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PubMedDate not supplied

[Correlation of antigenic properties of influenza viruses of the H3N2 subtype with changes in the amino acid sequence of hemagglutinins].

The effect of amino acid substitutions within the antigenic sites, the residues close to these sites, and the other parts of the hemagglutinin molecule on cross-reactions between influenza subtype H3N2 virus strains in hemagglutination-inhibition tests are considered. Previously we reported a method for calculation of the values of immunochemical cross-reactions between the homologous proteins based on the structural data. On this basis, a method for calculation of the titers of cross-reactions of influenza viruses in hemagglutination-inhibition tests is proposed. The values obtained by this method show a good correlation with the known experimental data. Analysis of the nature of amino acid replacements in region D located in the interface between the hemagglutinin subunits has shown that this region cannot bind with antibodies. The data on the limitation of the resource of the subtype H3N2 variability are presented.

Amino Acid Sequence↗
PubMed1986

Oral rimantadine hydrochloride therapy of influenza A virus H3N2 subtype infection in adults.

In a randomized, double-blind trial involving patients with uncomplicated influenza A H3N2 subtype virus infection, rimantadine treatment (200 mg/day for 5 days) was associated with significant reductions in nasal secretion viral titers (days 2 through 4), maximal temperature (days 2 and 3), time until defervescence (mean, 37 h shorter), and systemic symptoms compared with placebo treatment.

Adamantane↗
PubMed2006

A recombinant pseudorabies virus encoding the HA gene from H3N2 subtype swine influenza virus protects mice from virulent challenge.

The hemagglutinin (HA) gene of A/Swine/Inner Mogolian/547/2001 (H3N2) swine influenza virus (SIV) was recombined into the genome of pseudorabies virus (PRV) Bartha-K61 vaccine strain, generating a recombinant PRV expressing the HA gene, designated as rPRV-HA. One group of 15 mice was inoculated intranasally (i.n.) with 10(5.0) PFU of rPRV-HA, and another two control groups of mice (15 mice per group) were mock-inoculated or inoculated with Bartha-K61. Mice inoculated with rPRV-HA developed hemagglutination inhibition antibodies 3 weeks post-inoculation. Twenty-eight days post-inoculation, all mice were challenged i.n. with 10(5.0) TCID50 of A/Swine/Heilongjiang/74/2000 (H3N2). No challenge virus was isolated from vaccinated mice, and mild pathological lesions were observed only in lungs following challenge. The results demonstrate that the recombinant rPRV-HA expressing the HA gene from H3N2 SIV can protect mice from heterologous virulent challenge, and may represent a candidate vaccine against SIV.

Animals↗
PubMed1982

Prevalence of hemagglutination inhibition antibody to current strains of the H3N2 and H1N1 subtypes of influenza A virus in sera collected from the elderly in 1976.

Sera were collected in 1976 from 182 individuals born between 1876-1935, who included patients in a large local nursing home in Orange County, California, and patients and staff at the University of California, Irvine Medical Center. Sera were treated with receptor-destroying enzyme and assayed for hemagglutination inhibition (HI) antibody to recent strains of influenza A virus. The antigens tested were: A/Victoria/3/76 and A/Texas/1/77 for subtype H3N2; A/New Jersey/8/76, A/X53 and A/Swine/1976 for the A/swine influenza virus-like strains of subtype H1N1; and A/Brazil/11/78, A/Fort Monmouth/1/47 and A/Francis Warren/1/50 for the A/Fort Monmouth/47 virus-like strains of subtype H1N1. For individuals grouped by five- and 10-year intervals of the year of birth, the geometric mean and standard error for HI antibody to each antigen were calculated and plotted vs. date of birth. The results indicate that for a majority of individuals born between 1876-1900, the level of HI antibody would be protective against H3N2 but not against the strains of H1N1. In addition, a majority of individuals born between 1900-1925 had levels of antibody that should be protective against both H3N2 and the A/swine influenza virus-like strains of H1N1 but not against the A/Fort Monmouth/47 virus-like strains of H1N1. These findings could be important when deciding on the antigenic composition of vaccines to be used in those age groups that are most vulnerable to the complications of influenza. In addition, data were obtained that suggest that the A/Fort Monmouth/47 virus-like strains of H1N1 recycle in 35-40 years rather than in 65-70 years as has been demonstrated previously for H2N2 and H3N2.

Aged↗
PubMed2004

Protection of weaned pigs by vaccination with human adenovirus 5 recombinant viruses expressing the hemagglutinin and the nucleoprotein of H3N2 swine influenza virus.

Swine influenza virus (SIV), subtype H3N2, is a recent reassortant virus that emerged in 1998 in North American swine causing severe respiratory and reproductive disease. In this study, two replication-defective adenovirus recombinants were developed as potential vaccines against H3N2 influenza viruses. Three groups of 3-week-old pigs (10 pigs per group) were vaccinated intramuscularly (IM) with the recombinants; one group was vaccinated with the recombinant adenovirus expressing the influenza virus H3 hemagglutinin (HA) protein, one group was vaccinated with the recombinant adenovirus expressing the nucleoprotein (NP), and one group was vaccinated with both recombinants in a mixture. Two additional control groups (10 pigs per group) were included in the animal trial. One control group was challenged with a virulent H3N2 field strain and one control group remained unchallenged. The results showed that pigs in the groups given the recombinant adenovirus expressing HA alone and HA plus NP developed high levels of virus-specific hemagglutination-inhibition (HI) antibody by 4 weeks post vaccination. Pigs in the group vaccinated with both recombinant viruses in a mixture were completely protected. Complete protection was shown by the lack of nasal shedding of virus following challenge and by the lack of lung lesions at 1 week following the challenge infection. Thus, replication-incompetent adenovirus vaccines given simultaneously to pigs are efficacious for SIV and have the additional advantage over commercial vaccines that suckling piglets have no pre-existing maternally-derived antibody to block early life vaccination.

Adenoviridae↗
PubMed1986

Immunogenicity of a single dose of trivalent influenza vaccine including A/Philippines (H3N2): results of a field trial.

During 1982, a new A(H3N2) influenza virus subtype, A/Philippines/2/82, was identified, and this strain was combined with previous A(H1N1) and B influenza virus strains in the trivalent inactivated vaccine recommended for the 1983-1984 influenza season. Prior to the widescale use of this vaccine in Israel, a group of 106 young male soldiers was vaccinated under controlled conditions. Before vaccination, antibody titers greater than or equal to 1:40 were found in 14.1% against A/Philippines (H3N2), 18.1% against A/England/333/80 (H1N1), and 13.3% against B/Singapore/222/79. Two weeks following vaccination, 78.9% of the vaccinees for whom repeated blood samples were available, had antibody titers in this range for A/Philippines (H3N2), 92.9% for A/England (H1N1), and 80.0% for B/Singapore. The vaccine was only mildly reactogenic, and there were no cases of absence from work following vaccination. Thus the antibody response of young subjects to a single dose of a vaccine containing a new A(H3N2) subtype was found to be satisfactory, and the side effects experienced were minimal.

Antibodies, Viral↗
PubMed1995

Comparison of substrate specificities of sialidase activity between purified enzymes from influenza virus A (H1N1 and H3N2 subtypes) and B strains and their original viruses.

Sialidases possessing enzyme activity were solubilized from mouse-adapted influenza viruses A/PR/8/34 (A/PR8, H1N1), A/Guizhou/54/89 (A/Guizhou, H3N2) and B/Ibaraki/2/85 (B/Ibaraki) by proteolytic digestion and purified by affinity chromatography and/or sucrose density gradient centrifugation. The purified sialidases were observed as a single protein band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The optimum pH of purified sialidases from A/PR8, A/Guizhou and B/Ibaraki against sodium p-nitrophenyl-N-acetyl-alpha-D-neuraminate were 6.5, 7.5 and 5.5, respectively. The purified sialidase (N1) from A/PR8 and its original virus showed enzyme activity with similar substrate specificity, and preferentially hydrolyzed alpha (2-->3)sialyllactose and bovine submaxillary mucin (BSM). Purified sialidase from B/Ibaraki hydrolyzed alpha (2-->3)sialyllactose, alpha (2-->6)sialyllactose and most glycoproteins, especially BSM, but the intact virus showed higher sialidase activity against sialyllactoses than against glycoproteins and gangliosides. These results indicate that the purified enzyme and the original virus of B/Ibaraki have different substrate specificities of sialidase activity. Purified A/Guizhou sialidase (N2) hydrolyzed alpha (2-->3)sialyllactose and porcine stomach mucin but not alpha (2-->6)sialyllactose and BSM. The original virus of A/Guizhou showed substrate specificity similar to its purified enzyme, except that the virus was active against BSM.

Hydrogen-Ion Concentration↗
PubMed2005

Evaluation of a recombinant human adenovirus-5 vaccine administered via needle-free device and intramuscular injection for vaccination of pigs against swine influenza virus.

OBJECTIVE: To evaluate the safety and efficacy of a human adenovirus-5 vaccine for protecting weaned pigs against swine influenza virus subtype H3N2 infection when administered via 2 injection methods. ANIMALS: 76 pigs. PROCEDURE: 6 groups of weaned pigs received a 10-fold serial dilution of recombinant adenovirus expressing H3 hemagglutinin and a constant amount of recombinant adenovirus expressing nucleoprotein, either via a needle-free injection device or by traditional IM injection. In each group of 10 pigs, 1 served as a nonvaccinated contact pig to monitor whether there was spread of vaccinial virus from pig to pig. Vaccinated pigs and nonvaccinated controls were challenged or sham-inoculated 5 weeks later. After challenge, pigs were observed for clinical signs and nasal secretions were tested for virus. On day 5 after challenge, pigs were euthanatized; lungs were examined for gross lesions, and bronchoalveolar lavage specimens were tested for virus replication. RESULTS: A hemagglutination inhibition (HI) antibody response was elicited in a dose-dependent manner. Traditional IM administered vaccination induced consistently higher HI antibody responses than vaccination via needle-free injection, but the differences were not significant. Likewise, traditional IM administration was superior at reducing nasal virus shedding except at the highest dose, at which both methods blocked virus replication. The severity of lung lesions was reduced in a dose-dependent manner by both vaccination methods. Sentinel pigs did not seroconvert. CONCLUSIONS AND CLINICAL RELEVANCE: The human adenovirus-5 vaccine at high doses prevented nasal virus shedding after challenge exposure with both methods of administration. The replication-defective vaccine virus was not transmitted to sentinel pigs.

Adenoviridae↗
PubMed2006

Bacterial sinusitis and otitis media following influenza virus infection in ferrets.

Streptococcus pneumoniae is the leading cause of otitis media, sinusitis, and pneumonia. Many of these infections result from antecedent influenza virus infections. In this study we sought to determine whether the frequency and character of secondary pneumococcal infections differed depending on the strain of influenza virus that preceded bacterial challenge. In young ferrets infected with influenza virus and then challenged with pneumococcus, influenza viruses of any subtype increased bacterial colonization of the nasopharynx. Nine out of 10 ferrets infected with H3N2 subtype influenza A viruses developed either sinusitis or otitis media, while only 1 out of 11 ferrets infected with either an H1N1 influenza A virus or an influenza B virus did so. These data may partially explain why bacterial complication rates are higher during seasons when H3N2 viruses predominate. This animal model will be useful for further study of the mechanisms that underlie viral-bacterial synergism.

Animals↗
PubMedDate not supplied

Influenza and respiratory syncytial virus morbidity among 0-19 aged group in Yunus Emre Health Center.

The objective of the study was to determine the morbidity of influenza and respiratory syncytial virus (RSV) infection in the 0-19 years of age group with influenza-like illness among the outpatient cases. From 20 January to 31 March 2003 a total of 123 subjects with upper respiratory tract infection attended Yunus Emre Health Center. Ninety-one subjects fit the case definition of influenza-like illness, which consisted of acute fever of more than 38 degrees C, cough, and sore throat. After obtaining their consent, nasal swabs were taken for isolation of influenza and RSV. Of these, 10 were influenza A virus, 6 were influenza B virus and 20 were RSV. All of influenza virus A was typed as subtype H3N2. The rates of influenza virus among 5-9 and 1-4 years of age groups and of RSV among 1-4 years of age group were high. The average number of absentee days of schoolchildren with influenza was 3.33 days and of those with RSV infection was 1.43 days; this rate was calculated as 2.25 days for the influenza-like illness. Continuous surveillance and influenza vaccination for target groups are recommended for beneficial effects of reducing influenza morbidity and mortality in the community.

Adolescent↗
PubMed1990

Primary structure of the gene coding for the haemagglutinin of influenza virus A/Leningrad/385/80(H3N2): detection of a point mutation responsible for the antigenic drift.

Primary structure of the gene coding for haemagglutinin (HA-gene) of influenza virus A/Leningrad/385/80(H2N2) isolated during the epidemics of influenza in Leningrad in 1980 was determined. The close relationship of HA gene of this virus to the corresponding gene of the virus A/Bangkok/1/79(H3N2) was confirmed. It was shown that a single mutation in an antigenic site (the change from isoleucine to leucine at position 51 of HA1 gene) caused an antigenic drift. One silent mutation was detected (nucleotide 428 of HA1 gene) which points at the relatedness of strains A/Leningrad/385/80 with A/Bangkok/2/79 and with other more recent strains. These data allowed to determine the position of the strain A/Leningrad/385/80 HA gene regarding to the evolutionary relationships of HA genes of influenza A (H3N2 subtype) viruses. The branch leading to the above-mentioned strain is supposed to start from a point common for strains isolated following A/Bangkok/1/79. The mutations of HA genes presented in this subgroup were analysed supporting the notion on limited evolutionary potential of the subtype H3N2 influenza viruses.

Amino Acid Sequence↗