Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease

Experimental evidence from animal models has provided a framework for our current understanding of autoimmune disease pathogenesis and supports the importance of genetic predisposition, molecular mimicry, and immune dysregulation. However, only recently has evidence emerged to support the role of immune dysregulation in human organ-specific autoimmune disease. In the current study of the "late" manifestation of autoimmune thyroid disease (AITD) in a cohort of human immunodeficiency virus (HIV)-positive patients following highly active antiretroviral therapy (HAART), we discuss how immune dysregulation and factors associated with the immunopathology of HIV infection fit the current understanding of autoimmunity and provide a plausible basis for our clinical observations. De novo diagnoses of thyroid disease were identified between 1996 and 2002 in 7 HIV treatment centers (5/7 centers completed the study). Patients were diagnosed as clinical case entities and not discovered through thyroid function test screening. Paired plasma specimens were used to demonstrate sequential rise in thyroid antibodies.Seventeen patients were diagnosed with AITD (median age, 38 yr; 65% were of black African or black Caribbean ethnicity; and 82% were female). The median duration of immune reconstitution was 17 months. Graves disease (GD) was diagnosed in 15 of 17 patients. One patient developed hashithyrotoxicosis with atypically raised C-reactive protein, and another developed hypothyroidism. One GD patient had associated secondary hypoadrenalism. The estimated combined prevalence of GD for 4 treatment centers for female patients was 7/234 and for males was 2/1289. The denominator numbers were matched controls, from 4 centers able to provide data, who commenced HAART during the same time (January 1996 to July 2002) and who did not develop clinical AITD. The mean baseline pre-HAART CD4 count was 67 cells/mL, and the mean increase from nadir to AITD presentation was 355 cells/mL. AITD patients were more likely than controls (95% confidence interval, chi-square test) to be severely compromised at baseline (as defined by a CD4 count < 200 cells/mL or the presence of an acquired immunodeficiency syndrome [AIDS]-defining diagnosis), and to experience greater CD4 increments following HAART. AITD may be a late manifestation of immune reconstitution in HIV-positive patients taking HAART, and immune dysregulation may be an important factor.     

Recurrence of Mycobacterium avium infection in patients receiving highly active antiretroviral therapy and antimycobacterial agents.

The known effects of highly active antiretroviral therapy (HAART) on opportunistic infections (OIs) range from immune restoration disease to remission of specific OIs. In the present study, Mycobacterium avium complex infection recurred in 3 patients receiving antimycobacterial therapy and HAART. At the time of the initial M. avium infection, the mean CD4 cell count was 22.3 cells/mm3, and the HIV viral load was 181,133 copies/mL. Relapse occurred a mean of 14. 3 months after the first episode; the mean follow-up CD4 cell count was 89/mm3 (mean elevation of 66 cells/mm3), and the HIV viral load was <400 copies/mL in each patient. M. avium was isolated from blood (1 patient), blood and lymph node (1), and small-bowel tissue (1). M. avium infection may recur as a generalized or focal disease in those who are receiving antimycobacterial agents but whose HAART-associated CD4 cell recovery, although significant, is not optimal.     

Restoration of normal interleukin-2 production by CD4+ T cells of human immunodeficiency virus-infected patients after 9 months of highly active antiretroviral therapy.

The present study investigated immune restoration in patients at intermediate stages of human immunodeficiency virus (HIV) disease after initiation of highly active antiretroviral therapy (HAART). A progressive increase in both memory and naive CD4+ T cells was observed from the first weeks of therapy, concomitant with a decrease in the expression of activation markers on CD8+ T cells. The early-activation marker CD69 remained, however, overexpressed on T cells after suboptimal stimulation in vitro, indicative of persistent immune activation. The percentage of interleukin (IL)-2-producing CD4+ T cells significantly increased from 9 months of HAART. In most patients, CD4+ T cells recovered an ability to produce IL-2 on stimulation, similar to that of HIV-seronegative controls. Reversal of T-cell anergy may be a key event in immune restoration for achieving long-term clinical benefit with HAART.     

Change in transaminases in hepatitis C virus- and HIV-coinfected patients after highly active antiretroviral therapy: differences between complete and partial virologic responders?

Patients with HIV and hepatitis C virus (HCV) coinfection have more severe hepatitis-related disease than do patients with HCV infection alone. Highly active antiretroviral therapy (HAART) with protease inhibitor appears to restore pathogen-specific immune responses, especially in patients with persistent undetectable HIV viral load. To evaluate the potent impact of immune restoration induced by HAART on the course of HCV-related disease, HCV viremia and levels of transaminases were compared between two groups of patients: 10 HIV/HCV-coinfected patients with persistently undetectable HIV viremia (group A) and 12 HIV/HCV-coinfected patients with persistent detectable HIV viremia. No difference was detected in HCV viral load in either group. An increase in transaminases was found only in patients with persistent undetectable HIV viral load, which was correlated with the increase in CD8+ T cells. This may suggest that the restoration of CD8+ T cell cytotoxicity could lead to an enhancement of hepatitis C-related disease in HCV/HIV-coinfected patients receiving HAART.     

Spontaneous remission of cytomegalovirus retinitis in a patient infected with the human immunodeficiency virus

BACKGROUND: We report a case of CMV retinitis cured in an AIDS patient after two months of regular HAART therapy without CMV medications. CASE REPORT: A 37-year-old patient (baseline CD4 count 47/ml) receiving HAART (2 NRTI and 1 IP) showed poor compliance and had increased his CD4 count for two months reaching 263/ml although HIV viral load remained high (71,840 copies/ml). His fundus was normal. He was evaluated 8 months after a period of loss to follow-up: his CD4 count was 65/ml, HIV viral load was 123,000 copies/ml, CMV serology for IgV and viruria were positive, viremia was negative, his fundus revealed a healed CMV retinitis. Six months later and without any CMV therapy, no relapse has been observed while regularly taking HAART medications. CONCLUSION: Few cases have been reported in which HAART therapy with good immune response and reduced HIV viral load lead to complete regression of CMV retinitis without specific CMV medication. This case suggests that, even with an uncontrolled HIV viral load, HAART via transient immune restoration may contribute to resolving CMV retinitis.     

艾滋病的高效抗逆转录病毒治疗、疗效观察及其对免疫功能的影响

目的 为探讨艾滋病高效抗逆转录病毒治疗、疗效观察及其对免疫功能的影响.方法 应用HAART疗法对4例有严重免疫功能低下的HIV/AIDS病人进行治疗.结果 所有病人在治疗4周HIV复制被明显抑制,血浆病毒载量平均下降1.99log/ml(0.73～2.46log/ml),CD_8~ 、CD_4~ 细胞和血浆IL-2浓度在4～12周后持续性显著增高,上升幅度分别为67.2%,103.0%,255.1%,而血浆sIL-2R、IL-6、TNF-α、sTNFR-I、Neopterin浓度在治疗4～12周后持续下降至正常水平或以下.HAART治疗后各因素变化间的相关性分析显示,CD_4~ 细胞数与CD_8~ 、CD_3~ 细胞和血浆IL-2浓度之间,血浆病毒载量与sIL-2R、IL-6、TNF-α、sTNFR-I、Neopterin之间,sTNFR-I和Neopterin与sIL-2R、IL-6、TNF-α之间均存在明显正直线相关性;而CD_4~ 细胞数与血浆病毒载量、sIL-2R、sTNFR-I、Neopterin之间.以及IL-2和sIL-2R之间则有明显负直线相关性.结论 抗病毒治疗效果、病毒复制和免疫活化间具有密切关系,HAART治疗能快速有效地抑制HIV-1的复制,纠正机体免疫功能紊乱和重建免疫功能;外周血CD_4~ 细胞数、血浆病毒载量、IL-2、sIL-2R、TNF-α、sTNFR-I、Neopterin的浓度变化可以作为HAART治疗效果评价的重要指标.     

Percentage of CD3+CD4-CD8-gammadeltaTCR- T cells is increased HIV disease.

HIV patients given highly active antiretroviral therapy (HAART) experience a rapid rise in alphabetaT cell numbers, but changes in gammadeltaT cell populations have not been described. Here we investigate the effects of immune reconstitution and immune restoration diseases (IRDs) on expression of a pan-gammadeltaT cell receptor (TCR) marker on double-negative (CD3(+)CD4(-)CD8(-)) T cells and T cells expressing CD4 or CD8. IRDs are inflammatory disorders associated with preexisting infections in patients who have achieved immune reconstitution after HAART. Proportions of CD3(+)CD4(-)CD8(-) T cells and total gammadeltaT cells were not affected by CD4(+) T cell counts, HAART, or a history of IRD, but levels of CD4(-)CD8(-)gammadeltaTCR(-) T cells were higher in patients with <15% CD4(+) T cells.     

Herpes zoster as an immune restoration disease in AIDS patients during therapy including protease inhibitors

A prospective study to evaluate the incidence of herpes zoster (HZ) as an immune restoration disease in patients with AIDS during highly active antiretroviral therapy (HAART) was conducted in a series of 115 patients diagnosed with AIDS initiated on HAART between 1 January 2000 and 31 July 2001. Of these, a single dermatomal HZ episode occurred in 14 (12%) patients within one and 15 months of HAART (median eight months). The HZ patients were similar to the non-HZ patients in age, sex, and HIV transmission risk factor, but had a more advanced disease. Compared with the baseline values, the viral loads significantly (P<0.01) decreased, while the mean CD4+ T-cell counts increased by almost four-fold (P<0.01) in both groups at the time of the HZ episode (or equivalent in non-HZ), but remained below 400/mL in the HZ patients. HZ during HAART is an immunopathological consequence of the improvement of the host immuneresponse, correlating with the beginning of immune restoration.     

Oral candidosis as a clinical marker of immune failure in patients with HIV/AIDS on HAART

Oral candidosis (OC) has been proposed as a clinical marker of highly active antiretroviral therapy (HAART) success or failure. The principal objective of this work was to assess whether the presence OC is associated with immunologic or virologic failure in patients with HIV/AIDS undergoing HAART. One hundred fifty-one patients with HIV/AIDS from Regional Hospital "Carlos Haya," Malaga, Spain, were examined orally. All patients had been undergoing HAART for a minimum of 6 months prior to oral examination. OC diagnosis was in accordance with World Health Organization-Centers for Disease Control (WHO-CDC) criteria. Age, gender, route of HIV infection, CD4 lymphocyte counts, and viral load were taken from the medical records. In regard to HAART response the patients were classified as: virologic- responders (viral load < 50 copies per milliliter), virologic nonresponders (viral load >50 copies per milliliter); immunologic responders (CD4 cells counts > 500 per milliliter), and immunologic nonresponders (CD4 cells counts < 500 per milliliter). Prevalence of OC was determined for each group. The presence of OC was closely related to immune failure (p 0.006; odds ratio [OR] 3.38 95% confidence interval [CI] 1.262-12.046) in patients with HIV/AIDS undergoing HAART. The probability of immune failure in the presence of OC was 91% for men who have sex with men, 95.5% for heterosexuals, and 96% for intravenous drug users. In conclusion, OC should be considered a clinical marker of immune failure in patients with HIV/AIDS undergoing HAART.     

Effect of prolonged discontinuation of successful antiretroviral therapy on CD4+ T cell decline in human immunodeficiency virus-infected patients: implications for intermittent therapeutic strategies

This study evaluates the change in CD4(+) T cell counts among patients who achieved complete viral suppression and subsequently discontinued highly active antiretroviral therapy (HAART). We included 72 human immunodeficiency virus (HIV)-1-infected patients with plasma HIV RNA loads of <500 copies/mL for at least 3 months who then discontinued therapy for at least 12 weeks. The median CD4(+) T decay while off HAART was 16 cells/mm(3)/month (interquartile range, -6 to -34 cells/month). The mean follow-up after therapy ended was 45 weeks. The slope of the CD4(+) T cell decay was inversely correlated with the increase of CD4(+) T cells while receiving HAART, baseline virus load, CD4(+) T cell count at the time therapy was discontinued, age, and duration HIV RNA levels were undetectable. In a multiple regression analysis model, the increase of CD4(+) T cells while receiving therapy and age were independently associated with the rate of CD4(+) T cell loss.     

Development of opportunistic infections after diagnosis of active tuberculosis in HIV-infected patients

Despite advances in highly active antiretroviral therapy (HAART), its use during tuberculosis (TB) treatment is fraught with challenges, often leading to delayed therapy. This report describes the course of HIV infection and outcomes of 26 consecutive TB/HIV coinfected patients who received TB treatment in Rhode Island. HIV infection was diagnosed in 26 (4%) of 598 TB cases in during a 10-year period. Of these patients, TB was the first indication of HIV infection in 15 patients (58%). Of the 21 patients who were not on antiretrovirals at the time of TB diagnosis, 17 (81%) met criteria for immediate initiation of HAART. The median CD4 cell counts and HIV-1 plasma viral load were 80 cells per microliter (range, 2-800 cells per microliter) and 255,631 copies per milliliter (range, 50,000 to > 500,000 copies per milliliter), respectively, for the patients whose baseline measurements were available. CD4 lymphocyte count was less than 200 cells per microliter in 13 (76%) of the 17 patients whose measurements were available. Three (30%) of the 10 patients whose CD4 cell count was less than 100 cells per microliter developed subsequent AIDS-defining illness prior to the initiation of HAART and a fourth patient, within 30 days of starting HAART. None of the patients who had CD4 cell counts 100 cells per microliter or greater developed subsequent AIDS-defining illness during TB treatment. The median time to starting HAART after starting TB treatment was 12 weeks (range, 3-36 weeks). From our limited experience based on this case series, we recommend early initiation of HAART in coinfected patients with CD4 cell counts less than 100 cells per microliter.     

Highly active antiretroviral therapy as the sole treatment for AIDS-related primary central nervous system lymphoma: a case report with implications for treatment

A 40-year-old male presented to medical attention with Pneumocystis jiroveci pneumonia and HIV infection. His CD4+ count was 18 cells per microliter and his HIV viral load (VL) was more than 400,000 copies milliliter. After 3 weeks of antibiotic therapy, he continued to have global cognitive deficits. A brain imaging study showed a right temporal mass, which on biopsy proved to be primary central nervous system lymphoma (PCNSL). He began highly active antiretroviral therapy (HAART) but declined palliative whole-brain radiotherapy (WBRT). Four months later, his CD4+ count had improved to 153 cells per microliter and his HIV VL was less than 75 copies per milliliter. At 36 months follow-up, he remained in complete remission (CR). Through a literature review, we identified 4 additional PCNSL patients who achieved prolonged remission after the initiation of HAART. One patient required WBRT and ventriculo-peritoneal shunting for signs and symptoms of obstructive hydrocephalus. The other 3 patients presented with stable neurologic findings and were treated with HAART alone. The median initial CD4+ count for these patients was 50 cells per microliter (range, 2 to 220 cells per microliter). All 5 remained in CR with a median follow-up of 23.5 (range, 13 to 36) months. For patients who present with PCNSL as their initial AIDS-defining event, stable neurologic findings, and effective HAART options, initial treatment with HAART alone may be possible, reserving WBRT and corticosteroids for those who show signs of impending neurologic demise. Chemotherapy and other novel approaches could also be considered for selected patients with lesser degrees of immune suppression and high baseline functional status.     

300例艾滋病患者高效抗逆转录病毒治疗后免疫重建规律探讨

目的探讨高效抗逆转录病毒治疗（HAART）对中国南部地区艾滋病患者的免疫重建规律。方法收集近3年来300例患者的完整资料,按基线CD4^＋T细胞数分为A、B、C三组,观察基线及治疗1、3、6、12月末CD4^＋T淋巴细胞数、12月末血浆病毒载量（VL）、临床症状和毒副作用。结果抗病毒治疗12月末300例患者CD4^＋T淋巴细胞计数平均上升127个／1,以治疗3月后增长明显,3、12月末与基线CD4^＋T淋巴细胞计数比较差异有显著性（P〈0．05）;12月末273例（91％）患者血浆病毒载量（VL）〈5copies/ml,27例（9％）患者病毒载量（VL）〉50copies/ml,高病毒载量A组16例,C组4例;A组与C组比较差异有显著性（P〈0．05）;药物不良反应主要是外周神经炎（35．4％）、骨髓抑制（18．2％）、皮疹（15．2％）、肝功能损害（12．1％）、乳酸酸中毒（12．1％）和肾结石（6．1％）。结论HAART治疗对中国南部地区的艾滋病患者有效,能够实现免疫重建,但存在较多毒副作用。     

Immune activation in patients infected with HIV type 1 and maintaining suppression of viral replication by highly active antiretroviral therapy

Immune activation associated with HIV infection declines after highly active antiretroviral therapy (HAART), but may persist or recur in some patients. It is not clear whether this reflects a resurgence of HIV replication or another cause of immune activation, such as inflammatory reactions to opportunistic pathogens (immune restoration disease [IRD]). Here, we studied plasma and cellular immune activation markers in adult HIV-1 patients who had received HAART for >12 months and maintained plasma HIV RNA levels of <400 copies/ml for >6 months. Plasma interleukin 1 receptor antagonist and tumor necrosis factor receptor I levels were similar in patients and HIV-negative control subjects, but the highest levels occurred mainly in patients with a history of IRD. In contrast, expression of HLA-DR and CD38 on monocytes and of HLA-DR on CD8(+) T cells was higher in patients than in control subjects. Thus, cellular markers of immune activation are abnormal in some patients with a good virological response to HAART, and abnormalities of plasma immune activation markers correlate with a history of IRD.     

Retrospective analysis of suspending HAART in selected patients with controlled HIV replication

We sought to determine the consequences of stopping highly active antiretroviral therapy (HAART) in a group of 41 HIV-infected individuals with undetectable HIV viral loads and CD4+ counts greater than 500 cells per microliter for 6 months or more. Clinical and laboratory parameters were monitored, as was the time to HAART reinitiation. Three months after HAART interruption, the median CD4+ count declined by 162 cells per microliter and HIV viral load increased by 24,000 copies per milliliter. Over the next year, CD4+ counts continued to decrease by an average of 11 cells per microliter per 3-month intervals. In contrast, HIV viral loads remained stable over the same period. Five of 7 patients (71%) with elevated cholesterol levels and 6 of 13 patients (46%) with elevated triglyceride levels had these values normalize after stopping HAART. After a median of 21 months follow-up, 26 of 41 patients (63%) have restarted HAART. Patients with Centers for Disease Control (CDC) HIV/AIDS C classification were more likely to restart HAART than those with A or B classification (p = 0.008). Reasons for HAART restart included clinical events in 8 patients. Fifteen patients restarted HAART for immunologic reasons: CD4+ count less than 300 cells per microliter (n = 7); HIV viral load greater than 55,000 copies per milliliter (n = 3); or both (n = 5). Three patients restarted HAART because of personal preference. Within 4 months, all 26 patients who restarted HAART achieved HIV viral loads less than 50 copies per milliliter. Although patients were able to rapidly achieve nondetectable HIV viral loads after restarting HAART, the inability to foresee clinical events among 8 patients (20%) is disconcerting. We advise caution before HAART interruption, particularly for those patients with a preceding history of significant HIV-related complications.     

Recrudescent Kaposi's sarcoma after initiation of HAART: a manifestation of immune reconstitution syndrome

The objective of this case series and literature review is to characterize the clinical course and prognosis of HIV-infected patients with Kaposi's sarcoma (KS) flare during immune reconstitution inflammatory syndrome (IRIS), a heterogeneous and sometimes fatal disorder of immune perturbation after initiation of highly active antiretroviral therapy (HAART). Medical records of 9 HIV-infected patients with KS flare after virologic and immunologic response to HAART were reviewed from a single institution. An additional 10 cases were abstracted by computerized search of the medical literature. In our single institution series, mean time to onset of KS flare was 5 weeks. Pretreatment mean CD4+ count was 190 cells/mm(3) and mean HIV viral load was 153,934 copies per milliliter. During flare, mean CD4+ count was 256 cells/mm(3) and mean HIV viral load was 1156 copies per milliliter. Similar aggregate results are represented in the literature. Six fatalities are reported, 4 from pulmonary KS and 2 from unrelated causes. Systemic chemotherapy universally led to tumor regression, but was administered in only 10 of 19 cases. In no instance was HAART discontinued. Onset of IRIS-associated KS flare is observed as early as 3 weeks, with most cases diagnosed within 2 months after immunologic and virologic response to HAART. Such a flare does not necessarily portend a poor prognosis. Even for those patients with rapidly symptomatic KS, early systemic chemotherapy is effective in suppressing IRIS-associated flare. Close clinical supervision is warranted for the KS patient initiating, changing, or resuming HAART. Particular vigilance is recommended for pulmonary involvement.     

HIV-associated lymphoma successfully treated with peripheral blood stem cell transplantation

OBJECTIVE: To evaluate feasibility, safety, and efficacy of peripheral blood stem cell collection (PBSCC) and autologous stem cell transplantation (ASCT), to treat patients diagnosed of high-risk or relapsed HIV-associated lymphoma (HIV+ Ly), responding to highly active antiretroviral therapy (HAART). METHODS: Prospective and multicentric study in patients with high-risk or relapsed chemosensitive HIV+ Ly, candidate for consolidation with ASCT. Eligibility criteria were similar to those of HIV- lymphoma. HAART was aimed to be maintained during the procedure. RESULTS: Fourteen patients were admitted. Adequate PBSCC was obtained from all patients (median CD34+ cells was 4.7 x 10(6)/kg). Three patients died before ASCT; two had disease progression and one died from VHC-liver failure. Eleven transplanted patients showed neutrophil engraftment after a median time of 16 days (range, 9-33 days), and nine patients showed platelet engraftment after a median time of 20 days (range, 11-36 days). CD4+ cell counts and HIV viral load (VL) were appropriately preserved along the procedure. No patients died from treatment-related complications. One patient died from lymphoma progression (day +19), and another died in complete remission (CR) with undetectable VL, 15 months after transplant, due to infection. One patient relapsed at 32 months after ASCT. The remaining eight patients are alive in CR with an event-free survival of 65% and a median follow-up of 30 months after ASCT (range, 7-36 months). CONCLUSIONS: These results show that feasibility, safety, and efficacy of PBSCC and ASCT in HIV+ Ly patients responding to HAART are similar to those observed in the HIV- lymphoma setting.     

Down-regulation of interleukin-7 receptor (CD127) in HIV infection is associated with T cell activation and is a main factor influencing restoration of CD4(+) cells after antiretroviral therapy

BACKGROUND: Factors influencing the depletion of CD4(+) cells and the restoration of CD4(+) cells after antiretroviral therapy are not completely understood. Recently, attention has been paid to interleukin (IL)-7 and its receptor (CD127). We analyzed the influence of T cell activation and of suppression of viremia with antiretroviral therapy on this system, as well as its role in CD4(+) cell restoration after long-term antiretroviral therapy. METHODS: IL-7 levels and CD127 expression on several subsets of CD4(+) and CD8(+) T lymphocytes and the activation status (CD38) of these cells were examined at baseline and during 24 months of complete viral suppression under highly active antiretroviral therapy (HAART). RESULTS: A total of 42 individuals with human immunodeficiency virus (HIV) infection and 10 age-matched, uninfected control subjects were examined. Before HAART, IL-7 levels were increased and CD127 expression was decreased. Down-regulation of CD127 was mainly associated with T cell activation and reverted only partially after suppression of detectable plasma HIV RNA with HAART. In a multivariate analysis, CD127 expression on CD8(+) T cells was the main determinant of the extent of CD4(+) cell gains after successful HAART. CONCLUSIONS: The IL-7-CD127 system is impaired in HIV-infected patients. CD127 down-regulation is associated with T cell activation and with CD4(+) cell restoration after HAART.     

The clinical epidemiology of Hodgkin lymphoma in HIV-infected patients in the highly active antiretroviral therapy (HAART) era

Studies conducted before the introduction of highly active antiretroviral therapy (HAART) suggested that the risk of Hodgkin lymphoma in persons with human immunodeficiency virus (HIV) infection was increased. However, little is known about the features of this malignancy in patients receiving HAART. From January 1996 through December 2001, 23 cases of Hodgkin lymphoma were diagnosed among 3,945 HIV infected patients attending the Harris County Hospital District in Houston, Texas. Twenty (87%) of the HIV-infected patients diagnosed with Hodgkin lymphoma were receiving HAART and 3 (13%) were naive to antiretroviral therapy. The incidence per 1,000 patients of Hodgkin lymphoma in patients receiving HAART was 6.5. The median duration of HAART before the diagnosis of Hodgkin lymphoma was 16 months (range, 7-22 mo). The median CD4 cell count was 235 cells/mm(3) (range, 189-325 cells/mm(3)) for the 20 HIV-infected patients receiving HAART at the time of diagnosis of Hodgkin lymphoma and 90 cells/mm (range, 72-120 cells/mm(3)) for the 3 patients naive for antiretroviral therapy. Among patients with Hodgkin lymphoma receiving HAART, 50% (10/20) had an HIV-RNA viral load in plasma below the level of detection <400 copies/mL). Chemotherapy was administered to all patients, but a complete response was achieved in 30% (6/20) of the patients receiving HAART and 0% (0/3) of the patients naive to antiretroviral therapy. These results suggest that Hodgkin lymphoma has a low incidence in HIV-infected patients receiving HAART, but the malignancy is an aggressive disease with unfavorable clinical outcome in these patients.