cannot be identified at this time. Rotavirus and enteric adenovirus are two of the most prevalent and well-studied of the viral agents and have been reviewed extensively elsewhere. This review focuses on two broad groups of small round structured viruses (SRSV), astroviruses and caliciviruses (classic, Norwalk, and Norwalk-like). Although recognized in association with acute, nonbacterial gastroenteritis since the early 1970s, the study of these viruses has been hampered by the relatively low levels of viral shedding in feces, difficulty in propagating the virus in cell or organ culture, and the lack of widely available, well-standardized reagents for their detection. In spite of these obstacles, much has been learned about these viruses using standard virologic (electron microscopy, biophysical characterization, immunoassays) and epidemiologic methods. More recently, substantial progress has been made in studying astroviruses and caliciviruses at the molecular level. Molecular techniques are now being used as diagnostic aids to characterize the epidemiology of these agents in greater detail.

Animals↗
PubMed1991

The isolation and characterization of a Norwalk virus-specific cDNA.

Norwalk virus, an important cause of epidemic, acute, nonbacterial gastroenteritis in adults and children, has eluded adaptation to tissue culture, the development of an animal model, and molecular cloning. In this study, a portion of the Norwalk viral genome encoding an immunoreactive region was cloned from very small quantities of infected stool using sequence-independent single primer amplification. Six overlapping complementary DNA (cDNA) clones were isolated by immunologic screening. The expressed recombinant protein from a representative clone reacted with six of seven high titer. Norwalk-specific, postinfection sera but not with corresponding preinfection sera. Nucleic acid sequence for all clones defined a single open reading frame contiguous with the lambda gt11-expressed beta-galactosidase protein. Only oligonucleotide probes specific for the positive strand (defined by the open reading frame) hybridized to an RNaseA-sensitive, DNaseI-resistant nucleic acid sequence extracted from Norwalk-infected stool. Furthermore, RNA extracted from serial postinfection, but not preinfection, stools from three of five volunteers hybridized to a Norwalk virus cDNA probe. Clone-specific oligonucleotide probes hybridized with cesium chloride gradient fractions containing purified Norwalk virion. In conclusion, an antigenic, protein-coding region of the Norwalk virus genome has been identified. This epitope has potential utility in future sero- and molecular epidemiologic studies of Norwalk viral gastroenteritis.

Amino Acid Sequence↗
PubMed1990

Sequence analysis of gene 11 equivalents from "short" and "super short" strains of rotavirus.

The molecular basis for the aberrant migration pattern of the gene 11 equivalent in rotaviruses with "short" (human DS-1) and "super short" (human 69M and bovine VMRI) electropherotypes was investigated. The mRNAs of these viruses were synthesized in vitro, and the entire gene 11 equivalent of each of these viruses was sequenced with specific synthetic oligonucleotide primers. These sequences were compared with previously published sequences of "long" pattern rotavirus gene 11 segments. The increased lengths of the gene 11 equivalents of DS-1, 69M, and VMRI are due to a prolonged, 3' untranslated region in this gene segment. The 3' untranslated region of the VMRI gene 11 equivalent contains a clear duplication of a portion of its coding sequence. A stretch of 18 consecutive nucleotides within the 330-nucleotide, 3' untranslated region of 69M is identical to a section of UK coding sequence. The DS-1 and the remainder of the 69M 3'-end additional sequences are similar to each other, but neither is similar to any other currently available rotavirus gene sequence. This finding suggests that a process other than homologous duplication is involved in the evolution of these sequences. The widespread occurrence of human and animal rotaviruses with short and super short electropherotypes provides evidence that intragenic and possibly intergenic recombinational events associated with an error-prone viral RNA polymerase may play a role in increasing the genetic repertoire of rotaviruses.

Amino Acid Sequence↗
PubMed1989

Passive protection against rotavirus-induced diarrhea by monoclonal antibodies to the heterotypic neutralization domain of VP7 and the VP8 fragment of VP4.

A murine model was used to determine whether neutralizing monoclonal antibodies (MAbs) with heterotypic specificity directed to VP7 (MAb 57-8) or to the VP8 fragment of VP4 (MAb M14) passively protect mice against challenge with various strains of rotavirus. (The gene 4 product, an outer capsid protein, has traditionally been called VP3. It has been proposed, however, that the rotavirus gene 4 product be named VP4. The gene 3 product, a core protein, has been identified recently and named VP3 [M. Liu, P. A. Offit, and M. K. Estes, Virology 163:28-32, 1988]). Suckling mice orally inoculated with MAb 57-8 did not develop diarrhea when challenged with virulent serotype 3, 4, or 6 rotaviruses, while those inoculated with MAb M14 were passively protected from challenge with serotype 3 or 6 rotaviruses, as predicted by in vitro neutralization tests. These MAbs, however, did not protect mice from infection when the mice were challenged with rotaviruses of other serotypes. We conclude that specific neutralization epitopes on each surface protein are capable of mediating protection against one or several rotavirus serotypes.

Animals↗
PubMed1988

Characterization of homotypic and heterotypic VP7 neutralization sites of rhesus rotavirus.

The gene 9 nucleotide sequence was determined for rhesus rotavirus and each of 14 viral variants selected for their resistance to neutralizing monoclonal antibodies. Each variant contains a single gene 9, VP7, mutation which permits viral growth in the presence of the antibody. Variant mutations were identified in two distinct neutralization regions. Region A was identified by monoclonal antibodies that are involved in both serotype-specific and serotype cross-reactive neutralization. Region C was identified by serotype-specific neutralizing monoclonal antibodies. Heterotypic neutralizing monoclonal antibody 57-8 selected variants with a mutation at amino acid 94 in the A region, the same amino acid location selected by serotype-specific monoclonal antibodies. Monoclonal antibody 3 selected a VP7 mutation at amino acid 99 resulting in additional N-linked glycosylation of the VP7 protein. Despite the added VP7 glycosylation, variant v3 was not broadly resistant to additional VP7-specific neutralizing monoclonal antibodies.

Amino Acid Sequence↗
PubMed1988

The rhesus rotavirus gene encoding protein VP3: location of amino acids involved in homologous and heterologous rotavirus neutralization and identification of a putative fusion region.

The complete gene 4 nucleotide sequence was determined for rhesus rotavirus and each of 11 viral variants selected by neutralizing monoclonal antibodies. Gene 4 is 2362 bases in length and encodes a protein, VP3, of 776 amino acids with a calculated Mr of 86,500. A conserved trypsin cleavage site, located at amino acid 247, divides VP3 into VP8 and VP5. Neutralizing monoclonal antibodies directed at VP3 were used to select variants that escaped neutralization. Each variant contains a single gene 4 mutation that permits viral growth in the presence of the antibody. Variant mutations were identified in six distinct neutralization regions in VP8 and VP5. Five of the six neutralization regions were found in VP8. The VP8 regions were primarily associated with strain-specific or limited heterotypic rotavirus neutralization. One region was identified in VP5 by three monoclonal antibodies that neutralize a broad range of rotavirus serotypes. The VP5 neutralization region is largely hydrophobic and is similar to putative fusion sequences of Sindbis and Semliki Forest viruses.

Amino Acid Sequence↗
PubMed1983

The natural history of the inherited methylmalonic acidemias.

Six biochemical and genetic forms of methylmalonic acidemia have been defined previously: two (mut degrees and mut-) resulting from defects in the mutase apoenzyme, and four (cbl A, cbl B, cbl C, and cbl D) resulting from deficient adenosylcobalamin synthesis. We retrospectively surveyed the clinical presentation, response to cobalamin supplementation, and long-term outcome in the four most prevalent mutant classes by collecting detailed information on 45 patients (15 mut degrees, 5 mut-, 14 cbl A, and 11 cbl B). Most patients presented acutely with a common set of clinical and laboratory findings; however, there were significant differences between mutant classes: mut degrees patients presented earlier in infancy than did cbl A and cbl B patients; in response to cobalamin supplements, marked decreases in the concentration of methylmalonic acid in blood or urine were reported in most cbl A patients and in nearly half the cbl B patients, but not in mut degrees or mut- patients; and finally, most cbl A, cbl B, and mut- patients were still living, whereas most mut degrees patients died during the first few months of life. Our data indicate that genotypic classification of the methylmalonic acidemias has prognostic and therapeutic use as well as diagnostic value.

Amino Acid Metabolism, Inborn Errors↗