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Morphine potentiates neuropathogenesis of SIV infection in rhesus macaques
Sirosh M Bokhari1, Ramakrishna Hegde, Shannon Callen
1Department of Medicine, Division of Molecular Oncology, Washington University School of Medicine, St Louis, MO 63110, USA.
Abstract:
Despite the advent of antiretroviral therapy, complications of HIV-1 infection with concurrent drug abuse are an emerging problem. Opiates are well known to modulate immune responses by preventing the development of cell-mediated immune responses. Their effect on the pathogenesis of HIV-1 infection however remains controversial. Using the simian immunodeficiency virus/macaque model of HIV pathogenesis, we sought to explore the impact of morphine on disease progression and pathogenesis. Sixteen rhesus macaques were divided into two groups; four were administered saline and 12 others morphine routinely. Both groups of animals were then inoculated with SIVmacR71/17E and followed longitudinally for disease pathogenesis. The morphine group (M+V) exhibited a trend towards higher mortality rates and retardation in weight gain compared to the virus-alone group. Interestingly, a subset of M+V animals succumbed to disease within weeks post-infection. These rapid progressors also exhibited a higher incidence of other end-organ pathologies. Despite the higher numbers of circulating CD4+ and CD8+ T cells in the M+V group, CD4/CD8 ratios between the groups remained unchanged. Plasma and CSF viral load in the M+V group was at least a log higher than the control group. Similarly, there was a trend toward increased virus build-up in the brains of M+V animals compared with controls. A novel finding of this study was the increased influx of infected monocyte/macrophages in the brains of M+V animals.
Insights
Morphine use in macaques infected with simian immunodeficiency virus (SIV) accelerated disease progression, increasing mortality and viral load. This highlights potential risks of opiate abuse during HIV infection.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Antiretroviral therapy has improved HIV-1 outcomes, but complications from concurrent drug abuse, particularly opiates, are increasing.
- Opiates are known to modulate immune responses, but their specific impact on HIV-1 pathogenesis remains debated.
Purpose of the Study:
- To investigate the effect of morphine administration on simian immunodeficiency virus (SIV) disease progression and pathogenesis in a macaque model.
- To explore the influence of morphine on viral load, immune cell dynamics, and neuropathogenesis in SIV-infected rhesus macaques.
Main Methods:
- Rhesus macaques were divided into saline-treated (control) and morphine-treated groups.
- Both groups were inoculated with SIVmacR71/17E and monitored longitudinally for disease progression, viral load, immune cell counts, and neuropathology.
Main Results:
- The morphine-treated group showed a trend towards higher mortality rates, weight loss, and rapid disease progression.
- Viral loads in plasma and cerebrospinal fluid (CSF) were significantly higher in the morphine group.
- Increased infiltration of infected monocyte/macrophages into the brain was observed in morphine-treated animals.
Conclusions:
- Morphine administration exacerbates SIV pathogenesis in macaques, leading to accelerated disease and increased viral burden.
- Opiate use may worsen HIV-1 outcomes by promoting viral replication and neuroinvasion.
- These findings underscore the detrimental impact of concurrent opiate abuse on HIV-1 progression.
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