Function of Serum Adenosine Deaminase as an Indicator of Immune Status in HIV Patients treated with Combination Antiretroviral Therapy

Acquired immunodeficiency syndrome (AIDS) is one of the greatest public health and social problems threatening the human race. The trend of annual AIDS deaths is showing a steady decline since the implementation of the free Anti-Retroviral Therapy (ART) program in India (2004). HIV infection is characterized by replication of virus by abnormal non specific immune activation and persistent inflammation. Adenosine deaminase (ADA) has a cytokine-like co-stimulatory role in T cell proliferation which is independent of catalytic activity. Therefore, we decided to study the role of ADA as an indicator of immune status in HIV patients treated with combination antiretroviral therapy (cART). Adenosine deaminase activity (ADA) in HIV patients was estimated before and after 3 months interval of antiretroviral therapy (ART) up to 9 months. The study included 150 HIV positive patients between age group of 20-50 years from ICTC (Integrated Counseling and Testing Centre) and ART centre. Venous blood samples were collected in plain bulb to estimate serum ADA activity before and after 3 months interval upto 9 months of ART. Serum ADA activity was estimated using colorimetric method of Giusti and Galanti. Activity of serum ADA was significantly raised before and after 3 months interval of ART with decrease in CD4 cell count. After 6 months, increased ADA activity started declining and comes to near normal after 9 months of ART (p<0.001). Elevated serum adenosine deaminase activity in HIV patients is an indicator of T-cell activation. Serum ADA activity along with other markers can be used as a prognostic marker to monitor response to antiretroviral therapy and immunocompetence in HIV patients.

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Plasma adenosine deaminase activity among HIV1 Clade C seropositives: Relation to CD4 T cell population and antiretroviral therapy

Clinica Chimica Acta ◽

10.1016/j.cca.2006.09.006 ◽

2007 ◽

Vol 377 (1-2) ◽

pp. 133-137 ◽

Cited By ~ 14

Author(s):

Seetharamaiah Chittiprol ◽

P. Satishchandra ◽

R.S. Bhimasenarao ◽

G.R. Rangaswamy ◽

S.V. Sureshbabu ◽

...

Keyword(s):

T Cell ◽

Antiretroviral Therapy ◽

Adenosine Deaminase ◽

Cell Population ◽

Cd4 T Cell ◽

Adenosine Deaminase Activity ◽

Clade C ◽

Plasma Adenosine

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European mitochondrial haplogroups are associated with CD4+ T cell recovery in HIV-infected patients on combination antiretroviral therapy

Journal of Antimicrobial Chemotherapy ◽

10.1093/jac/dkt206 ◽

2013 ◽

Vol 68 (10) ◽

pp. 2349-2357 ◽

Cited By ~ 11

Author(s):

María Guzmán-Fulgencio ◽

Juan Berenguer ◽

Dariela Micheloud ◽

Amanda Fernández-Rodríguez ◽

Mónica García-Álvarez ◽

...

Keyword(s):

T Cell ◽

Antiretroviral Therapy ◽

Cd4 T Cell ◽

Combination Antiretroviral Therapy ◽

Cell Recovery ◽

Mitochondrial Haplogroups

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Could natural killer cells compensate for impaired CD4+ T-cell responses to CMV in HIV patients responding to antiretroviral therapy?

Clinical Immunology ◽

10.1016/j.clim.2009.03.518 ◽

2009 ◽

Vol 132 (1) ◽

pp. 63-70 ◽

Cited By ~ 2

Author(s):

Dino Bee Aik Tan ◽

Sonia Fernandez ◽

Martyn French ◽

Patricia Price

Keyword(s):

T Cell ◽

Antiretroviral Therapy ◽

Natural Killer Cells ◽

Natural Killer ◽

T Cell Responses ◽

Cd4 T Cell ◽

Hiv Patients ◽

Killer Cells ◽

Cell Responses

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Low CD4+ T-cell counts in HIV patients receiving effective antiretroviral therapy are associated with CD4+ T-cell activation and senescence but not with lower effector memory T-cell function

Clinical Immunology ◽

10.1016/j.clim.2006.04.570 ◽

2006 ◽

Vol 120 (2) ◽

pp. 163-170 ◽

Cited By ~ 42

Author(s):

Sonia Fernandez ◽

Patricia Price ◽

Elizabeth J. McKinnon ◽

Richard C. Nolan ◽

Martyn A. French

Keyword(s):

T Cell ◽

Antiretroviral Therapy ◽

T Cell Activation ◽

Cell Activation ◽

Cell Function ◽

Cd4 T Cell ◽

Effector Memory ◽

Hiv Patients ◽

Memory T Cell ◽

Cell Counts

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Impact of hepatitis C virus co-infection on HIV patients before and after highly active antiretroviral therapy: an immunological and clinical chemistry observation, Addis Ababa, Ethiopia

BMC Immunology ◽

10.1186/1471-2172-14-23 ◽

2013 ◽

Vol 14 (1) ◽

Cited By ~ 13

Author(s):

Solomon Taye ◽

Mekuria Lakew

Keyword(s):

Hepatitis C Virus ◽

Hepatitis C ◽

Antiretroviral Therapy ◽

Highly Active Antiretroviral Therapy ◽

Clinical Chemistry ◽

Addis Ababa ◽

Hiv Patients ◽

Highly Active ◽

Before And After

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Study of serum adenosine deaminase activity and c-reactive protein in patients of rheumatoid arthritis

International Journal of Research in Pharmaceutical Sciences ◽

10.26452/ijrps.v11i4.4724 ◽

2020 ◽

Vol 11 (4) ◽

pp. 7990-7993

Author(s):

Sangeetha R ◽

Ramesh Raju K A P ◽

Hemapriya S ◽

Suganthi V ◽

Panneerselvam P

Keyword(s):

Rheumatoid Arthritis ◽

Adenosine Deaminase ◽

Treatment Plan ◽

Colorimetric Method ◽

Disease Score ◽

C Reactive Protein ◽

Positive Correlation ◽

Reactive Protein ◽

Adenosine Deaminase Activity

Rheumatoid arthritis (RA) is a chronic disease that causes inflammatory synovitis. The treatment plan of RA includes reducing inflammation and improving the quality of life. Hence, understanding the role of Adenosine deaminase (ADA) and C-reactive protein helps for a better plan of treatment. The present study was undertaken to determine the serum ADA activity and CRP in RA patients and correlate with the severity of the progression of the disease. 25 patients diagnosed with RA as per 2010 ACR/EULAR criteria and 25 age and sex matched healthy controls were included in the study after informed consent. Blood samples were collected from all the subjects after an overnight fast, serum separated was analyzed immediately for Adenosine deaminase(ADA) activity measured using colorimetric method of Guisti and Galanti. Disease score, C-reactive protein, RA factor, ADA and ESR were significantly higher in cases when compared with controls. Significant positive correlation was present between the disease score and C-reactive protein, RA factor among cases. A positive correlation was observed between the disease score and ADA, but it was not statistically significant among cases.

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Alteration of tumor necrosis factor–α T-cell homeostasis following potent antiretroviral therapy: contribution to the development of human immunodeficiency virus–associated lipodystrophy syndrome

Blood ◽

10.1182/blood.v95.10.3191 ◽

2000 ◽

Vol 95 (10) ◽

pp. 3191-3198 ◽

Cited By ~ 117

Author(s):

Eric Ledru ◽

Névéna Christeff ◽

Olivier Patey ◽

Pierre de Truchis ◽

Jean-Claude Melchior ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

T Cell ◽

Antiretroviral Therapy ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Interleukin 2 ◽

Hiv Patients ◽

Immunodeficiency Virus ◽

Necrosis Factor

Abstract Highly-active antiretroviral therapy (HAART) has lead to a dramatic decrease in the morbidity of patients infected with the human immunodeficiency virus (HIV). However, metabolic side effects, including lipodystrophy-associated (LD-associated) dyslipidemia, have been reported in patients treated with antiretroviral therapy. This study was designed to determine whether successful HAART was responsible for a dysregulation in the homeostasis of tumor necrosis factor- (TNF-), a cytokine involved in lipid metabolism. Cytokine production was assessed at the single cell level by flow cytometry after a short-term stimulation of peripheral blood T cells from HIV-infected (HIV+) patients who were followed during 18 months of HAART. A dramatic polarization to TNF- synthesis of both CD4 and CD8 T cells was observed in all patients. Because it was previously shown that TNF- synthesis by T cells was highly controlled by apoptosis, concomitant synthesis of TNF- and priming for apoptosis were also analyzed. The accumulation of T cells primed for TNF- synthesis is related to their escape from activation-induced apoptosis, partly due to the cosynthesis of interleukin-2 (IL-2) and TNF-. Interestingly, we observed that LD is associated with a more dramatic TNF- dysregulation, and positive correlations were found between the absolute number of TNF- CD8 T-cell precursors and lipid parameters usually altered in LD including cholesterol, triglycerides, and the atherogenic ratio apolipoprotein B (apoB)/apoA1. Observations from the study indicate that HAART dysregulates homeostasis of TNF- synthesis and suggest that this proinflammatory response induced by efficient antiretroviral therapy is a risk factor of LD development in HIV+ patients.

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