Henry M. Gelfand
Tulane University
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American Journal of Public Health | 1958
John P. Fox; Henry M. Gelfand; Dorothy R. LeBlanc; Dighton F. Rowan
IT IS commonly recognized that immunity to an infecting agent may range in degree from absolute resistance to infection down to minimal modification of its morbid consequences. For the individual, distinction between absolute and relative resistance is not of importance provided that the infection permiiitted shall not result in disease. For the group, the distinction is of practical importance only if the immune but infected individual is capable of serving as a link in the chain of continued disseinination of the agent or if the maintenance of immunity in the individual, and hence, in the herd, depends upon natural restimulation by infection. Our present interest is in immunity to poliomyelitis. From the characteristic age distribution of clinically evident infections, it appears that immunity initiated by natural infection during childhood ordinarily protects adults from disease. Serosurveys of isolated populations, such as those of certain Alaskan Eskimo communities,1 afford proof that in many persons seroimmunity may persist indefinitely after infection. However, such studies leave unanswered questions as to the actual proportion of infections that are followed by long persisting iiimunity, whether or not reinfections are important at all to the maintenance of both individual and herd immunity, and, if reinfections occur, whether the reinfected individual can play a significant role in virus dissemination. Obviously, rather similar questions relate to immunity which is induced artificially. Major interest centers in the possibility that artificially induced immunity, resulting from either killedvirus vaccine or inifection with live avirulent strains, may not only prevent disease but also either prevent or so imodify alimentary infection that the immune individual can play no effective role in virus transmission. If such were the case, it is clear that extensive but partial immunization of the population might create a significant barrier to virus spread and so afford a measure of protection to those not vaccinated. Some have suggested that the greatly reduced occurrence of paralytic polioinyelitis in the United States in 1957 is out of proportion to the extent of vaccine application and may indicate that a vaccine-induced immune barrier to virus spread actually has been erected. However, in this connection it should be noted that as recently as 1942 the na-
American Journal of Epidemiology | 1959
Henry M. Gelfand; Dorothy R. LeBlanc; Louis Potash; John P. Fox
Maternal, umbilical cord, and serially-collected infant blood samples, were available incidental to the “Louisiana Study” of natural infection with polioviruses. By means of the simultaneous titration of series of these specimens, the passive transfer of circulating maternal antibody to the infant and the decline in the infant of the maternally-derived antibody were investigated by the neutralization test. Sixty-six maternal cord blood pairs permitted observation on 188 typespecific comparisons, and showed that the titer of humoral antibody varies, in general, very little within each pair, but that there is a greater tendency for type 3 transfer to be inefficient as compared with types 1 and 2. However, specific transfer inefficiency of any antibody type may be associated with individual women. Since the antibody comparison possessed by children at birth is a function of maternal titer and since the passively acquired antibody gradually disappears, the percentage of seropositive infants in a population gradually diminishes with postpartum age. In this highly endemic area, over 50% of infants were seronegative, at a serum dilution of 1:10, against any one antibody type, by 3 months of age. The implications of this finding to early vaccination were discussed. The half-life for passive polioantibody was calculated by a study of the mean titer of antibody at successive monthly intervals of infants born of mothers with various antibody levels. The decline was found to be exponential in nature and not to vary appreciably or consistently with maternal titer. The half-life of the passive antibody was found to be approximately 25 days.
American Journal of Tropical Medicine and Hygiene | 1984
Henry M. Gelfand
Only the oldest among Americans and Europeans have had personal experience of the horror and tragedy of epidemic smallpox in their countries. A smaller number of younger physicians and epidemiologists have had this experience during the course of eradication campaigns, mostly in tropical areas. Soon, with the total elimination of smallpox since 1977, it will be merely a historical curiosity. It is most timely, therefore, that Dr. Hopkins has undertaken the task of assembling widely scattered records to produce this concise, authoritative, easily readable story of the devastating impact of smallpox on individuals, populations, and the history of mankind. The book opens with a superb chapter which, in remarkably few but well chosen words, reviews the virology, pathogenesis, clinical presentation, inter-person transmission, the geographic origin and spread, and the history of thought about the cause and propagation of smallpox in relation to its treatment and prevention.
Journal of Immunology | 1960
Henry M. Gelfand; John P. Fox; Dorothy R. LeBlanc; Lila R. Elveback
American Journal of Epidemiology | 1957
Henry M. Gelfand; Dorothy R. LeBlanc; John P. Fox; Donald P. Conwell; Margaret S. Brooks; Barbara F. Yaeger
American Journal of Epidemiology | 1966
James E. Froeschle; Paul M. Feorino; Henry M. Gelfand
JAMA | 1959
Henry M. Gelfand; Louis Potash; Dorothy R. LeBlanc; John P. Fox
American Journal of Epidemiology | 1963
Henry M. Gelfand; Alfonso H. Holguin; George E. Marchetti; Paul M. Feorino; Frances R. Richardson; Dorreth D. Humphrey
American Journal of Epidemiology | 1962
James H. Nakano; Henry M. Gelfand
American Journal of Epidemiology | 1963
James H. Nakano; Henry M. Gelfand; Jura T. Cole
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University of Texas Health Science Center at San Antonio
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