Secondary Logo

Journal Logo

Clinical Science

Brief Report: Higher ART Adherence Is Associated With Lower Systemic Inflammation in Treatment-Naive Ugandans Who Achieve Virologic Suppression

Castillo-Mancilla, Jose R. MD*; Morrow, Mary MS; Boum, Yap PhD; Byakwaga, Helen MBChB, PhD§,║; Haberer, Jessica E. MD, MS; Martin, Jeffrey N. MD, MPH; Bangsberg, David MD, MPH#; Mawhinney, Samantha ScD; Musinguzi, Nicholas MSc§; Huang, Yong PhD; Tracy, Russell P. PhD**; Burdo, Tricia H. PhD††; Williams, Kenneth PhD‡‡; Muzzora, Conrad MBBCh, MMed§; Hunt, Peter W. MD; Siedner, Mark J. MD, MPH§,¶

Author Information
JAIDS Journal of Acquired Immune Deficiency Syndromes: April 15, 2018 - Volume 77 - Issue 5 - p 507-513
doi: 10.1097/QAI.0000000000001629



Antiretroviral therapy (ART) prevents AIDS-related morbidity and mortality1–3 and reduces HIV transmission.4 In addition, ART reduces systemic inflammation,5–7 immune activation,8 and coagulopathy9 by achieving and sustaining viral suppression but only partially to levels observed in HIV-negative individuals.6,10,11 This chronic residual inflammation and coagulopathy have been linked to the development of non-AIDS complications, including cardiovascular disease, cancer, and death.12–19 Although multiple interventions aimed at improving residual inflammation have been evaluated (eg, ART intensification, anti-inflammatories, treating coinfections),20–25 most have shown modest or no beneficial effect. Thus, effective strategies to reduce residual inflammation in treated HIV infection are needed.26

Sustained ART adherence is required to achieve durable virological suppression, yet the relationship between adherence and viral suppression is complex and dynamic.27–30 Perfect (ie, 100%) adherence is not required to achieve or sustain viral suppression, and viral suppression is not necessarily a perfect surrogate for complete adherence (ie, ART can be interrupted for short periods without the development of viremia using conventional assays).31–35 However, the consequences of suboptimal adherence, beyond suppression, are unknown. Recently, low self-reported adherence was associated with higher levels of residual inflammation and immune activation in chronically suppressed men living with HIV.36 This association has not been replicated nor has been evaluated in women, treatment-naive individuals, or in cohorts using objective measures of ART adherence. To address this gap, we aimed to determine whether ART adherence, measured by electronic monitoring, is associated with biomarkers of systemic inflammation and coagulopathy among treatment-naive individuals living with HIV who initiate nonnucleoside reverse transcriptase inhibitors (NNRTI) and thymidine analog–based ART.



We evaluated treatment-naive adults living with HIV who initiated first-line ART between 2005 and 2010 and were enrolled in the Uganda AIDS Rural Treatment Outcomes cohort (UARTO, NCT01596322) at a regional referral hospital in Mbarara, Uganda.37–39 In UARTO, participants were followed every 3–4 months; blood was collected for plasma and cell isolation, including CD4+ T-cell count and HIV viral load (VL; Amplicor HIV Monitor 1.5 test; Roche, Branchburg, NJ), at baseline and subsequent visits. For this analysis, we evaluated participants who (1) had available biomarker levels at baseline and after 6 (±1) months of ART; (2) had HIV VL <400 copies per milliliter at the 6-month visit, and; (3) had available ART adherence data for at least 3 months in the 6-month period.

Adherence Measurement

ART adherence (across the 6-month study period) was measured using the medication event monitoring system (MEMS) electronic pill bottle (Aardex Group, Sion, Switzerland), which recorded the date and time for each bottle opening. Average ART adherence was calculated based on the number of observed cap openings divided by the number of prescribed doses/day in the 6-month period (capped at 100%).

Biomarkers of Inflammation, Coagulopathy, and CD8+ T-Cell Activation

Plasma was centrifuged and stored at −80°C until analysis. Most (95%) samples were stored in acid citrate dextrose, whereas the remaining in EDTA; to account for this difference, an adjustment factor of 1.276 was used for biomarkers tested from acid citrate dextrose tubes.39 D-dimer (Diagnostico Stago, Parsippany, NJ), interleukin 6 (IL-6; Human IL-6 Ultra-Sensitive Kit; Meso Scale Diagnostics, Rockville, MD), soluble (s)CD14 (sCD14; R&D Systems, Minneapolis, MN), sCD163 (sCD163; Trillium Diagnostics, Bangor, ME), and the kynurenine/tryptophan ratio were measured in thawed plasma samples, as previously reported.38,39 The percentage of human leukocyte antigen-D–related (HLA-DR)+/CD38+ CD8+ T cells was measured in fresh whole-blood specimens processed on the day of collection, as previously described.37

Statistical Analysis

Demographic and baseline cohort characteristics were summarized. Biomarker concentrations were log transformed, except the proportion of HLA-DR+/CD38+/CD8+ T cells, which was analyzed as an absolute value. The crude change in biomarkers and CD8+ T-cell activation between baseline and the 6-month visit was analyzed using paired t tests. Average ART adherence was considered to be continuous. We used scatter plots to graphically evaluate the relationship between average ART adherence and the outcomes of interest at the 6-month visit, assessing for a linear relationship between the explanatory and outcome variables. We then fit linear regression models to estimate the change in biomarkers and CD8+ T-cell activation after 6-month on ART with changes in ART adherence, adjusting for baseline biomarker values. We initially evaluated a model where average ART adherence was the primary predictor of interest. We then used a model that adjusted for potential confounders, including age, gender, CD4+ T-cell count, baseline HIV VL, depression (using the Hopkins symptoms checklist score40,41), and heavy alcohol use (using the Alcohol Use Disorders Identification Test-C questionnaire42). Variables excluded from the unadjusted model because of missing data and/or collection later during the study included smoking status, illicit drug use, food security, body mass index, and anemia. Because biomarkers of inflammation and CD8+ T-cell activation were analyzed as related and complementary outcomes, we did not correct for multiple comparisons.43 We also performed sensitivity analyses, limiting our sample to participants with an HIV VL of <40 copies per milliliter at the 6-month visit (as the HIV VL assay evolved throughout the course of the study) and removing high-influence observations with DFBETA values outside the range of ±2/sqrt (n) or a Cook D value of >1.0. Statistical analyses were performed using SAS 9.4 (SAS Institute, Inc, Cary, NC). A P value of <0.05 was considered to be statistically significant.

Ethical Considerations

Study procedures were reviewed and approved by the Institutional Review Boards of the Mbarara University of Science and Technology and Partners Healthcare/Massachusetts General Hospital and the Ugandan National Council of Science and Technology. All participants provided written informed consent.


Study Population

Of a total of 546 participants enrolled in the UARTO cohort during the study period, 282 met our evaluation criteria for at least 1 outcome and were included in the unadjusted analysis. Reasons for exclusion were as follows: baseline visit only (24%), no 6-month visit within study window (8%), <3 month MEMS data (8%), no ART initiation within study window (8%), and no HIV VL or HIV VL of >400 copies per milliliter at 6-month visit (4%). The median age was 35 years [interquartile range (IQR) 30–40 years], and 196 (70%) of the participants were women. Heavy alcohol use and depression were reported at least once in 39 (15%) and 92 (34%) of participants, respectively. Most ART regimens were NNRTI based [244 (89%) nevirapine and 21 (7%) efavirenz], with a nucleoside reverse transcriptase inhibitor backbone consisting of zidovudine/lamivudine (68%), stavudine/lamivudine (28%), or other (4%). Median CD4+ T-cell count was 134 cells per cubic millimeter (IQR, 80–198 cells/mm3), and 54% of participants had a baseline HIV VL of >100,000 copies per milliliter. Baseline characteristics of virologically suppressed participants who were included in the adjusted analysis vs. those excluded because of missing data are presented in Table 1.

Baseline Characteristic of Participants Who Achieved Virologic Suppression (<400 copies/mL) at the 6-Month Visit and Were Included in the Multivariate Analysis vs. Those Who Achieved Virologic Suppression (<400 copies/mL) and Were Excluded From the Multivariate Analysis Because of Missing Data (ie, Missing MEMS and/or Covariates, Such as Age, Baseline CD4+ T Cells, Baseline HIV VL, Depression Score† and Alcohol Use‡)

ART Adherence and Biomarkers of Inflammation and Coagulopathy

The median ART adherence was 93% (IQR, 84%–98%); 13 (5%) participants had a mean 6-month adherence of 100%, 194 (68%) had an adherence of 85%–100%, and 75 (27%) had an adherence of <85%. We observed a significant decrease in all biomarkers between the pre-ART and 6-month visits (P < 0.0001 for all biomarkers, except sCD14 P = 0.003). In the analyses adjusted for baseline values of biomarkers only, we identified a statistically significant inverse linear relationship between average ART adherence and biomarkers of inflammation and coagulopathy (Supplemental Digital Content Table 1,, Fig. 1). After additionally adjusting for age, gender, a positive depression screen, heavy alcohol use, and baseline CD4+ T-cell count, and HIV VL (Table 2), these relationships remained statistically significant for IL-6 (15% decrease; P < 0.0001), D-dimer (10% decrease; P = 0.017), and sCD14 (3% decrease; P = 0.028) in participants who achieved virologic suppression to <400 copies per milliliter at the 6-month visit. In the adjusted model for participants who achieved virologic suppression to <40 copies per milliliter, IL-6 (11% decrease; P = 0.040) and sCD163 (7% decrease; P = 0.009) remained statistically significant, despite a smaller sample size (Table 2). These findings were similar (and the slopes in all biomarkers remained negative) when removing highly influential observations (Supplemental Digital Content Table 2, A sensitivity analysis adjusting for the most prevalent ART regimens (limited to participants on 3 TC/AZT/NVP or 3 TC/d4T/NVP, which corresponded to 88% of the ART regimens in this cohort) did not show any additional effect on biomarker levels (data not shown).

Antiretroviral adherence and biomarkers of inflammation, coagulopathy, and CD8+ T-cell activation in virologically suppressed Ugandans living with HIV 6 months after treatment initiation. Scatter plots represent biomarkers values at the 6-month visit by average antiretroviral adherence. K/T ratio, kynurenine/tryptophan ratio; sCD14, soluble CD14; sCD163, soluble CD163.
Antiretroviral Adherence and Biomarkers of Inflammation, Coagulopathy, and CD8+ T-Cell Activation 6 Months After Treatment Initiation in Study Participants Who Achieved an HIV VL of <400 Copies Per Milliliter and <40 Copies Per Milliliter


We demonstrated an inverse relationship between ART adherence, measured using electronic monitoring, and plasma concentrations of biomarkers of inflammation and coagulopathy in treatment-naive Ugandan adults who achieved virologic suppression after 6 months of ART. These relationships remained significant for IL-6, D-dimer, and sCD14 after adjusting for several covariates, including pre-ART CD4+ T-cell count and VL, with decreases of 3%–15% in each biomarker for each 10% increase in average adherence. Interestingly, our observations were the strongest for IL-6, which has also been found to be the strongest predictor of adverse outcomes in comparison with other markers16 and could have been influenced by our overall low CD4 T cell at baseline, as has been previously proposed.44 To our knowledge, this study is the first to demonstrate a relationship between electronically monitored adherence using MEMS, inflammation, and coagulopathy among virologically suppressed patients. Collectively, these findings suggest that variations in ART adherence could have biological consequences that extend beyond achieving and sustaining virologic suppression.

Our findings are consistent with previous observations, where <100% ART adherence (measured subjectively through self-report) was associated with higher levels of inflammatory biomarkers in virologically suppressed men on ART in the United States.36 Among the possible explanations for our findings is that suboptimal ART adherence could lead to low-level viral replication below the limit of detection of most clinically available assays,45–47 which may result in spurts of inflammation and immune activation.48,49 Likewise, incomplete ART adherence could also be associated with intermittent episodes of viremia that are not captured between visits. Further research to evaluate these and other possible mechanisms is needed.

The findings in this study could have clinical implications that deserve further evaluation. Given the relationship between low ART adherence and higher levels of IL-6, which has been associated with higher morbidity and mortality in HIV,12,15,16 suboptimal ART adherence could conceivably also be associated with worse clinical outcomes that extend beyond those prevented by sustained virologic control, although this relationship remains unknown. It is also unclear whether strategies to improve ART adherence can reduce chronic residual inflammation and its downstream consequences in treated HIV infection. Interestingly, in a recent clinical trial of ART intensification among individuals maintaining plasma HIV RNA levels of <40 copies per milliliter, a significant reduction of at least 1 biomarker of immune activation (activated CD4+ T cells) was observed in the placebo arm.23 This was coupled with an early reduction in low-level viremia using a highly sensitive single-copy assay,23 which was also reported in the placebo arm of a second intensification study.24 Although the mechanisms behind these findings in the participants randomized to placebo remain unclear, it is plausible that they could have been mediated, at least partially, by an improvement in ART adherence after enrollment in a clinical trial (ie, Hawthorne effect). Although any single intervention is unlikely to completely reverse residual inflammation and its clinical consequences, ART adherence could play a significant synergistic role to achieve this goal. Future studies evaluating the impact of adherence optimization beyond virologic suppression are necessary to corroborate these hypotheses.

Among the strengths of our study are the inclusion of a diverse population with a large proportion of women in resource-limited settings, the use of an objective adherence measure that is more informative than self-report,50 and the inclusion of multiple biomarkers of systemic inflammation, innate and acquired immune activation, and coagulopathy. The main limitations include the use of a relatively high VL cutoff (<400 copies/mL), the evaluation of primarily older NNRTI-based ART regimens, and the potential influence of unmeasured confounders (ie, smoking and diet). Further studies to determine if these findings persist with even lower VL thresholds and during long-term virologic control are needed.

In addition, these findings should be replicated in the era of modern ART, to determine if the relationships between adherence and inflammation in suppressed patients are generalizable to those taking more forgiving antiretrovirals, such as the integrase strand transfer inhibitors.

In summary, we demonstrated that lower ART adherence is associated with higher inflammation and coagulopathy in treatment-naive Ugandans who achieved virologic suppression after 6 months of therapy. These findings confirm previous observations and suggest that optimal adherence may be required to maximize the biological benefit or ART.


The authors thank the UARTO participants and staff who made this study possible.


1. Group ISS, Lundgren JD, Babiker AG, et al. Initiation of antiretroviral therapy in early asymptomatic HIV infection. N Engl J Med. 2015;373:795–807.
2. Murphy EL, Collier AC, Kalish LA, et al. Highly active antiretroviral therapy decreases mortality and morbidity in patients with advanced HIV disease. Ann Intern Med. 2001;135:17–26.
3. Zolopa A, Andersen J, Powderly W, et al. Early antiretroviral therapy reduces AIDS progression/death in individuals with acute opportunistic infections: a multicenter randomized strategy trial. PLoS One. 2009;4:e5575.
4. Cohen MS, Chen YQ, McCauley M, et al. Antiretroviral therapy for the prevention of HIV-1 transmission. N Engl J Med. 2016;375:830–839.
5. Palella FJ Jr, Gange SJ, Benning L, et al. Inflammatory biomarkers and abacavir use in the Women's Interagency HIV Study and the Multicenter AIDS Cohort Study. AIDS. 2010;24:1657–1665.
6. Wada NI, Jacobson LP, Margolick JB, et al. The effect of HAART-induced HIV suppression on circulating markers of inflammation and immune activation. AIDS. 2015;29:463–471.
7. Baker JV, Neuhaus J, Duprez D, et al. Changes in inflammatory and coagulation biomarkers: a randomized comparison of immediate versus deferred antiretroviral therapy in patients with HIV infection. J Acquir Immune Defic Syndr. 2011;56:36–43.
8. Hileman CO, Kinley B, Scharen-Guivel V, et al. Differential reduction in monocyte activation and vascular inflammation with integrase inhibitor-based initial antiretroviral therapy among HIV-infected individuals. J Infect Dis. 2015;212:345–354.
9. Sereti I, Krebs SJ, Phanuphak N, et al. Persistent, albeit reduced, chronic inflammation in persons starting antiretroviral therapy in acute HIV infection. Clin Infect Dis. 2017;64:124–131.
10. Neuhaus J, Jacobs DR Jr, Baker JV, et al. Markers of inflammation, coagulation, and renal function are elevated in adults with HIV infection. J Infect Dis. 2010;201:1788–1795.
11. French MA, King MS, Tschampa JM, et al. Serum immune activation markers are persistently increased in patients with HIV infection after 6 years of antiretroviral therapy despite suppression of viral replication and reconstitution of CD4+ T cells. J Infect Dis. 2009;200:1212–1215.
12. Tenorio AR, Zheng Y, Bosch RJ, et al. Soluble markers of inflammation and coagulation but not T-cell activation predict non-AIDS-defining morbid events during suppressive antiretroviral treatment. J Infect Dis. 2014;210:1248–1259.
13. Borges AH, Silverberg MJ, Wentworth D, et al. Predicting risk of cancer during HIV infection: the role of inflammatory and coagulation biomarkers. AIDS. 2013;27:1433–1441.
14. McKibben RA, Margolick JB, Grinspoon S, et al. Elevated levels of monocyte activation markers are associated with subclinical atherosclerosis in men with and those without HIV infection. J Infect Dis. 2015;211:1219–1228.
15. Kuller LH, Tracy R, Belloso W, et al. Inflammatory and coagulation biomarkers and mortality in patients with HIV infection. PLoS Med. 2008;5:e203.
16. Borges AH, O'Connor JL, Phillips AN, et al. Interleukin 6 is a stronger predictor of clinical events than high-sensitivity C-Reactive protein or d-dimer during HIV infection. J Infect Dis. 2016;214:408–416.
17. Tien PC, Choi AI, Zolopa AR, et al. Inflammation and mortality in HIV-infected adults: analysis of the FRAM study cohort. J Acquir Immune Defic Syndr. 2010;55:316–322.
18. Sandler NG, Wand H, Roque A, et al. Plasma levels of soluble CD14 independently predict mortality in HIV infection. J Infect Dis. 2011;203:780–790.
19. Knudsen TB, Ertner G, Petersen J, et al. Plasma soluble CD163 level independently predicts all-cause mortality in HIV-1-infected individuals. J Infect Dis. 2016;214:1198–1204.
20. Hunt PW, Martin JN, Sinclair E, et al. Valganciclovir reduces T cell activation in HIV-infected individuals with incomplete CD4+ T cell recovery on antiretroviral therapy. J Infect Dis. 2011;203:1474–1483.
21. Funderburg NT, Jiang Y, Debanne SM, et al. Rosuvastatin reduces vascular inflammation and T-cell and monocyte activation in HIV-infected subjects on antiretroviral therapy. J Acquir Immune Defic Syndr. 2015;68:396–404.
22. O'Brien MP, Hunt PW, Kitch DW, et al. A randomized placebo controlled trial of aspirin effects on immune activation in chronically human immunodeficiency virus-infected adults on virologically suppressive antiretroviral therapy. Open Forum Infect Dis. 2017;4:ofw278.
23. Hunt PW, Shulman NS, Hayes TL, et al. The immunologic effects of maraviroc intensification in treated HIV-infected individuals with incomplete CD4+ T-cell recovery: a randomized trial. Blood. 2013;121:4635–4646.
24. Hatano H, Hayes TL, Dahl V, et al. A randomized, controlled trial of raltegravir intensification in antiretroviral-treated, HIV-infected patients with a suboptimal CD4+ T cell response. J Infect Dis. 2011;203:960–968.
25. Wilkin TJ, Lalama CM, McKinnon J, et al. A pilot trial of adding maraviroc to suppressive antiretroviral therapy for suboptimal CD4(+) T-cell recovery despite sustained virologic suppression: ACTG A5256. J Infect Dis. 2012;206:534–542.
26. Hunt PW, Lee SA, Siedner MJ. Immunologic biomarkers, morbidity, and mortality in treated HIV infection. J Infect Dis. 2016;214(suppl 2):S44–S50.
27. Gardner EM, Burman WJ, Maravi ME, et al. Durability of adherence to antiretroviral therapy on initial and subsequent regimens. AIDS Patient Care STDS. 2006;20:628–636.
28. Nachega JB, Marconi VC, van Zyl GU, et al. HIV treatment adherence, drug resistance, virologic failure: evolving concepts. Infect Disord Drug Targets. 2011;11:167–174.
29. Lima VD, Bangsberg DR, Harrigan PR, et al. Risk of viral failure declines with duration of suppression on highly active antiretroviral therapy irrespective of adherence level. J Acquir Immune Defic Syndr. 2010;55:460–465.
30. Parienti JJ, Ragland K, Lucht F, et al. Average adherence to boosted protease inhibitor therapy, rather than the pattern of missed doses, as a predictor of HIV RNA replication. Clin Infect Dis. 2010;50:1192–1197.
31. Musinguzi N, Mocello RA, Boum Y II, et al. Duration of viral suppression and risk of rebound viremia with first-line antiretroviral therapy in rural Uganda. AIDS Behav. 2017;21:1735–1740.
32. Viswanathan S, Detels R, Mehta SH, et al. Level of adherence and HIV RNA suppression in the current era of highly active antiretroviral therapy (HAART). AIDS Behav. 2015;19:601–611.
33. Bangsberg DR. Less than 95% adherence to nonnucleoside reverse-transcriptase inhibitor therapy can lead to viral suppression. Clin Infect Dis. 2006;43:939–941.
34. Shuter J, Sarlo JA, Kanmaz TJ, et al. HIV-infected patients receiving lopinavir/ritonavir-based antiretroviral therapy achieve high rates of virologic suppression despite adherence rates less than 95%. J Acquir Immune Defic Syndr. 2007;45:4–8.
35. Haberer JE, Musinguzi N, Boum Y II, et al. Duration of antiretroviral therapy adherence interruption is associated with risk of virologic rebound as determined by real-time adherence monitoring in rural Uganda. J Acquir Immune Defic Syndr. 2015;70:386–392.
36. Castillo-Mancilla JR, Brown TT, Erlandson KM, et al. Suboptimal adherence to combination antiretroviral therapy is associated with higher levels of inflammation despite HIV suppression. Clin Infect Dis. 2016;63:1661–1667.
37. Hunt PW, Cao HL, Muzoora C, et al. Impact of CD8+ T-cell activation on CD4+ T-cell recovery and mortality in HIV-infected Ugandans initiating antiretroviral therapy. AIDS. 2011;25:2123–2131.
38. Byakwaga H, Boum Y II, Huang Y, et al. The kynurenine pathway of tryptophan catabolism, CD4+ T-cell recovery, and mortality among HIV-infected Ugandans initiating antiretroviral therapy. J Infect Dis. 2014;210:383–391.
39. Siedner MJ, Kim JH, Nakku RS, et al. Persistent immune activation and carotid atherosclerosis in HIV-infected Ugandans receiving antiretroviral therapy. J Infect Dis. 2016;213:370–378.
40. Psaros C, Haberer JE, Boum Y II, et al. The factor structure and presentation of depression among HIV-positive adults in Uganda. AIDS Behav. 2015;19:27–33.
41. Tsai AC, Bangsberg DR, Frongillo EA, et al. Food insecurity, depression and the modifying role of social support among people living with HIV/AIDS in rural Uganda. Soc Sci Med. 2012;74:2012–2019.
42. Bush K, Kivlahan DR, McDonell MB, et al. The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med. 1998;158:1789–1795.
43. Bacchetti P, Deeks SG, McCune JM. Breaking free of sample size dogma to perform innovative translational research. Sci Transl Med. 2011;3:87ps24.
44. Salter ML, Lau B, Mehta SH, et al. Correlates of elevated interleukin-6 and C-reactive protein in persons with or at high-risk for HCV and HIV infections. J Acquir Immune Defic Syndr. 2013;64:488–495.
45. Pasternak AO, de Bruin M, Jurriaans S, et al. Modest nonadherence to antiretroviral therapy promotes residual HIV-1 replication in the absence of virological rebound in plasma. J Infect Dis. 2012;206:1443–1452.
46. Podsadecki TJ, Vrijens BC, Tousset EP, et al. Decreased adherence to antiretroviral therapy observed prior to transient human immunodeficiency virus type 1 viremia. J Infect Dis. 2007;196:1773–1778.
47. Li JZ, Gallien S, Ribaudo H, et al. Incomplete adherence to antiretroviral therapy is associated with higher levels of residual HIV-1 viremia. AIDS. 2014;28:181–186.
48. Mavigner M, Delobel P, Cazabat M, et al. HIV-1 residual viremia correlates with persistent T-cell activation in poor immunological responders to combination antiretroviral therapy. PLoS One. 2009;4:e7658.
49. Ostrowski SR, Katzenstein TL, Pedersen BK, et al. Residual viraemia in HIV-1-infected patients with plasma viral load <or=20 copies/ml is associated with increased blood levels of soluble immune activation markers. Scand J Immunol. 2008;68:652–660.
50. Williams AB, Amico KR, Bova C, et al. A proposal for quality standards for measuring medication adherence in research. AIDS Behav. 2013;17:284–297.

adherence; inflammation; antiretroviral therapy; Uganda

Supplemental Digital Content

Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc.