Fibroblast interferon in HBsAg-positive chronic active hepatitis.
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Biomedical subjects
Publications and source records attributed to N Masurel.
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RSV complement fixation antibodies were established in 200 paired maternal and cord blood sera. Geometric mean titres in cord sera were significantly higher than in matermal sera. The differences did not depend on the virus strain used. Half of the paired sera (taken at random) were also submitted to microneutralization tests. No differences were found between geometric mean titres in maternal and cord sera.
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Sera collected in 1967 and 1972 from people in the 0-100 age-group showed haemagglutination-inhibition (H.I.) antibody to swine virus A/Iowa/15/30 (Hsw1N1) in greatest number and with highest titre in people born before 1918. A slight decrease was observed from 1967 to 1972 in the number of sera with antibody to swine virus and in the height of the titres. The recently isolated A/New Jersey/10/76 (Hsw1N1) virus showed a result comparable to that of the Swine/1930 virus in sera of 1972. On the analogy of the findings in 1968, when the Hong Kong virus became epidemic in human populations and antibody to this virus was found in sera of people over 70 years, the suggestion is made that the recurrence of swine virus as an epidemic agent of human influenza may be expected around 1986. Fourfold or greater increase of antibody to Swine/1930 virus was observed in about 4--5% of people infected by or immunised with H3N2 viruses. This response occurred in people who had been in touch with the epidemic influenza-A viruses Hsw1N1, H0N1, and H1N1 during the swine era of 1918 to 1956. Following immunisation with H3N2 viruses of persons showing no response to H3N2 viruses in their serum 5% did show a fourfold or greater heterotypic H.I. antibody rise to swine virus. This finding is of consequence for the diagnostic serology of influenza.
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Ferrets were sequentially infected at time intervals of 3 weeks with different influenza virus A strains. It was found that secondary infection can result in the appearance of antibodies highly cross-reacting with a virus strain closely related to the strain of first infection. Such highly cross-reacting antibodies were designated as HCR antibodies. Evidence is presented that HCR antibodies were not antineuraminidase antibodies and, in addition, were not specifically oriented to the strain with which the crossing was observed. When using time intervals of 3 weeks between infections, no increase after secondary infection of antibodies oriented to the strain of first infection was recorded. However, when time intervals of 4 to 5 months between infections were used, secondary infections resulted in an increase of antibodies oriented to the strain of first infection ("original antigenic sin") but not in the appearance of HCR antibodies. In addition, antibodies combining specifically with both infecting strains, designated as doubly specific antibodies, were found. Thus, the conclusion was reached that the original antigenic sin phenomenon and the appearance of HCR antibodies are mutually exclusive events.
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