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Biomedical subjects

R Jennings

Publications and source records attributed to R Jennings.

At least 145 records · Page 8Linked to original sources

Assessment of resistance to influenza virus infection in animal models.

The antibody response and immunity to challenge infection were determined in ferrets immunized with inactivated influenza vaccine in saline or adjuvant. Adjuvanated vaccines induced variable titres of serum antibody, and the degree of immunity to challenge infection was directly related to the titre of serum HI antibody induced by these vaccines. Conventional doses of saline vaccine did not induce serum HI antibody, and the ferrets were completely susceptible to challenge infection. Infection with live virus produced a more solid immunity to challenge infection than immunization with a adjuvant vaccines, even though immunization induced higher titres of serum HI antibody. Ferrets previously infected with a heterotypic influenza A virus, but not other viruses, produced serum HI antibody in response to subsequent immunization with inactivated influenza vaccine. Similar results were obtained in hamsters and mice. Thus, the failure of animals to produce antibody in response to immunization with saline inactivated vaccines was due to the absence of a previous priming infection; this prior experience would be a feature of most volunteers. Live virus infection produced nasal antibody in ferrets, but inactivated vaccines only induced serum antibody. This may explain the more solid immunity observed following infection; however, at the time of challenge infection, no nasal wash antibody could be detected. Immunization with inactivated vaccine in Freund's complete adjuvant and influenza virus infection both produced a cell-mediated immune response; thus, the difference in the degree of immunity induced by these two immunization procedures are probably not due to differences in the cell-mediated immune response. However, cell-mediated immunity was measured by skin tests and by macrophage migration inhibition tests with spleen cells; the reaction of cells from the respiratory tract may be more important, but was not measured in these studies.

Administration, Intranasal↗

Immunity to influenza in ferrets. XI. Cross-immunity between A/Hong Kong/68 and A/England/72 viruses: serum antibodies produced by infection or immunization.

The degree of immunity due to cross-reactions between antibody to influenza virus A/Hong Kong/1/68 and A/England/42/72 was studied in ferrets. Ferrets were immunized with the viruses by either live infection or by inoculation with inactivated virus vaccines. The vaccines were given with Freund's incomplete adjuvant or were given to ferrets previously infected with influenza virus A/PR/8/34. As a result of these immunizations the animals all produced similar titres of serum HI antibody to the immunizing virus, although the degree of cross-reaction with the other virus strain was variable. After immunization the animals were challenged by infection with an A/Eng/42/72-like virus and their degree of immunity was measured. It was found that the greatest immunity was in ferrets previously infected with the homologous A/Eng/42/72 virus. Animals previously infected with A/HK/68 virus also showed a measurable degree of immunity to A/Eng/42/72 infection, and this was greater than that found in animals given inactivated virus vaccines. The immunity produced by the vaccines was approximately equal, regardless of which vaccine or method of immunization was used. Thus, live infection produced a more effective, broader immunity than did the use of inactivated virus vaccines.

Animals↗

Immunity to influenza in ferrets. X. Intranasal immunization of ferrets with inactivated influenza A virus vaccines.

The response of ferrets after intranasal inoculation of inactivated A/Hong Kong/68 (H3N2) influenza virus vaccines is reported. Normal ferrets given either saline vaccine in drops or freeze-dried vaccine in an aerosol intranasally did not produce detectable serum or nasal hemagglutination inhibiting antibody and were found to be completely susceptible to challenge infection with A/Hong Kong/68 virus. Intranasal saline vaccine did not produce an additive effect on the response of ferrets simultaneously given the same vaccine intramuscularly with adjuvant. Ferrets primed by previous infection with A/PR/8/34 (H0N1) influenza virus, however, responded to intranasal immunization with saline A/Hong Kong/68 virus vaccine and produced serum and nasal antibody. These animals were found to be partially resistant to challenge infection, in contrast to similar animals given saline vaccine intramuscularly which were completely resistant to challenge infection. Primed ferrets did not respond after immunization with the freeze-dried aerosol vaccine, but this may have been due to a failure of the aerosol to be inhaled satisfactorily.

Administration, Intranasal↗

Antibody response of hamsters to A2-Hong Kong virus vaccine after priming by heterotypic virus infection.

Hamsters previously infected with influenza virus A1/FM/1/47 produced serum hemagglutination inhibition (HI) antibody in response to 1/100 the antigenic dose of inactivated influenza virus A2/Hong Kong vaccine necessary to induce antibody in normal animals. This priming effect was believed to be due to the virus infection which caused an immune response to a virus antigen common to both the infecting virus and the virus vaccine; this antigen acted as a carrier for the specific vaccine virus hemagglutinin and potentiated the immune response to the new antigen. This theory, which has been established in other immune systems, was tested, and the results obtained did not contradict the conditions imposed in the above explanation. Thus, the priming effect could be transferred to normal hamsters by inoculation of spleen cells from virus-infected animals, and the HI antibody response to the virus vaccine was characteristic of a secondary response. The theory also required that the new antigen be coupled to the carrier protein; however, primed hamsters produced serum HI antibody after inoculation with ether-Tween-split virus vaccine, but there was no proof that this vaccine was completely dissociated.

Animals↗

Studies on type C influenza virus in the chick embryo.

The effect of varying conditions of inoculation and incubation on the growth of type C influenza virus in the allantoic cavity of the developing chick embryo were investigated. It was found that the highest yields of both virus haemagglutinin and infectious virus were obtained following the inoculation of chick embryos at 8 days with subsequent incubation at 32 degrees C. Using the chick embryo allantoic cavity for titration of infectious virus, growth curves of allantoically propagated virus under varying inoculation and incubation conditions were determined.

Animals↗

Interferon induction by influenza type C.

The presence of a heat-stable interferon-like inhibitor in allantoic and amniotic fluids collected from chick embryos infected with type C influenza virus was determined. This inhibitor was characterized as an interferon and the ability of both live and ultra-violet-irradiated influenza type C virus to induce the substance was examined under various conditions.

Animals↗

Adenovirus, parainfluenza virus and respiratory syncytial virus antibodies in the sera of Jamaicans.

Surveys for respiratory virus antibodies in the Jamaican population have shown that adenovirus, respiratory syncytial virus and parainfluenza types 1 and 3 virus antibodies are acquired early in life. The incidence of haemagglutination-inhibiting antibodies to parainfluenza viruses increases rapidly with age and almost all adults possess parainfluenza type 3 antibody, usually in high titre. Parainfluenza type 1 antibodies are only slightly less common. Complement-fixing antibodies to the adenovirus group were also observed to increase in incidence with age.Complement-fixing antibody to respiratory syncytial virus was less common in Jamaican sera than antibody to the other respiratory viruses described here. The highest titres were observed in the youngest age-group.

Adenoviridae↗