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www.ncbi.nlm.nih.gov/pubmed/15116311?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P
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J Infect Dis. 2004 May 1;189(9):1721-8. Epub 2004 Apr 19. Links
Age-associated decline in resistance to Babesia microti is
genetically determined.
Vannier E, Borggraefe I, Telford SR 3rd, Menon S, Brauns T, Spielman
A, Gelfand JA, Wortis HH.
Division of Infectious Diseases, Tufts-New England Medical Center,
Boston, Massachusetts 02111, USA.
BACKGROUND: Although infection by the protozoan Babesia microti is
rarely symptomatic in immunocompetent young people, healthy
individuals aged >50 years may experience life-threatening disease.
To determine the basis for this age relationship, we developed a
mouse model of babesiosis using a novel clinical isolate of B.
microti.
METHODS: Mice were infected at 2, 6, 12, or 18 months. Parasitemia
was monitored on Giemsa-stained blood smears or by flow cytometry.
RESULTS: In DBA/2 mice, early and persistent parasitemias increased
with age at infection. BALB/c and C57BL/6 mice were resistant,
regardless of age, which indicates that allelic variation determines
resistance to B. microti. Unlike immunocompetent mice, SCID mice,
which retain an innate immune system but****lack the lymphocytes
needed for adaptive immunity, developed high and persistent levels
of parasitemia**** that were markedly reduced by transfer of naive
BALB/c or DBA/2 splenocytes. BALB/c cells reduced the persistent
parasitemia to a greater extent than did age-matched DBA/2 cells.
****Of importance, there was an age-associated loss of protection by
cells of both strains.
CONCLUSION: The resistance to B. microti infection conferred by the
adaptive immune system is genetically determined and associated with
age. We postulate that there are age-related differences in the
expression of alleles critical for adaptive immunity to B. microti.
PMID: 15116311 [PubMed - indexed for MEDLINE
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