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The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

ABSTRACT: Fentanyl enhanced expression of CXCR4 and CCR5 protein levels and viral expression in a dose-dependent manner in multiple HIV-susceptible and HIV-infected cell lines. Multiple genes associated with apoptosis, antiviral / interferon response, chemokine. signaling, and NFκB signaling were differentially regulated by fentanyl. Thus fentanyl impacts HIV replication and chemokine co-receptor expression in HIV-susceptible and HIV-infected lymphocyte cell lines suggesting that opioid use may increase the likelihood of transmission to others and accelerate disease progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216124 | GEO | 2022/10/20

REPOSITORIES: GEO

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The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:The illicit use of synthetic opioids such as fentanyl has led to a serious public health crisis in the United States. People with opioid use disorder are more likely to contract infections such as HIV and viral hepatitis. While several drugs of abuse are known to enhance viral replication and to suppress immunologic responses, the effects of synthetic opioids on HIV pathogenesis have not been investigated thoroughly. Thus, we examined the impact of fentanyl on HIV-susceptible and HIV-infected cell types and chemokine receptor expression in vitro. TZM-bl and HIV-infected lymphocyte cells were incubated with fentanyl at concentrations of 1 ng, 100 ng, and 10 ug. Expression levels of the CXCR4 and CCR5 chemokine receptors were measured in cell lysates, and HIV p24 antigen was quantified in culture supernatants by ELISA. HIV proviral DNA was quantified in cells using SYBR RT-PCR targeting the pol gene. Cell viability in the presence of drug was detected by the MTT Cell Proliferation Assay. RNA-seq and miRNAseq was performed to characterize cellular gene regulation in the presence of fentanyl. Fentanyl enhanced expression of CXCR4 and CCR5 protein levels in a dose-dependent manner in HIV-susceptible and HIV-infected cells. Similarly, fentanyl induced viral expression in HIV-exposed TZM-bl cells and in multiple HIV-infected lymphocyte cell lines. Multiple genes associated with apoptosis, antiviral / interferon response, chemokine signaling, and NFκB signaling were differentially regulated by fentanyl. These data demonstrate that the synthetic opioid fentanyl impacts HIV replication and chemokine co-receptor expression in HIV-susceptible and HIV-infected cells. Increased virus levels also suggest that opioid use may increase the likelihood of transmission to others and accelerate disease progression.

2022-10-19 | GSE216044 | GEO

The synthetic opioid fentanyl increases HIV replication expression in macrophages

Project description:The illicit use of synthetic opioids such as fentanyl has led to a serious public health crisis in the US. People with opioid use disorder are more likely to contract infections such as HIV and viral hepatitis and experience more severe disease. While several drugs of abuse are known to enhance viral replication and to suppress immunologic responses, the effects of synthetic opioids on HIV pathogenesis have not been investigated thoroughly. Thus, we examined the impact of fentanyl on macrophage cell line U937 and monocyte derived macrophage cells and chemokine receptor expression in vitro.

2024-08-28 | GSE241769 | GEO

Opioid withdrawal produces sex-specific effects on fentanyl-vs.-food choice and mesolimbic transcription

Project description:Background: Opioid withdrawal is a key driver of opioid addiction and an obstacle to recovery. However, withdrawal effects on opioid reinforcement and mesolimbic neuroadaptation are understudied and the role of sex is largely unknown. Methods: Male (n=13) and female (n=12) rats responded under a fentanyl-vs.-food “choice” procedure during daily 2h sessions. In addition to the daily choice sessions, rats were provided extended access to fentanyl during 12h self-administration sessions. After two weeks of this selfadministration regimen, the nucleus accumbens (NAc) and ventral tegmental area (VTA) of a subset of rats were subjected to RNA sequencing. In the remaining rats, a third week of this self-administration regimen was conducted, during which methadone effects on fentanyl-vs.-food choice were determined. Results: Prior to opioid dependence, male and female rats similarly allocated responding between fentanyl and food. Abstinence from extended fentanyl access elicited similar increases in somatic withdrawal signs in both sexes. Despite similar withdrawal signs and extended access fentanyl intake, opioid withdrawal was accompanied by a maladaptive increase in fentanyl choice in males, but not females. Behavioral sex differences corresponded with a greater number of differentially expressed genes in the NAc and VTA of opioidwithdrawn females relative to males. Methadone blocked withdrawal-associated increases in fentanyl choice in males, but failed to further decrease fentanyl choice in females. Conclusions: These results provide foundational evidence of sex-specific neuroadaptations to opioid withdrawal, which may be relevant to the female-specific resilience to withdrawal-associated increases in opioid choice and aid in the identification of novel therapeutic targets.

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The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

| PRJNA891755 | ENA

The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

Project description:The synthetic opioid fentanyl increases HIV replication and chemokine co-receptor expression in lymphocyte cell lines

| PRJNA892117 | ENA

The synthetic opioid fentanyl increases HIV replication expression in macrophages

Project description:The synthetic opioid fentanyl increases HIV replication expression in macrophages

| PRJNA1009840 | ENA

The synthetic opioid fentanyl elicited transcriptomic alterations related to viral replication, immune response, and inflammation in vitro.

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microRNA expression and opioid signaling

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