Mitochondrial oxidative phosphorylation in [PBMCs] is decreased in chronic HIV and correlates with immune dysregulation, 2020, Ganguangco et al

Full title: Mitochondrial oxidative phosphorylation in peripheral blood mononuclear cells is decreased in chronic HIV and correlates with immune dysregulation

Abstract
Background
Cellular immunometabolism among people living with HIV (PLWH) on antiretroviral therapy (ART) remains under investigated. We assessed the relationships between mitochondrial oxidative phosphorylation (OXPHOS) in peripheral blood mononuclear cells (PBMCs) and blood parameters associated with HIV immune dysregulation.

Methods
PLWH ≥40 years old and on stable ART ≥3 months were enrolled (N = 149). OXPHOS complex I (CI, NADH dehydrogenase) and complex IV (CIV, cytochrome c oxidase) protein levels in PBMCs were quantified using immunoassays. Monocyte subsets and markers of T-cell activation, senescence, and exhaustion were measured on PBMC by flow cytometry. Plasma inflammatory mediators were quantified using a multiplex assay. HIV-uninfected group (N = 44) of similar age, gender, and ethnicity had available OXPHOS levels.

Results
PLWH had a median age of 51 years. Majority were male (88.6%), Caucasian (57.7%), and with undetectable plasma HIV RNA <50 copies/mL (84.6%). Median CI level was lower in PLWH compared with the HIV-seronegative group (65.5 vs 155.0 optical density/μg protein x 103, p <0.0001). There was no significant difference in median CIV levels. Lower OXPHOS levels correlated with lower CD4% and CD4/CD8 ratio. On multivariable linear regression adjusted for age, current use of zidovudine/didanosine, and HIV RNA (detectable versus undetectable), lower OXPHOS levels were significantly associated with higher MPO, SAA, SAP, and sVCAM, and higher frequencies of intermediate (CD14++CD16+) monocytes and TIGIT+TIM3+ CD4 T-cell (p<0.01).

Conclusion
CI PBMC protein levels were decreased in PLWH on ART. Decreased OXPHOS correlated with disease severity and inflammation. Further studies on the relationship between immunometabolism and immune dysregulation in HIV are warranted.

Open access, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0231761

 

Similarly: Frontiers | Mitochondrial functions are compromised in CD4 T cells from ART-controlled PLHIV | Immunology (frontiersin.org)

Seems to me that T Cell exhaustion, while a trendy research topic, seems worth understanding well for ME/CFS. After all people often experience a long time period of flu-like symptoms before 'something changes' and that point of something changing essentially equals the beginning of ME/CFS proper. In HIV the complexity of impact of the virus on the immune system is huge, but it is a lot better understood than in ME/CFS and has resulted in clinical treatment approaches.

Worth stating clearly, with regards to the research I link to in this post: The relevant mitochondria are those of the T Cells investigated, rather than a body-wide impact.