Intervention Strategies for High Risk Infants and Young Children

1977 ◽  
Vol 142 (12) ◽  
pp. 917-917
Author(s):  
Ogden C. Bruton
1993 ◽  
Vol 329 (21) ◽  
pp. 1524-1530 ◽  
Author(s):  
Jessie R. Groothuis ◽  
Eric Simoes ◽  
Myron J. Levin ◽  
Caroline B. Hall ◽  
Christine E. Long ◽  
...  

2009 ◽  
Vol 22 (1) ◽  
pp. 13-36 ◽  
Author(s):  
Denise L. Doolan ◽  
Carlota Dobaño ◽  
J. Kevin Baird

SUMMARY Naturally acquired immunity to falciparum malaria protects millions of people routinely exposed to Plasmodium falciparum infection from severe disease and death. There is no clear concept about how this protection works. There is no general agreement about the rate of onset of acquired immunity or what constitutes the key determinants of protection; much less is there a consensus regarding the mechanism(s) of protection. This review summarizes what is understood about naturally acquired and experimentally induced immunity against malaria with the help of evolving insights provided by biotechnology and places these insights in the context of historical, clinical, and epidemiological observations. We advocate that naturally acquired immunity should be appreciated as being virtually 100% effective against severe disease and death among heavily exposed adults. Even the immunity that occurs in exposed infants may exceed 90% effectiveness. The induction of an adult-like immune status among high-risk infants in sub-Saharan Africa would greatly diminish disease and death caused by P. falciparum. The mechanism of naturally acquired immunity that occurs among adults living in areas of hyper- to holoendemicity should be understood with a view toward duplicating such protection in infants and young children in areas of endemicity.


PEDIATRICS ◽  
1991 ◽  
Vol 88 (5) ◽  
pp. 1031-1036
Author(s):  
Roland A. Levandowski ◽  
Helen L. Regnery ◽  
Eldridge Staton ◽  
B. Gail Burgess ◽  
Michael S. Williams ◽  
...  

The cocirculation in several parts of the world of influenza viruses B/Yamagata/16/88 and B/Victoria/2/87, which are genetically and antigenically divergent, has prompted the question of whether immunization with one viral antigen is sufficient for protection against both strains. Twenty-three high-risk infants and young children were immunized with a commercial trivalent influenza vaccine containing the antigens of influenza virus B/Yamagata/16/88. When antibodies against influenza viruses B/Yamagata/16/88 and B/Victoria/2/87 were determined, increases developed uniformly to both in the sera of primed children previously exposed to influenza virus B/Victoria/2/87 by immunization or infection. Antibodies against B/Yamagata/16/88 developed in the sera of unprimed children with titers similar to those of the primed children. However, antibodies to B/ Victoria/2/87 were not detected in the sera of the unprimed children. These data suggest that children with out appropriate immunologic priming may not be protected against an infection with a B/Victoria/2/87 strain after vaccination with a B/Yamagata/16/88 strain. Immunization with more than one influenza B virus strain may be desirable in some high-risk pediatric patients if divergent influenza B viruses circulate.


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