Disease relevance of Influenza A Virus, H3N2 Subtype

• By complementation tests against a set of prototype WSN ts mutants with a defined genetic lesion, the ts lesion of two H3N2 viruses (HK/8/68 and Xia-ts) was located on the NP gene and that of two H1N1 viruses (Tianjin/78/77 and Beijing/1/79) was located on the M protein gene [1].
• Antibodies to type A influenza virus matrix protein (M) were assayed by single radial diffusion in 180 paired sera of volunteers challenged intranasally with live H3N2 viruses of varying degrees of virulence [2].
• Virulence of rimantadine-resistant human influenza A (H3N2) viruses in ferrets [3].
• All clinical isolates of influenza A viruses from patients in Huntington, West Virginia, during the decade 1978-1988 were tested, and 65 of 65 H1N1 and 176 of 181 H3N2 viruses were susceptible to the antiviral action of amantadine and rimantadine [4].
• The matrix (M) protein of the H2N2 virus A/Ann Arbor/6/60 may be distinguished from M protein of several H3N2 viruses and A/New Jersey/76 (HSWINI) by SDS acrylamide gel electrophoresis using a discontinuous buffer system [5].

High impact information on Influenza A Virus, H3N2 Subtype

• Point mutations were introduced into the epitopes derived from the NP and PA such that they no longer bound the presenting H2Db MHC class I glycoprotein, and reassortant H1N1 and H3N2 viruses were made by reverse genetics [6].
• METHODS: Ten influenza A (H3N2) viruses isolated during the outbreaks were examined for resistance to amantadine and rimantadine by means of an enzyme immunoassay and by sequencing of the viral nucleic acid that encodes the transmembrane domain of the M2 protein [7].
• The seroreactivity levels in swine serum samples and the nucleotide sequences of six additional 1999 isolates, all of which were of the triple-reassortant genotype, suggested that H3N2 viruses containing avian PA and PB2 genes had spread throughout much of the country [8].
• Antibodies to neuraminidase may contribute to the enhanced uptake of viruses of a different subtype, because N2-specific monoclonal antibodies augmented the uptake of both A/Japan/305/57 (H2N2) and A/Port Chalmers/1/73 (H3N2) viruses [9].
• Ferrets as a transmission model for influenza: sequence changes in HA1 of type A (H3N2) virus [10].

Chemical compound and disease context of Influenza A Virus, H3N2 Subtype

• Reactogenicity and immunogenicity of parenteral monovalent influenza A/Victoria/3/75 (H3N2) virus vaccine in healthy adults [11].
• T cell lines, established from mice primed by intranasal infection with X31 (H3N2) virus, were cross-stimulated with natural variant viruses of known primary sequence (either A/TEXAS/1/77 or A/ENG878/69) and proliferating cells eliminated by treatment with the cell cycle-specific drug 5-bromodeoxyuridine [12].
• Thirty-nine influenza A (H1N1) and (H3N2) virus isolates were examined for their susceptibility to amantadine in allantois-on-shell (AOS) cultures [13].
• The smallest RNA (RNA 8) of the A/Ann Arbor/6/60 virus may be distinguished from RNA 8 of several H3N2 viruses by acrylamide gel electrophoresis in 3% or 3-6% gels in the absence of urea, if electrophoresis is done at 30 to 36 degrees C or 20 degrees C respectively [5].
• When subjected to electrophoresis at 33 degrees C in 3% polyacrylamide gels with no urea added, the nucleoprotein and neuraminidase genes of an H2N2 and H3N2 virus migrate as RNA bands 5 and 6 respectively [14].

Biological context of Influenza A Virus, H3N2 Subtype

• Vaccines were equally antigenic, and delineation of antibody specificities revealed antibody cross-reacting with A/Hong Kong/68 (H3N2) virus in all sera [15].
• Amino acid sequence identity between the HA1 of influenza A (H3N2) viruses grown in mammalian and primary chick kidney cells [16].

Anatomical context of Influenza A Virus, H3N2 Subtype

• These results indicate that SP-A mediates internalization of FITC-labeled influenza A (H3N2) virus by alveolar macrophages [17].
• Therefore, we have studied the induction of IFN in cultures of human leukocytes exposed under standardized conditions to various concentrations of adenovirus type 7A, coronavirus 229E, an influenza type A virus (H3N2), a rhinovirus, and respiratory syncytial virus (RSV) [18].

Gene context of Influenza A Virus, H3N2 Subtype

• In contrast to the well-characterized laboratory strain A/PR/8/34, several, but not all, recent isolates of H3N2 viruses resulted in moderate IFN-beta stimulation [19].
• Twenty-six infants from whom cord sera were available had culture-documented infections with influenza A/Victoria (H3N2) virus when younger than four months [20].
• Infection with influenza H3N2 viruses circulating during this study occurred with comparable low frequency in CF patients after ca (14 infections/100 subject-years of observation) or triv vaccine (10 infections/100 subject-years of observation) [21].
• The H3N2 viruses presently circulating in the U.S. swine population are triple reassortants containing avian-like (PA and PB2), swine-like (M, NP, and NS), and human-like (HA, NA, and PB1) gene segments [22].
• The California (H1N1) strain isolated in 1978 had acquired by reassortment the NP gene of a human H3N2 virus circulating at about 1977 as had been previously suggested by investigations involving RNase fingerprint or hybridization techniques [23].

Analytical, diagnostic and therapeutic context of Influenza A Virus, H3N2 Subtype

• When the TR FIA was performed with 96 nasopharyngeal aspirate specimens collected during outbreaks of influenza A (H3N2) virus and the results were compared with serodiagnosis results with paired sera, the specificity and sensitivity of TR FIA for the demonstration of influenza A infections were 95 and 85%, respectively [24].
• The optimal conditions required to obtain the maximum recovery of HA and NA activity from purified influenza X47 (H3N2) virus concentrate after treatment with Empigen, and the nature and the morphological appearance of the Empigen-treated preparations both before and following a sucrose density gradient purification step, are described [25].
• The NA genes of H3N2 viruses used for primary infection or vaccination showed higher amino acid homology with H1N2 (88.3-92.6%), while nucleoprotein (95.5-96.3% nucleotide identity) and matrix (96.8-98.4%) genes were most conserved between the three subtypes [26].
• Healthy, nonsmoking, young adult volunteers who were seronegative to influenza A/Korea/82 (H3N2) virus were randomly assigned to breathe either filtered clean air (control group) or NO2 for 2 h/day for 3 consecutive days [27].

References