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Methadone induces CCR5 and promotes AIDS virus infection
Author(s) -
Suzuki Shunji,
Carlos Maria P,
Chuang Linda F,
Torres José V,
Doi Roy H,
Chuang Ronald Y
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02746-1
Subject(s) - methadone , virology , simian immunodeficiency virus , virus , syncytium , concomitant , reverse transcriptase , opioid , human immunodeficiency virus (hiv) , receptor , μ opioid receptor , medicine , immunology , biology , pharmacology , rna , gene , biochemistry
Methadone, a regimen for the treatment of opioid dependency, was found to induce the expression of CCR5, a co‐receptor for human immunodeficiency virus (HIV)/simian form of HIV (SIV) entry, on human CEM x174 lymphocytes. Both CCR5 mRNA and protein were elevated in methadone‐treated cells. A concomitant increase of mu opioid receptors was also observed. Upon methadone exposure, SIVmac239‐infected CEM x174 cells released greater amounts of virus particles as revealed by both the number of syncytia formation and reverse transcriptase activities. Similar methadone effect was not observed on CEM x174 cells infected with other simian retroviruses that do not depend on CCR5 for cellular entry. These studies raise concerns considering methadone as an innocuous morphine substitute.