rubella/tyrosine

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A single-amino-acid substitution of a tyrosine residue in the rubella virus E1 cytoplasmic domain blocks virus release.

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Rubella virus particles, consisting of a nucleocapsid surrounded by a lipid envelope in which two virus-encoded glycoproteins E1 and E2 are embedded, assemble on intracellular membranes and are secreted from cells, possibly via the cellular secretory pathway. We have recently demonstrated that the

Microarray profiling analysis uncovers common molecular mechanisms of rubella virus, human cytomegalovirus, and herpes simplex virus type 2 infections in ECV304 cells.

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To study the common molecular mechanisms of various viruses infections that might result in congential cardiovascular diseases in perinatal period, changes in mRNA expression levels of ECV304 cells infected by rubella virus (RUBV), human cytomegalovirus (HCMV), and herpes simplex virus type 2

Protease and helicase domains are related to the temperature sensitivity of wild-type rubella viruses.

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Wild-type rubella viruses grow well at 39°C (non-temperature sensitivity: non-ts), while vaccine strains do not (temperature sensitivity: ts). Histidine at position 1042 of the p150 region of the KRT vaccine strain was found to be responsible for ts, while wild-type viruses had tyrosine at position

Humoral beta-cell autoimmunity is rare in patients with the congenital rubella syndrome.

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The congenital rubella syndrome (CRS) is associated with increased risk for diabetes and thyroid disease. However, the mechanisms by which the rubella virus may cause these diseases are poorly characterized. Previous studies were carried out before modern immunological methods were available. The

Genome-wide SNP associations with rubella-specific cytokine responses in measles-mumps-rubella vaccine recipients.

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Genetic polymorphisms are known to affect responses to both viral infection and vaccination. Our previous work has described genetic polymorphisms significantly associated with variations in immune response to rubella vaccine from multiple gene families with known immune function, including HLA,

[Characteristics of the plasma amino acid spectrum of neonatal intrahepatic cholestasis caused by citrin deficiency].

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OBJECTIVE To investigate the plasma amino acid spectrum in infants more than 1-year-old with neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) in order to identify potential diagnostic markers of NICCD. METHODS Infants less than 1 year of age who had been referred to our hospital

Herpes simplex encephalitis in a patient with a distinctive form of inherited IFNAR1 deficiency

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Inborn errors of TLR3-dependent IFN-α/β- and -λ-mediated immunity in the central nervous system (CNS) can underlie herpes simplex virus 1 (HSV-1) encephalitis (HSE). The respective contributions of IFN-α/β and -λ are unknown. We report a child homozygous for a genomic deletion of the entire coding

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