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J Med Virol 2013 Dec;85(12):2139-40

CCR5 deficiency and severe polio infection in the 1984 outbreak in Finland.

Rosenberg AS, Roivainen M, Hovi T, Liu Q, Murphy PM

Abstract

CCR5, a leukocyte chemoattractant receptor for chemokines CCL3, CCL4, and CCL5, promotes innate and adaptive immune responses by mediating leukocyte trafficking within lymph nodes and to peripheral tissues and is also known as a co-receptor for HIV cell entry. Homozygous inheritance of a complete loss-of-function mutation in CCR5 (CCR5Delta32/CCR5Delta32) is associated with symptomatic neuroinflammatory disease in humans with West Nile and Tickborne Encephalitis flavivirus infections. This study sought to establish whether CCR5 deficiency could also be a determinant of clinical outcome after infection by poliovirus which results in central nervous system damage in only a small proportion of cases. We analyzed serum samples from seven patients and 79 controls, collected during the 1984-1985 polio outbreak in Finland, where CCR5Delta32 is relatively common in the general population. The results excluded CCR5 deficiency as the sole determinant of severe neurologic disease after poliovirus infection in this population. J. Med. Virol. 9999:1-2, 2013. (c) 2013 Wiley Periodicals, Inc.


Category: Journal Article
PubMed ID: #24037958 DOI: 10.1002/jmv.23739
Includes FDA Authors from Scientific Area(s): Drugs
Entry Created: 2013-09-17 Entry Last Modified: 2013-11-02
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