People living with the human immunodeficiency virus (HIV) have an elevated risk of
opioid misuse due to both prescriptions for HIV-associated
chronic pain and because injection drug use remains a primary mode of HIV transmission. HIV pathogenesis is characterized by chronic immune activation and microbial
dysbiosis, and translocation across the gut barrier exacerbating
inflammation. Despite the high rate of co-occurrence, little is known about the microbiome during chronic
opioid use in the context of HIV and combination antiretroviral therapy (cART). We recently demonstrated the reduction of the CD4 + T-cell reservoir in lymphoid tissues but increased in microglia/macrophage reservoirs in CNS by using
morphine-treated, simian immunodeficiency virus (SIV)-infected rhesus macaques with
viremia suppressed by cART. To understand whether
morphine may perturb the gut-brain axis, fecal samples were collected at necropsy,
DNA isolated, and
16S rRNA sequenced and changes of the microbiome analyzed. We found that
morphine treatment led to
dysbiosis, primarily characterized by expansion of Bacteroidetes, particularly Prevotellaceae, at the expense of Firmicutes and other members of healthy microbial communities resulting in a lower α-diversity. Of the many genera in Prevotellaceae, the differences between the saline and
morphine group were primarily due to a higher relative abundance of Prevotella_9, the taxa most similar to Prevotella copri, an inflammatory pathobiont in the human microbiome. These findings reinforce previous research showing that
opioid abuse is associated with
dysbiosis, therefore, warranting additional future research to elucidate the complex interaction between the host and
opioid abuse during HIV and SIV
infection.