Objectives: To determine effects of opiate dependency on development of simian AIDS.
Design: Assessments of viral, immune, and clinicopathological status were conducted on rhesus macaques before and after establishment of opiate dependency and Simian Immunodeficiency Virus, sooty mangabey, strain-9 (SIVsmm9) infection. Controls received saline.
Methods: Blood was collected at baseline, before opiate dependencies, and viral infections were established and then after SIVsmm9 infection, longitudinally, through 216 weeks. Plasma viral titers were assessed using the branched chain DNA assay and CD4 and CD8 counts via cytofluorometry. Clinicopathological assessments of AIDS were founded on Centers for Disease Control and Prevention and other selected criteria.
Results: AIDS progression rates seemed to be decelerated and survival times increased by opiate dependency. Mean viral titers were unaffected by opiate exposure. Opiate-dependent monkeys that evidenced high initial viral titers survived significantly longer than controls. Several opiate-dependent monkeys maintained high viral titers for atypically extended durations. Several (5/19) opiate-dependent monkeys died or were removed early from the study due to "non-AIDS" causes.
Conclusions: Long-term opiate dependency seemed to decelerate the rate of progression to AIDS in the SIVsmm9 monkey model. This effect was most evident in monkeys with high initial viral titers/set points. "Non-AIDS" morbidities and mortalities were noted as potential confounds of epidemiological assessments of the role of opiates in HIV/AIDS.
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http://dx.doi.org/10.1097/QAI.0b013e3181967354 | DOI Listing |
BMC Psychiatry
December 2024
Department of Economics, University of Bergen, Postboks, Bergen, 7802, 5020, Norway.
Background: Opioid use disorders constitute a vast disease burden, need for comprehensive treatment, and substantial costs to individuals, families, and society. The multifaceted needs of people with opioid dependence call for integrated care. The study aims to assess the added value of an integrated medically assisted rehabilitation (MAR) program providing opioid agonist therapy for patients with opioid dependence as compared to the standard of care (SoC) in Norway.
View Article and Find Full Text PDFHarm Reduct J
December 2024
Sexual and Reproductive Health Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
J Assoc Physicians India
December 2024
Professor and Head, Department of Internal Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India.
This case report discusses an interesting instance of acute respiratory distress syndrome (ARDS) induced by heroin abuse. Heroin, a potent opioid, has been linked to this life-threatening condition. A young man in his early twenties was found unconscious, displaying atypical symptoms such as tachycardia and tachypnea; later he landed up in ARDS.
View Article and Find Full Text PDFExp Brain Res
December 2024
Department of Physiology, Faculty of Medicine, Istanbul Medeniyet University, Istanbul, Turkey.
Heroin addiction is one of the neuropsychiatric burdens that affects many genetic and epigenetic systems. While it is known that heroin may change the expressions of some genes in the brain during dependence, there is no detailed study related to which gene are mostly affected. Therefore, in the current study, we aimed to determine alterations in the miRNA profiles of rats' brains for providing a detailed analysis of molecular mechanisms in heroin addiction-related toxicology.
View Article and Find Full Text PDFBiochemistry (Mosc)
November 2024
Federal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, Moscow, 125315, Russia.
The accumulated evidence suggests that varying levels of tyrosine kinase receptor signaling pathway activity may regulate opiate-associated neuroadaptation of noradrenergic system. Neurotrophin-3 (NT-3) interacts with tropomyosin receptor kinases (TRKs), binding mainly to TRKC receptors, which are expressed within noradrenergic neurons in the blue spot (, LC). Considering the difficulties in delivering full-length neurotrophins to the CNS after systemic administration, low-molecular mimetics of loop 4 in NT-3, hexamethylenediamide bis-(N-monosuccinyl-L-asparaginyl-L-asparagine) (GTS-301), and hexamethylenediamide bis-(N-γ-oxybutyryl-L-glutamyl-L-asparagine) (GTS-302), activating TRKC and TRKB receptors, were synthesized.
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