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Infection and Immunity, July 2002, p. 3701-3706, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3701-3706.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Deletion of T Cells Bearing the Vß8.1 T-Cell Receptor following Mouse Mammary Tumor Virus 7 Integration Confers Resistance to Murine Cerebral Malaria

Unité d'Immunophysiopathologie Infectieuse (CNRS URA 1961),¹ Unité de Génétique des Mammifères (CNRS URA 1960), Département d'Immunologie, Institut Pasteur, 75724 Paris Cedex 15,³ INSERM U511, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires, CHU Pitié-Salpêtrière, 75643 Paris Cedex 13, France²

Received 30 October 2001/ Returned for modification 24 January 2002/ Accepted 25 March 2002

Plasmodium berghei ANKA induces a fatal neurological syndrome known as cerebral malaria (CM) in susceptible mice. Host genetic elements are among the key factors determining susceptibility or resistance to CM. Analysis of mice of the same H-2 haplotype revealed that mouse mammary tumor virus 7 (MTV-7) integration into chromosome 1 is one of the key factors associated with resistance to neurological disease during P. berghei ANKA infection. We investigated this phenomenon by infecting a series of recombinant inbred mice (CXD2), derived from BALB/c (susceptible to CM) and DBA/2 (resistant to CM) mice, with P. berghei ANKA. We observed differences in susceptibility to CM induced by this Plasmodium strain. Mice with the MTV-7 sequence in their genome were resistant to CM, whereas those without integration of this gene were susceptible. Thus, an integrated proviral open reading frame or similar genomic sequences may confer protection against neuropathogenesis during malaria, at least in mice.

Editor: S. H. E. Kaufmann

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