Search

New technologies now enable virologists to study small genetic and antigenic differences between field isolates of animal viruses at a higher level of discrimination than has been possible using conventional serological techniques. The most important of the laboratory techniques revolve around the use of monoclonal antibodies, peptide mapping, fingerprinting of whole RNA virus genomes, RNA:RNA hybridization, ‘electropherotyping’ of virus RNA or polypeptides, restriction enzyme analysis of virus DNA genomes, cloning of genes and rapid sequencing of viral DNAs and RNAs, in the latter case using primer extension techniques (reviewed by Palese & Roizman, 1980). From a practical point of view, genetic and phenotypic heterogeneity among viruses may be of considerable importance in attempts to control certain virus diseases by chemo- or immunoprophylaxis. [ABSTRACT FROM PUBLISHER]

Four antigenic variants of the neuraminidase (NA) of A/Texas/77 (H3N2) virus were selected using monoclonal antibody at a frequency of one variant in 105 parental virions. The antigenic variants failed to react serologically with the monoclonal antibody used for their selection in vitro. The antigenic variants failed also to react serologically with a proportion of sera from children and adults although all of the sera reacted with the parental A/Texas/77 virus. Thus, certain human sera have a restricted antibody repertoire to influenza NA antigen which might enable virus antigenic variants to avoid anti-NA antibody-mediated neutralization in nature. [ABSTRACT FROM PUBLISHER]

A newly developed lectin neuraminidase test (LNT) and a panel of mouse monoclonal and post-infection ferret antibodies have been used to analyse antigenic drift in N1 neuraminidases of influenza A viruses isolated between 1933 and 1957 and also between 1977 and 1980. Significant antigenic differences were detected among the ‘early’ (1933–57) viruses since the NA of viruses isolated one year apart could be distinguished serologically. The NA ofthe ‘re-emerged’ virus A/USSR/92/77 (H1N1) was antigenically related but not identical to influenza A viruses isolated in 1949 (A/Paris/49 (H1N1), A/Geneva/49 (H1N1)) which thus predates the previously observed antigenic similarity of A/USSR/77 with A/FW/50 (H1N1) virus. [ABSTRACT FROM PUBLISHER]

Antibodies have been used for the last five decades in the laboratory diagnosis of a wide range of diseases caused by viruses and in detailed investigations of virus structure. However, immunological and serological assays have always had problems of interpretation, reproducibility and standardization, resulting partly from the unavoidable heterogeneity of the antibodies in the test. When a mouse, for example, is immunized with a virus, the animal may easily recognise 10–20 different antigenic determinants. As many as five distinct antibodies can be produced by the mouse against each determinant and these will often differ from antibodies made by another mouse against the same antigenic determinant. The method of lymphocyte fusion and the subsequent generation of monoclonal antibodies (Kohler & Milstein, 1975; Kohler, 1980) overcomes these limitations. [ABSTRACT FROM PUBLISHER]

The single radial haemolysis (SRH) technique detected anti-B/HK/8/73 HA antibody rises in 59–85 % of paired sera from persons immunized with different influenza vaccines. In contrast, analysis of the same sera by the haemagglutination inhibition (HI) test indicated significant antibody rises in only 27–54% of paired sera. High levels of antibody were detected to influenza B/HK/8/73 and B/Singapore/222/79 viruses in post-immunization sera analysed by SRH, whereas the HI test indicated comparatively low geometric mean antibody titres. Most adults responded to immunization with influenza B virus by producing cross-reactive (CR) antibody which reacted with different influenza B viruses including the early isolate B/Lee/40. [ABSTRACT FROM PUBLISHER]

Antigenic variants of A/Texas/77 (H3N2) virus were selected in vitro using monoclonal antibody to virus haemagglutinin (HA). The antigenic variants and parental A/Texas/77 viruses were used to evaluate the frequency of anti-HA antibodies in the sera of children and adults using single-radial-haemolysis (SRH) tests. Twenty to 41 % of selected sera from adults, which contained antibody to the parental A/Texas/77 virus, failed to react with the different antigenic mutant viruses. A higher proportion of sera from children (37–58%) failed to react with the antigenic variants. Certain human sera and particularly those of children would appear to possess a more limited antibody repertoire to influenza HA, potentially allowing new antigenic variants to escape neutralization and spread in the community. [ABSTRACT FROM PUBLISHER]

The specificity of serum anti-HA antibody from children immunized or infected with A/Victoria/75 (H3N2) or A/Texas/77 (H3N2) virus was examined using the single radial haemolysis test together with adsorption of antibody with three antigenic variants A/Hong Kong/68 (H3N2), A/Port Chalmers/73 (H3N2) and A/Victoria/75 (H3N2). The majority of young children reacted to vaccination or infection by producing strain-specific (SS) antibody to the homologous virus. A small proportion of children's sera contained cross-reacting (CR) antibodies capable of reacting with the haemagglutinins of all antigenic variants of the subtype including A/HK/1/68. In contrast, most adults reacted immunologically to either vaccination or infection by producing CR antibody, reacting with all variants of the antigenic subtype including the prototype virus A/HK/1/68 (H3N2). [ABSTRACT FROM PUBLISHER]

The anti-haemagglutinin antibody response in adult human volunteers to inactivated whole virus or tween ether split influenza A/Victoria/75 (H3N2) and A/Scotland/74 (H3N2) virus vaccines was investigated using antibody adsorption and single-radial-haemolysis (SRH) techniques. The concentrations of haemagglutinin (HA), nucleoprotein (NP) and matrix (M) antigens measured by single radial diffusion (SRD) and rocket immunoelectrophoresis were similar for both the whole virus and split vaccines. Whole virus and split vaccines induced cross-reactive (CR) antibody in 87% of vaccinees. Strain specific (SS) antibody to A/Hong Kong/1/68 or the homologous virus was induced less frequently than CR antibody. Higher anti-haemagglutinin antibody titres were detected in persons receiving the split virus vaccines than in those receiving the whole virus vaccines. No antibody to the type-specific matrix protein was detectable, but 33% of volunteers developed an antibody rise to type-specific nucleoprotein antigen.The specificity of the anti-haemagglutinin antibody response in human adults to natural infection with A/Port Chalmers/73 (H3N2) virus was similar to that induced by inactivated vaccines in that a high proportion of subjects developed CR anti-haemagglutinin antibody, which reacted with A/Hong Kong/68 virus and the homologous A/Port Chalmers/73 virus, and SS antibody for A/Hong Kong/68 virus but SS antibody for A/Port Chalmers/73 virus was infrequently stimulated by natural infection. [ABSTRACT FROM PUBLISHER]

After one passage of influenza A2/Singapore/l/57 virus in mice treated with 150 mg./kg./day of aminoadamantane, a partially drug-resistant strain of virus was detected in 1 of 12 mice. The isolation rate of aminoadamantane-resistant viruses increased to 8 after three passages in drug-treated mice. Some virus strains showed a 500-fold increase in resistance to aminoadamantane and to the structurally related compounds α-methyl-1-adamantane methylamine and 2-adamantanamine sulphate. No aminoadamantane-resistant viruses were detected after passage of influenza four times in mice treated with lower (15 or 1·5 mg./kg./day) concentrations of aminoadamantane. Aminoadamantane had no detectable effect on the development of lung lesions in mice infected with the drug-resistant influenza strain, whereas lung lesions were reduced in aminoadamantane treated mice infected with a control strain of influenza A2/Singapore virus. No differences were detected in the buoyant density in caesium chloride, morphology or serology between control and aminoadamantane-resistant strains of virus. These drug-resistant influenza viruses may be useful for detailed studies of the mode of action of aminoadamantane. [ABSTRACT FROM PUBLISHER]

The haemagglutinin of influenza virus A 2/Hong Kong/1/68 was shown to be markedly different from that of previously isolated A 2 virus strains. No haemagglutination-inhibiting (HI) antibody to A 2/Hong Kong/1/68 virus was detected in serum specimens collected in 1966 from persons aged 60 years or less. In contrast, HI antibody tests with 270 sera collected in 1968 indicated that 9·6% had demonstrable HI antibody at low titres, and 35·2% of 454 postepidemic (1969) sera had demonstrable HI antibody at relatively high titres. Most sera from persons aged 80 years and more collected in 1968 and 1969 had demonstrable HI anti-body to influenza virus A 2/Hong Kong/1/68. No HI antibody to the Hong Kong virus was detected in pre-epidemic sera from children aged 6 months to 3 years, whereas 32 % of postepidemic sera had HI antibody. The acquisition of HI antibody to A 2/Hong Kong/1/68 was not accompanied by an increase hi the incidence or titres of HI antibody to heterotypic A 2 influenza viruses. For sera from children aged 4–11 years, an increase of HI titre to heterotypic A 2 influenza was found. [ABSTRACT FROM PUBLISHER]

The inactivation kinetics of CELO virus were studied in the presence of 1/4000 formaldehyde. Inactivation of the virus by formaldehyde at 4° C. was not complete after 14 days incubation. Formaldehyde inactivation at 36° C., however, was rapid and no virus was detected after 24 hr. incubation.Neutralizing antibody to CELO virus was detected in 20–88% of sera tested from five flocks of hens. This suggested dissemination of the virus in England and Scotland. However, no CELO virus neutralizing antibody at a serum dilution of 1/8 was detected in 142 normal human sera or in 229 sera from persons who had been immunized with egg grown, inactivated influenza virus vaccine.We would like to thank Professor C. H. Stuart-Harris and Drs J. E. Wilson, D. A. Martin and D. Breeze for their help and their criticisms of the manuscript.Dr G. C. Schild kindly supplied a number of the human sera used in the study. The study was financed in part by the National Fund for Research in Poliomyelitis and other Crippling Diseases and by the British Empire Cancer Campaign. [ABSTRACT FROM PUBLISHER]

The haemagglutinin of influenza virus A2/Hong Kong/1/68 was shown to be markedly different from that of previously isolated A2 virus strains. No haemagglutination-inhibiting (HI) antibody to A2/Hong Kong/1/68 virus was detected in serum specimens collected in 1966 from persons aged 60 years or less. In contrast, HI antibody tests with 270 sera collected in 1968 indicated that 9.6% had demonstrable HI antibody at low titres, and 35.2% of 454 postepidemic (1969) sera had demonstrable HI antibody at relatively high titres. Most sera from persons aged 80 years and more collected in 1968 and 1969 had demonstrable HI antibody to influenza virus A2/Hong Kong/1/68. No HI antibody to the Hong Kong virus was detected in pre-epidemic sera from children aged 6 months to 3 years, whereas 32% of postepidemic sera had HI antibody. The acquisition of HI antibody to A2/Hong Kong/1/68 was not accompanied by an increase in the incidence or titres of HI antibody to heterotypic A2 influenza viruses. For sera from children aged 4-11 years, an increase of HI titre to heterotypic A2 influenza was found.