Differences in survival according to malignancy type and degree of immunodeficiency in HIV-infected patients

Fernández-Ruiz, Alexia; Sanjoaquín-Conde, Isabel; Letona-Carbajo, Santiago; Lambea-Sorrosal, Julio José; Crusells-Canales, María José

doi:10.1016/j.medcle.2019.06.023

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…This aligns with the prevailing consensus that HIV infection impairs the immune system by preferentially destroying CD4-positive T cells. Indeed, the altered immunological profiles of the HIV-positive study population are consistent with previous research on the detrimental effect of HIV infection on immune system functionality [ 52 , 53 ]. Moreover, the observation of a negative correlation between CD4 count and MDA concentrations provides further evidence for the probable influence of both HIV infection and chemical exposures on cellular pathways associated with oxidative stress and apoptosis.…”

Section: Discussionsupporting

confidence: 87%

Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver

Udah,

Bakarey,

Anetor

et al. 2024

PLOS Glob Public Health

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The growing exposure to occupational chemicals and the spread of human immunodeficiency virus (HIV) infection are major global health issues. However, there is little data on the carcinogenic risk profile of HIV-infected individuals who have been occupationally exposed to chemical mixtures. This study therefore investigated the levels of cancer risk biomarkers in HIV-infected individuals exposed to occupational chemicals, exploring the relationship between apoptotic regulatory and oxidative response markers as a measure of cancer risk. Study participants (mean age 38.35±0.72 years) were divided into four groups according to their HIV status and occupational chemical exposure: 62 HIV-positive exposed (HPE), 66 HIV-positive unexposed (HPU), 60 HIV-negative exposed (HNE), and 60 HIV-negative unexposed (HNU). Serum p53, β-cell lymphoma-2 (bcl2), 8-hydroxydeoxyguanosine (8-OHdG), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured using standard methods. Clusters of differentiation 4 (CD4+) T-lymphocytes were enumerated using flow cytometry. Serum p53 and bcl2 levels in HPE (0.91±0.11ng/ml and 122.37±15.77ng/ml) were significantly lower than HNU (1.49±0.15ng/ml and 225.52±33.67ng/ml) (p < 0.05), respectively. Wildtype p53 and bcl2 were positively and significantly correlated with 8-OHdG (r = 0.35, p<0.001; r = 0.36, p<0.001) and SOD (r = 0.38, p<0.001; r = 0.39, p<0.001). After controlling for gender, age, BMI, and cigarette smoking, both HIV status and SOD activity were significantly associated with wildtype p53 and bcl2 (p < 0.05). Malondialdehyde was significantly higher in the HPE (0.72 ± 0.01 mg/ml) than in the HNE (0.68 ± 0.01 mg/ml) and HNU (0.67 ± 0.01 mg/ml) groups (p < 0.05). The HPE group showed significantly lower CD4 counts than the HNE and HNU groups. Individuals who are HIV-infected and occupationally exposed to chemicals have a constellation of depressed immunity, elevated oxidative stress, and loss of tumour suppressive functions, which together intensify cancer risk, providing valuable scientific and public health bases for preventive measures in this vulnerable population.

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Section: Discussionsupporting

confidence: 87%

Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver

Udah,

Bakarey,

Anetor

et al. 2024

PLOS Glob Public Health

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show abstract

“…This aligns with the prevailing consensus that HIV infection impairs the immune system by preferentially destroying CD4-positive T cells. Indeed, the altered immunological profiles of the HIV-positive study population are consistent with previous research on the detrimental effect of HIV infection on immune system functionality [50,51]. Moreover, the observation of a negative correlation between CD4 count and MDA concentrations provides further evidence for the probable influence of both HIV infection and chemical exposures on cellular pathways associated with oxidative stress and apoptosis.…”

Section: Discussionsupporting

confidence: 86%

Occupational cancer risk surveillance in HIV-infected individuals exposed to chemicals: Role of p53 molecular marker

Udah,

Bakarey,

Anetor

et al. 2024

Preprint

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The growing exposure to occupational chemicals and HIV infection are both major global health issues. However, there is little data on the carcinogenic risk profile of HIV-infected individuals who have been occupationally exposed to chemical mixtures. This study therefore investigated the levels of cancer risk biomarkers in HIV-infected individuals exposed to occupational chemicals, exploring the relationship between apoptotic regulatory markers and DNA oxidative response markers as a measure of cancer risk.Apparently healthy adults (mean age 38.35±0.72years) were divided into four groups according to their HIV status and occupational chemical exposure: 62 HIV positive exposed (HPE), 66 HIV positive unexposed (HPU), 60 HIV negative exposed (HNE), and 60 HIV negative unexposed (HNU). Serum p53, bcl2, 8-hydroxydeoxyguanosine (8-OHdG), superoxide dismutase (SOD), and malondialdehyde (MDA) were estimated by standard methods. Blood samples were analysed for CD4 cell count by flow cytometry.Serum p53 and bcl2 levels in HPE (0.91±0.11ng/ml and 122.37±15.77ng/ml) were significantly lower than HNU (1.49±0.15ng/ml and 225.52±33.67ng/ml) (p < 0.05), respectively. Wildtype p53 and bcl2 were positively and significantly correlated with 8-OHdG (r=0.35, p<0.001; r=0.36, p<0.001) and SOD (r=0.38, p<0.001; r=0.39, p<0.001). After controlling for gender, age, BMI, and cigarette smoking, both HIV status and SOD activity were significantly associated with wildtype p53 and bcl2 (p < 0.05). Malondialdehyde was significantly higher in the HPE (0.72 ± 0.01 mg/ml) than in the HNE (0.68 ± 0.01 mg/ml) and HNU (0.67 ± 0.01 mg/ml) groups (p < 0.05). Additionally, the HPE group (578.87±33.64 cells/µL) exhibited significantly lower CD4 counts than the HNE (785.35±36.8 cells/µL) and HNU (862.15±43.29 cells/µL) groups. Individuals infected with HIV and occupationally exposed to chemical substances exhibit compromised immunity, elevated oxidative stress, and depressed p53 (loss of tumour suppressive capacity) and bcl2; a convergence promoting the carcinogenic pathway and elevated cancer risk. These findings provide a mechanistic basis of cancer risk and scientific justification for preventive strategies against carcinogenesis in individuals who are HIV-infected.

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“…People living with HIV are at a higher risk of developing NHL due to their weakened immune system. The risk of developing NHL increases with the degree of immune suppression and other factors such as co-infection with other viruses and lifestyle factors [1,[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Aids and Non-Hodgkin Lymphoma: Report of a Case

2023

Int J Virol AIDS

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A 49-year-old male resident of Cancun has the following significant history: full immunization, SARS-CoV-2, 2 AstraZeneca doses, previous hospitalizations on two occasions in the last three years for pneumonia, transfusions in March 2022 for anemia, alcoholism for 29 years at a rate of 14 gr/day suspended 8 months ago. HIV positive for 20 years with intermittent adherence to treatment, currently with a third treatment scheme with ritonavir, darunavir, dolutegravir and tenofobir with emtricitabine.

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Differences in survival according to malignancy type and degree of immunodeficiency in HIV-infected patients

Cited by 3 publications

References 27 publications

Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver

Increased cancer risk in HIV-infected individuals occupationally exposed to chemicals: Depression of p53 as the key driver

Occupational cancer risk surveillance in HIV-infected individuals exposed to chemicals: Role of p53 molecular marker

Aids and Non-Hodgkin Lymphoma: Report of a Case

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