Such haplotype preferences were consistent among HLA-identical siblings, indicating that the specificity of the T-cell response to influenza virus in association with HLA-A and -B antigens is controlled by genes linked to HLA.
The pattern of virus-immune cytotoxicity among siblings demonstrated T-cell recognition of influenza virus predominantly (greater than 90%) in association with determinants which are coded by genes linked to HLA (P less than 0.0002).
The kinetics of cellular mRNA decay in influenza virus-infected cells have been studied by means of blot hybridization using as probes cloned cDNAs of alpha- and beta-actin, alpha- and beta-tubulin and vimentin.
The kinetics of cellular mRNA decay in influenza virus-infected cells have been studied by means of blot hybridization using as probes cloned cDNAs of alpha- and beta-actin, alpha- and beta-tubulin and vimentin.
In this study, panels of monoclonal antibodies (Mabs) produced against the matrix proteins (M1) of A/WSN and A/PR/8/34 and the nucleoprotein (NP) of A/WSN were assessed for their value in identifying the hosts of origin of the M1 and NP genes in influenza virus isolates and in mapping the proteins' functional domains.
Production of DR3 molecules having the conformation-dependent 16.23 epitope and efficient DR1-restricted presentation of influenza viral epitopes occurred in a B cell line that has a mutation specifically eliminating expression of the TAP1 transporter gene, which is in the approximately 230 kb interval and is needed for production of HLA class I/peptide complexes.
We surveyed 161 clinical isolates of ampicillin-resistant, beta-lactamase-producing isolates of Haemophilus influenzae obtained between 1975 and 1985 to determine whether they produced TEM-1 or Rob beta-lactamase.
The most common cause of ampicillin resistance in Haemophilus influenzae type b is production of TEM-1 beta-lactamase; however, a novel enzyme with a similar substrate profile but a quite different isoelectric point has also been described.
Influenza virus infection has adverse effects on the metabolism of two representative RNA polymerase II transcripts in chicken embryo fibroblasts, those coding for beta-actin and for avian leukosis virus (ALV) proteins.
Influenza virus infection has adverse effects on the metabolism of two representative RNA polymerase II transcripts in chicken embryo fibroblasts, those coding for beta-actin and for avian leukosis virus (ALV) proteins.
Documented ampicillin treatment failures of systemic Haemophilus influenzae type b infections have been associated with synthesis of a TEM-1 beta-lactamase.
For example, the H3N2 virus has been found to be a recombinant deriving seven of its eight genes from an H2N2 strain and gene 4 (which encodes for the HAG) from some other virus, possibly an avian influenza virus of the H3 subtype [1-3].
The frequencies of erythrocyte MNSs antigens and certain histocompatibility leukocyte antigen (HLA) specificities (HLA-A, HLA-B, and HLA-DR) were determined in white patients with meningitis or epiglottitis due to Haemophilus influenzae type b and in controls.
The frequencies of erythrocyte MNSs antigens and certain histocompatibility leukocyte antigen (HLA) specificities (HLA-A, HLA-B, and HLA-DR) were determined in white patients with meningitis or epiglottitis due to Haemophilus influenzae type b and in controls.