Modulation of Infection and Type 1 Cytokine Expression Parameters by Morphine During In Vitro Coinfection with Human T-Cell Leukemia Virus Type I and HIV-1

Authors:
  • CCChuanhai Cao
    Chuanhai Cao
  • YBYun Bai
    Yun Bai
  • TLThomas P. Loughran
    Thomas P. Loughran
  • KUKenneth E. Ugen
    Kenneth E. Ugen
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Abstract
Infection of injection drug users (IDUs) with the human T-cell leukemia viruses (HTLVs) or HIV is considerably higher than in the non-IDU population. Also, coinfection with HIV-1 and HTLV type I (HTLV-I) occurs more frequently. There is little or no information on the effects of opiates (i.e., morphine) on HTLV infection alone or on coinfection of HTLV-I-infected cells with HIV-1. Therefore, in this report, we analyzed the in vitro effects of morphine on HIV or HTLV infection alone as well as on dual infection with HTLV-I and HIV-1. Morphine decreased the in vitro levels of interferon-γ (IFNγ) and IL-2 during single infections, and this effect was reversed by the addition of the opioid antagonist naloxone. In contrast, treatment with morphine resulted in a 31% and 36% increase in IFNγ and IL-2 levels, respectively, during dual infection. In addition, naloxone had an apparent additive effect on the morphineassociated enhancement of IFNγ and IL-2 expression in the dual-infection model. Despite the high levels of IFNγ expression, the viability of the coinfected cells in the presence of morphine was maintained. Importantly, morphine treatment was associated with augmented viral reverse transcription activity in dually infected cultures, apparently to the benefit of HTLV-I. If a similar putative morphine-induced advantage for HTLV-I production also occurs during in vivo coinfection, opiates such as morphine could contribute to the observed increased rate of HIV-1/HTLV-I infection in the IDU population in a more direct fashion than was previously believed.

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