Experience with Vaccination Against Influenza in the Spring of 1947

Francis, Thomas; Salk, Jonas; Quilligan, J. J.

doi:10.2105/ajph.37.8.1013

Cited by 127 publications

(65 citation statements)

References 4 publications

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“…The problems encountered in the prophylaxis of influenza by vaccination as a result of strain deviation in the Type A group are well established (17,18). Recent evidence (19) of major antigenic changes occurring in the B group points up the importance of this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Antigenic Variants of Influenza a Virus (Pr8 Strain)

Gerber

Hamre

Loosli

1956

The Journal of Experimental Medicine

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In an attempt to simulate conditions in the human population between epidemics of influenza, the influenza A virus (PR8 strain) has been serially passed in mice partially immunized with this virus. The antigenic variant which emerged in the course of these passages has been described (1). This variant was capable of multiplying in the lungs of vaccinated mice which were fully resistant to challenge with the parent PR8 strain. It was shown by cross-serological tests that the variant contained a new dominant antigen, but that it also retained antigens related to the parent PR8 strain. Because there was no further alteration in the antigenic composition of the variant after the 17th passage in PRS-immunized mice, passages were carried in mice immunized to the variant. The present report describes the production and characterization of a series of three variants, each derived in succession from the previous one, and compares them with the parent PR8 strain and the first variant strain (1). Materials and MethodsSeveral of the methods employed are similar to those previously described in detail (1). These will be briefly reviewed in the present report. The additional techniques used include the complement-fixation test and antibody absorption.The PR8 influenza A strain was initially employed as the parent virus (1). The stock suspensions of PR8-infected mouse lung were prepared from mice infected by the air-borne route in a closed chamber and sacrificed 48 hours later (2). 10 per cent suspensions were frozen in aliquots and stored at --40°C. Broth used for lung suspensions and for all dilutions contained 1,000 units/ml, of penicillin and 1 mg./ml, of dihydrostreptomyein. Viral antigens

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Section: Discussionmentioning

confidence: 99%

Antigenic Variants of Influenza a Virus (Pr8 Strain)

Gerber

Hamre

Loosli

1956

The Journal of Experimental Medicine

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“…In particular, it violates a basic rule in immunology established by McFarlane Burnet; that rule predicts that the second antigen would activate specific lymphocytes that proliferate and differentiate into effector cells capable of reacting better with that antigen compared with the first one [11]. More importantly, OAS compromises effector immune responses to infectious agents that cross-react with previously encountered antigens [4][5][6][7][8], with deleterious consequences on an individual's ability to control an infection.…”

Section: Introductionmentioning

confidence: 99%

A simple mechanistic explanation for original antigenic sin and its alleviation by adjuvants

Ndifon

2015

J. R. Soc. Interface.

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A large number of published studies have shown that adaptive immunity to a particular antigen, including pathogen-derived, can be boosted by another, cross-reacting antigen while inducing suboptimal immunity to the latter. 0912458109)). Here, focusing on the humoral aspects of adaptive immunity, I propose a simple and testable mechanism: that OAS occurs when T regulatory cells induced by the first antigen decrease the dose of the second antigen that is loaded by dendritic cells and available to activate naive lymphocytes. I use both a parsimonious mathematical model and experimental data to confirm the deductive validity of this proposal. This model also explains the puzzling experimental observation that administering certain dendritic cell-activating adjuvants during antigen exposure alleviates OAS. Specifically, the model predicts that such adjuvants will attenuate T regulatory suppression of naive lymphocyte activation. Together, these results suggest additional strategies for redeeming adaptive immunity from the destructive consequences of antigenic 'sin'.

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“…This phenomenon was first described by Thomas Francis, Jr., in 1960 (3) on the basis of analysis in the late 1940s and 1950s of the antibody responses to an antigenically distinct H1N1 influenza A virus that emerged in 1947 (designated A prime) in individuals previously vaccinated with older H1N1 influenza viruses (designated classical H1N1 viruses) (1)(2)(3)(4)(5). Those studies showed that after an A prime H1N1 virus infection, previously vaccinated individuals produced higher titers of antibody against the older, classical H1N1 viruses and a diminished antibody response against the A prime H1N1 virus (1)(2)(3)(4)(5).…”

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confidence: 99%