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Novel BTK mutation presenting with vaccine-associated paralytic poliomyelitis.

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Oral polio vaccine (OPV) has been used safely and efficiently for more than 40 years in preventive medicine. Vaccine-associated paralytic poliomyelitis (VAPP) is a rare adverse event of OPV due to reversion of the vaccine strain virus to a neurovirulent strain. VAPP can occur in healthy recipients

[The oldest case with X-linked agammaglobulinemia in Japan lacking Bruton-type tyrosine kinase protein detected by flow cytometry].

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We report a case of sporadic X-linked agammaglobulinemia previously diagnosed as variable immunodeficiency (VID). An 39-year-old male had recurrent episodes of respiratory tract infection since his early childhood. At the age of four, he developed partial paresis of the left limbs after polio

Survival of wild polio by a patient with XLA.

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BACKGROUND X-linked agammaglobulinemia (XLA) is a primary immunodeficiency characterized by failure of B-cell differentiation and hypogammaglobulinemia. In addition to being susceptible to bacterial infections, patients with XLA are also susceptible to enteroviruses. Systemic enterocytopathogenic

O4-(5'-uridylyl)tyrosine is the bond between the genome-linked protein and the RNA of poliovirus.

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Virion RNA of poliovirus type 1 has been analyzed for the linkage between genome-protein VPg and the polyribonucleotide chain. Hydrolysis of the linkage with acid or alkali and enzymatic degradation lead to the conclusion that the bond is neither a phosphodiester such as nucleotidyl-(P-O)-serine (or

Studies on the attenuation phenotype of polio vaccines: poliovirus RNA polymerase derived from Sabin type 1 sequence is temperature sensitive in the uridylylation of VPg.

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Determinants of temperature sensitivity and/or attenuation in Sabin type 1 poliovirus reside in the 5' NTR and coding sequences of the capsid proteins and viral RNA polymerase, 3D(pol). Previous studies have implicated at least two mutations in 3D(pol) of Sabin 1 vaccine strain [PV1(S)], including a

Stable isotope labeling by amino acids in cell culture and differential plasma membrane proteome quantitation identify new substrates for the MARCH9 transmembrane E3 ligase.

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The regulation of cell surface receptor expression is essential for immune cell differentiation and function. At the plasma membrane ubiquitination is an important post-translational mechanism for regulating expression of a wide range of surface proteins. MARCH9, a member of the RING-CH family of

[Clinical features of X-linked agammaglobulinemia: analysis of 8 cases].

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OBJECTIVE X-linked agammaglobulinemia (XLA), caused by mutations in Bruton's tyrosine kinase (BTK), is a common form of inherited antibody deficiency. There were very few case reports of this disease that were diagnosed only based on clinical findings in China. The purpose of this study was to

An aspartic acid at amino acid 108 is required to rescue infectious virus after transfection of a poliovirus cDNA containing a CGDD but not SGDD amino acid motif in 3Dpol.

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The poliovirus RNA-dependent RNA polymerase (3Dpol) contains a region of homology centered around the amino acid motif YGDD (amino acids 326 to 329), which has been postulated to be involved in the catalytic activity of the enzyme. Previous studies from this laboratory have used oligonucleotide

[Characteristics of an enzyme hydrolyzing the covalent bond between RNA and protein VPg of the encephalomyocarditis virus].

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The enzyme termed by us as uridilylpolynucleotide-(5'P----O)-tyrosine phosphodiesterase (Y-pUpN PDE) was isolated from mouse ascites Krebs II cells by ion-exchange and affinity chromatography. The enzyme was found to specifically split the natural covalent bond between VPg and EMC or polio viral

A Btk transgene restores the antiviral TI-2 antibody responses of xid mice in a dose-dependent fashion.

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X-linked agammaglobulinemia in humans and X-linked immunodeficiency (xid) in mice are both caused by mutations in Bruton's tyrosine kinase (Btk). Xid mice lack the early T cell-independent type 2 (TI-2) antibody response to polio virus and to a recombinant vaccinia virus (Vacc-IND-G) expressing the

Enterovirus infection may induce humoral immune response reacting with islet cell autoantigens in humans.

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Molecular mimicry is one of the mechanisms by which enterovirus infections have been postulated to have a role in the pathogenesis of type 1 diabetes. Immunogenic epitopes in enterovirus capsid protein VP1 and procapsid protein VP0 have sequence similarities with diabetes-associated epitopes in

Clinical approach to the weak patient in the intensive care unit.

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Motor weakness in a patient in the intensive care unit (ICU) may be related to (1) pre-existing neuromuscular disorder that leads to ICU admission, (2) new-onset or previously undiagnosed neurological disorder, or (3) complications of non-neuromuscular critical illness. Neuromuscular syndromes

Poliovirus entry into human brain microvascular cells requires receptor-induced activation of SHP-2.

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Viruses use specific receptor molecules to bind selectively to target cells. Receptors have often been considered as mere docking sites, but they may also possess intrinsic signaling capacities that serve to prime the cell for entry and infection. Poliovirus (PV) initiates infection by binding to

Comparison of Common Monogenic Defects in a Large Predominantly Antibody Deficiency Cohort.

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BACKGROUND Predominantly antibody deficiencies (PADs) are the most common primary immunodeficiencies, characterized by hypogammaglobulinemia and inability to generate effective antibody responses. OBJECTIVE We intended to report most common monogenic PADs and to investigate how patients with PAD who

X-linked agammaglobulinemia. A clinical and molecular analysis.

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X-linked agammaglobulinemia (XLA), characterized by a profound deficiency of B lymphocytes due to an arrest in B lymphocyte development, is caused by mutations in the gene encoding Btk (Bruton tyrosine kinase). The BTK gene has been cloned and the genomic organization determined. BTK codes for 19

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