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Sequential determination of viral load and phenotype in human immunodeficiency virus type 1 infection.

Detailed studies of HIV viral load and phenotype were performed on sequentially cryopreserved peripheral blood mononuclear cells (PBMCs) from eight infected individuals followed in the Los Angeles Multicenter AIDS Cohort Study. Three individuals remained clinically and immunologically stable over a 5- to 8-year period, three demonstrated precipitous and two gradual declines in CD4+ T lymphocytes. Viral load in PBMCs was quantitated by limiting dilution culture and DNA PCR, while minimally passaged viral isolates were studied for their ability to induce syncytium formation in vitro and, when relevant, sensitivity to zidovudine (ZDV). Viral burden remained relatively low in those who remained clinically and immunologically stable, while increasing substantially in all five individuals who experienced a decline in CD4+ T lymphocytes. Two subjects were noted to have a switch from non-syncytium-inducing (NSI) to syncytium-inducing (SI) isolates immediately preceding a precipitous decline in CD4+ T lymphocytes, while the third individual who experienced such a decline and the two who had gradual declines did not develop SI isolates. Moreover, of the three subjects who experienced a decrease in CD4+ T lymphocyte number and were given ZDV during the study period, none were noted to develop resistance to this agent. In summary, the virology in clinically and immunologically stable individuals was characterized by relatively low viral burden in PBMCs and a predominance of NSI isolates.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

Human papillomavirus, viral load and proliferation rate in recurrent respiratory papillomatosis in response to alpha interferon treatment.

The aim of this study was to identify recurrent respiratory papillomatosis patients who may benefit from interferon (IFN)-alpha treatment and to determine the means of IFN-alpha action. The presence of human papillomavirus (HPV) and viral load and proliferation rate in pre-, ongoing and post-treatment respiratory papillomatosis biopsies were examined retrospectively in 25 patients, 18 of whom were IFN-alpha treated and seven of whom were IFN-alpha non-treated. Using PCR, HPV was found to be present in 20/25 respiratory papillomatosis patients and HPV type was determined for 18/25 patients (12 HPV6 and six HPV11). Eighteen of the patients were treated with IFN-alpha, 14 of whom were HPV positive (eight HPV6, five HPV11 and one undefined HPV). Response to IFN-alpha therapy was observed in 12 patients (7/8 HPV6, 3/5 HPV11, 1/1 undefined HPV and 1/4 HPV negative), while six patients (1/8 HPV6, 2/5 HPV11 and 3/4 HPV negative) did not respond to therapy. Viral load, determined by quantitative real-time PCR (between 0.03 and 533 HPV copies per cell), and proliferation rate, determined as the percentage of Ki-67-positive cells (between 8 and 54 %), were similar in IFN-alpha-treated and non-treated patients and were generally unaffected by IFN-alpha treatment. In summary, most (12/18) IFN-alpha-treated patients responded to therapy. Moreover, there was a tendency for patients with HPV6-positive (7/8) respiratory papillomatosis to respond more frequently to IFN-alpha therapy than patients with HPV11 (3/5) or HPV-negative (1/4) respiratory papillomatosis. Finally, the presence of HPV and viral load and proliferation in respiratory papillomatosis biopsies was similar in patients treated or not with IFN-alpha and were in general unaffected by IFN-alpha treatment.

Adolescent↗

Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study.

BACKGROUND: We investigated the temporal progression of the clinical, radiological, and virological changes in a community outbreak of severe acute respiratory syndrome (SARS). METHODS: We followed up 75 patients for 3 weeks managed with a standard treatment protocol of ribavirin and corticosteroids, and assessed the pattern of clinical disease, viral load, risk factors for poor clinical outcome, and the usefulness of virological diagnostic methods. FINDINGS: Fever and pneumonia initially improved but 64 (85%) patients developed recurrent fever after a mean of 8.9 (SD 3.1) days, 55 (73%) had watery diarrhoea after 7.5 (2.3) days, 60 (80%) had radiological worsening after 7.4 (2.2) days, and respiratory symptoms worsened in 34 (45%) after 8.6 (3.0) days. In 34 (45%) patients, improvement of initial pulmonary lesions was associated with appearance of new radiological lesions at other sites. Nine (12%) patients developed spontaneous pneumomediastinum and 15 (20%) developed acute respiratory distress syndrome (ARDS) in week 3. Quantitative reverse-transcriptase (RT) PCR of nasopharyngeal aspirates in 14 patients (four with ARDS) showed peak viral load at day 10, and at day 15 a load lower than at admission. Age and chronic hepatitis B virus infection treated with lamivudine were independent significant risk factors for progression to ARDS (p=0.001). SARS-associated coronavirus in faeces was seen on RT-PCR in 65 (97%) of 67 patients at day 14. The mean time to seroconversion was 20 days. INTERPRETATION: The consistent clinical progression, shifting radiological infiltrates, and an inverted V viral-load profile suggest that worsening in week 2 is unrelated to uncontrolled viral replication but may be related to immunopathological damage.

Administration, Oral↗

Prospective study of emotional reactions to changes in HIV viral load.

Advances in antiretroviral therapies for HIV infection have given rise to new hope for the long-term survival of people living with HIV/AIDS. The current study examined changes in depression, anxiety, and HIV treatment attitudes that may co-occur with improvements and setbacks in HIV disease progression in a prospective cohort of 166 HIV-positive men and women. Results from a 9-month prospective observation period showed that persons who experienced increases in viral load, as indexed by medical chart abstraction, reported modest increases in depression and decreases in positive attitudes toward HIV treatments. Persons who experienced substantive decreases in viral load to undetectable levels demonstrated meaningful reductions in depression, particularly affective symptoms of depression after statistically controlling for years living with HIV, HIV symptoms, and age. Results suggest that emotional distress and perceptions of HIV treatments change in parallel to markers of HIV disease progression, especially with regard to reduced emotional distress in response to clinically significant changes in viral load.

Adult↗

Comparison of the sensitivities and viral load values of the AMPLICOR HIV-1 MONITOR version 1.0 and 1.5 tests.

This study compared the sensitivity and viral load values of the AMPLICOR HIV-1 MONITOR microwell version 1.0, microwell version 1.5, and COBAS version 1.5 tests. Based on the percentage of positive replicates, the microwell version 1.5 and COBAS version 1.5 tests are more sensitive than the microwell version 1.0 test. Viral load values obtained with the COBAS version 1.5 test are lower than those obtained with either the microwell version 1.0 or microwell version 1.5 test.

HIV Infections↗

Plasma viral load of Epstein-Barr virus and risk of multiple sclerosis.

Elevated antibody titers to Epstein-Barr virus (EBV) have been found prior to the onset of multiple sclerosis (MS) and EBV has been found in serum of patients with MS exacerbations. We conducted a prospective, nested case-control study in the Nurses' Health Study and Nurses' Health Study II cohorts to determine whether plasma EBV viral load in healthy adults predicts the risk of MS. MS cases with blood collected before onset (n = 18) or diagnosis (n = 13) and 62 healthy controls were matched by age and time of blood collection. EBV viral load in plasma was measured by real time polymerase chain reaction. Presence of EBV in plasma was associated with an increased risk of MS (relative risk = 2.5, 95% CI 0.78-7.8, P = 0.12). Adjusting for smoking, ancestry, and latitude of residence at birth did not materially change this result. However, no association was found between the EBV viral load and risk of MS. These results support a role for EBV in the etiology of MS, but need to be confirmed in a larger study.

Antibodies, Viral↗

Relationships of human papillomavirus type, qualitative viral load, and age with cytologic abnormality.

Persistent cervical infections with carcinogenic human papillomaviruses (HPV) cause virtually all cervical cancer. Cytologic abnormalities are the manifestations of HPV infections used to identify women at risk. To compare the potential of the full range of anogenital HPV genotypes to induce cytopathic effects, we examined the influences of HPV type, viral load, and age on cytopathology among 1,222 women having a single HPV type at enrollment into a 10,000-woman population-based study in Costa Rica. Cervical specimens were tested for approximately 40 HPV types by MY09/MY11 L1 primer PCR and type-specific dot blot hybridization. Types were organized by phylogenetic species and cancer risk. PCR signal strength served as a qualitative surrogate for viral load. Overall, 24.8% [95% confidence interval (95% CI), 22.4-27.3] of single prevalent HPV infections had concurrent abnormalities (atypical squamous cells or worse) ranging from 0.0% to 80.0% based on HPV type. Noncarcinogenic alpha3/alpha15 types, although highly prevalent, uncommonly caused cytologic abnormalities (13.1%; 95% CI, 9.8-17.0). In contrast, one quarter to nearly one half of infections with a single major carcinogenic species type (alpha9/alpha11/alpha7/alpha5/alpha6) produced abnormalities. Greater abnormalities were observed with increasing qualitative viral load of carcinogenic types; fewer abnormalities were observed among older women (>54 years). A high percentage (46.2%) of detected abnormalities in women infected with HPV16 or related alpha9 types were high grade or worse, consistent with strong carcinogenicity, compared with 10.7% in women infected with alpha7 types, including HPV18, a major cause of adenocarcinoma. The lack of evident severe abnormalities associated with HPV18 and related HPV types might have implications for screening for poorly detected glandular and alpha7-related lesions.

Adult↗

Lowering the detection limits of HIV-1 viral load using real-time immuno-PCR for HIV-1 p24 antigen.

Presently, the assay that attains maximal sensitivity and dynamic range of HIV-1 viral copy number (50 copies per milliliter) is nucleic acid amplification of HIV RNA in plasma. Enzyme-linked immunosorbent assay (ELISA) methods for quantification of HIV-1 p24 antigen have been relatively insensitive. In this report, we show data that indicate real-time immuno-polymerase chain reaction (IPCR), a combination of the ELISA and PCR techniques, is more sensitive for HIV-1 p24 antigen detection than other currently reported methods. When derived from an IPCR standard curve, a dose response was observed from patient samples with known viral loads diluted within a 3-log range (1.68-6,514 viral RNA copies per milliliter). IPCR detected 42% (22/52) of patient samples that had fewer than 50 viral RNA copies per milliliter by reverse transcriptase-PCR. IPCR shows the potential to become the most analytically sensitive test available for determination of HIV-1 viral load by the detection of HIV-1 p24 antigen.

Animals↗

CMVR diagnoses and progression of CD4 cell counts and HIV viral load measurements in HIV patients on HAART.

AIM: To assess the impact of highly active antiretroviral therapy (HAART) on the prevalence and progression of CMV retinitis (CMVR) among AIDS patients with baseline CD4 cell counts <100 cells x 10(6)/l. METHODS: A longitudinal cohort study of 1292 patients. CD4 cell counts and HIV viral load measurements were obtained before commencing therapy, at 3 months, 1 year, 2 years, and at last follow up. The CMVR prevalence rate was measured for the subgroup with baseline CD4 cell counts <100 cells x 10(6)/l. CMVR adverse event (AE) rates per 100 person days at risk were calculated for the subgroup with CMVR and baseline CD4 cell counts <100 cells x 10(6)/l. RESULTS: 1292 patients were started on HAART. 8% of patients had CD4 counts <50 cells x 10(6)/l and 40% had detectable HIV viral load at last follow up. The prevalence of CMVR for the subgroup with baseline CD4 <100 cells x 10(6)/l was 10%. For those with baseline CD4 <100 cells x 10(6)/l, the mean CMVR AE rate was greatest during the first 6 months of follow up after HAART commencement (p <0.003). The mean AE rate per 100 person days at risk was 0.36 (95% CI 0.167 to 0.551) before starting HAART, and 0.14 (95% CI 0.085 to 0.199) after starting HAART (p = 0.03). CONCLUSIONS: HAART significantly prolongs the disease-free intervals in patients with pre-existing disease but recurrences persist within the first 6 months of starting therapy. AE were absent beyond 18 months of follow up in all patients including those with persistently low CD4 counts and detectable HIV viral load indicating clinical immunorestoration. New methods for monitoring the response to therapy are needed to identify those at risk.

Adult↗

Markers of immune activation and viral load in HIV-associated sensory neuropathy.

BACKGROUND: HIV infection is associated with a painful distal sensory polyneuropathy (DSP) that can severely limit the quality of life of affected subjects. The pathogenesis of DSP is unknown, although both HIV proteins and products of immune activation triggered by HIV infection have been implicated. OBJECTIVE: To assess the association between baseline markers of immune activation and HIV RNA levels (viral load) and time to symptomatic DSP (SDSP). METHODS: A cohort of 376 subjects, most receiving highly active antiretroviral therapy (HAART), were followed semiannually for up to 48 months. Blood and CSF levels of HIV viral load, monocyte chemotactic protein-1, macrophage colony-stimulating factor (M-CSF), matrix metalloproteinase-2, and tumor necrosis factor-alpha were measured in addition to CD4 lymphocyte cell count. RESULTS: In subjects without SDSP at baseline (62.5% of the cohort), among the virologic and immunologic markers, only baseline CSF M-CSF levels were associated with time to SDSP (hazard ratio = 2.97, p = 0.05). The Kaplan-Meier estimate of the 1-year incidence of SDSP was 21%, a 15% decrease from that observed in the Dana cohort, a pre-HAART cohort enrolled with the same inclusion/exclusion criteria. CONCLUSION: Highly active retroviral therapy (HAART) has changed the natural history of HIV-associated symptomatic distal sensory polyneuropathy (SDSP), which may explain, in contrast with studies from the pre-HAART era, the lack of association between SDSP and baseline HIV viral load and CD4 cell count.

Adult↗

A randomized controlled trial investigating the efficacy and safety of switching from a protease inhibitor to nevirapine in patients with undetectable viral load.

OBJECTIVE: To assess the antiviral efficacy and safety of switching from a protease inhibitor (PI) to nevirapine in patients with long-term HIV-1 RNA suppression on PI-containing regimens, and to assess its influence in the adherence to treatment. METHODS: In an open-label multicentre study, 160 HIV-infected patients with undetectable viral load for at least 6 months on a PI-containing regimen were randomized to either continue with their PI regimen (n=79) or replace PI with nevirapine (n=81). Clinical assessment included plasma HIV-1 RNA, blood chemistry, haematology, lymphocyte counts and adverse events reports. Adherence to treatment and lipodystrophy syndrome were assessed by patient self-reporting. RESULTS: Treatment efficacy was equivalent in the two arms, for patients with viral loads either above or below 100 000 HIV-1 RNA copies/mL. The increase in CD4 cell count was significant in both arms (P<0.00001) but the average CD4 cell count at 48 weeks was slightly higher in the nevirapine arm (596 vs. 569; P=0.1588). The number of patients with severe hypertriglyceridaemia (>400 mg/dL) after 48 weeks of treatment decreased in the nevirapine arm (from 11 to six), but increased in the PI arm (from four to 11) and led to treatment discontinuation in two patients. Lipodystrophy changes increased in 15% of patients in the PI arm but decreased in 4% of patients in the nevirapine arm. Finally, although adherence was similar in the two arms, patients reported that it required significantly less effort to stay on treatment in the nevirapine arm. Conclusions The results indicate that switching from PI to nevirapine is as effective as continuing with PI for maintaining viral control, even in patients with baseline viral load above 100,000 copies/mL. In addition, reductions in hypertriglyceridaemia and lipodystrophy and in the effort required to stay on treatment were observed.

Adult↗

A time-to-prescription-refill measure of antiretroviral adherence predicted changes in viral load in HIV.

OBJECTIVE: The goal of this study was to determine the validity and utility of a pharmacy-based time-to-refill measure of antiretroviral therapy adherence. METHODS: We performed an observational cohort study of 110 HIV-infected subjects on a stable, highly active antiretroviral regimen for at least 3 months at a Veterans' Affairs Medical Center in Philadelphia, Pennsylvania. RESULTS: The viral load decreased by 0.12 log c/mL (95% confidence interval [CI] 0.01-0.23 log c/mL) for each 10% increase in pharmacy-based time-to-refill defined adherence as compared with 0.05 log c/mL (95% CI -0.14-0.25 log c/mL) for the self-reported adherence measure. Thus, only the refill-defined measure was statistically significantly associated with viral load change. When adherence was classified as good (> or = 85%) versus poor (<85%), both measures demonstrated a significant difference in outcome between groups. Yet, in individuals self-reporting 100% adherence, those classified as good adherers using the pharmacy-based measure had greater viral load reductions than poor adherers (2.4 log c/mL [interquartile range 1.4-3.4] vs. 1.5 log c/mL [interquartile range 0.8-2.4, P=.03). CONCLUSIONS: The pharmacy-based technique is a valid measure of antiretroviral therapy adherence. Because it provides clinically relevant information in subjects who self-report 100% adherence, it should be incorporated into clinical practice and adherence research.

Adult↗

HIV-1 viral load, phenotype, and resistance in a subset of drug-naive participants from the Delta trial. The National Virology Groups. Delta Virology Working Group and Coordinating Committee.

BACKGROUND: The Delta trial showed that combination therapy (zidovudine plus didanosine and zidovudine plus zalcitabine) substantially lengthened life and reduced disease progression compared with zidovudine monotherapy. We did a nested virological study in three countries (France, the Netherlands, and the UK) to investigate changes in markers for viral load and antiretroviral-drug resistance during therapy. METHODS: 240 zidovudine-naive HIV-1-infected patients were randomly assigned zidovudine only (n = 87), zidovudine plus didanosine (n = 80), or zidovudine plus zalcitabine (n = 73). Viral load in peripheral-blood mononuclear cells and plasma was measured by quantitative culture. Plasma HIV-1 RNA was measured by reverse-transcriptase PCR amplification, and serum p24 antigen by ELISA. Resistance to antiretroviral drugs was measured phenotypically by culture and genotypically by detection and quantification of drug-related point mutations in the pol gene. Analyses were done by intention to treat. FINDINGS: The reduction in viral load was greatest 4-12 weeks after the start of therapy and was most pronounced in the combination-therapy study groups (median reductions of RNA at 4 weeks 1.58, 1.28, and 0.49 log10 copies/mL for zidovudine plus didanosine, zidovudine plus zalcitabine, and zidovudine only, respectively). RNA levels at 8 weeks were predictive of disease progression and death after allowance for baseline values. At 48 weeks, the proportion of participants with phenotypic zidovudine resistance was similar in all three groups: didanosine and zalcitabine resistance were rare; zidovudine genomic resistance correlated with phenotypic resistance (r = 0.54, p < 0.0001) and developed earlier in the combined-therapy groups. However, participants in the zidovudine monotherapy group had higher circulating loads of resistant virus than those in the combined-therapy groups. INTERPRETATION: Combined antiretroviral therapy was more efficient at lowering virus load than monotherapy. Although zidovudine resistance was common in monotherapy and combined-therapy groups, circulating concentrations of resistant virus were substantially lower in the combination groups, which is likely to be a result of the continued antiviral activity of didanosine or zalcitabine.

Anti-HIV Agents↗

Serum retinol and HIV-1 RNA viral load in rapid and slow progressors.

Few studies have addressed the relation between serum vitamin A level and HIV disease progression. Thirty HIV-infected women in Rwanda were studied over a time span of 26 to 99 months. Fourteen subjects seroconverted and died of HIV-related disease at a mean of 44 months (range, 26-69 months) after their first HIV-positive test and were termed "rapid progressors," (RPs). A comparison group of 16 "slow progressors" (SPs) were HIV-positive at the time of their first HIV serology and had asymptomatic HIV infections at a mean of 96 months (range, 93-99 months) after their first HIV serology. Baseline mean serum retinol values were the same in RPs and SPs: 0.65 + 0.08 mmol/L versus 0.67 + 0.09 micromol/L (p = .7). Lower serum retinol levels were observed in RPs compared with SPs for the second and third measurements, obtained at a median of 12 and 24 months past baseline: 0.51 + 0.07 mmol/L versus 0.76 + 0.14 mmol/L (p = .3) and 0.44 + 0.09 mmol/L versus 0.64 + 0.08 mmol/L (p = .08), respectively. Median retinol levels for the third sample measurement were similar in RPs with lower viral load (LVL) and SPs (0.49 mmol/L and 0.52 mmol/L, respectively) compared with only 0.19 mmol/L in RPs with higher viral load (HVL; p = .02). A trend toward decreasing serum retinol levels and increasing HIV-1 RNA viral load was observed at the third sample measurement (p = .04). Subjects with LVL, higher serum retinol levels (> or =0.70 mmol/L), or both had more favorable rates of survival than subjects with HVL, low serum retinol levels (<0.70 mmol/L), or both. Although sample size does not permit definitive conclusions, this study demonstrates an association of high HIV load, rapid progression, and low serum retinol late but not early in disease progression.

Adult↗

Serum retinol and HIV-1 RNA viral load in rapid and slow progressors.

Few studies have addressed the relation between serum vitamin A levels and HIV disease progression. Thirty HIV-infected women in Rwanda were studied over a time span of 26 to 99 months. Fourteen subjects seroconverted and died of HIV-related disease at a mean of 44 months (range, 26-69 months) after their first HIV-positive test and were termed "rapid progressors," (RPs). A comparison group of 16 "slow progressors" (SPs) were HIV-positive at the time of their first HIV serology and had asymptomatic HIV infections at a mean of 96 months (range, 93-99 months) after their first HIV serology. Baseline mean serum retinol values were the same in RPs and SPs: 0.65 + 0.08 micromol/L versus 0.67 + 0.09 micromol/L (p = .7). Lower serum retinol levels were observed in RPs compared with SPs for the second and third measurements, obtained at a median of 12 and 24 months past baseline: 0.51 + 0.07 micromol/L versus 0.76 + 0.14 micromol/L (p = .3) and 0.44 + 0.09 micromol/L versus 0.64 + 0.08 micromol/L (p = .08), respectively. Median retinol levels for the third sample measurement were similar in RPs with lower viral load (LVL) and SPs (0.49 micromol/L and 0.52 micromol/L, respectively) compared with only 0.19 micromol/L in RPs with higher viral load (HVL; p = .02). A trend toward decreasing serum retinol levels and increasing HIV-1 RNA viral load was observed at the third sample measurement (p = .04). Subjects with LVL, higher serum retinol levels (> or =0.70 micromol/L), or both had more favorable rates of survival than subjects with HVL, low serum retinol levels (<0.70 micromol/L), or both. Although sample size does not permit definitive conclusions, this study demonstrates an association of high HIV load, rapid progression, and low serum retinol late but not early in disease progression.

Adult↗

[Importance of measurement of plasma viral load for the therapeutic follow-up of children infected with HIV-1. Study of its evolution according to modifications of treatment in 55 children].

Since 1987 we started to treat all vertically HIV-1 infected newborns by an antiretroviral therapy as soon as the diagnosis was confirmed. From the study of 55 HIV-1 infected children followed at Armand Trousseau Hospital (Paris, France) we retrospectively evaluated the use of the plasma viral load as a marker of the treatment efficiency. This parameter and CD4 counts were measured the day of any modification in antiviral therapy (Day 0), 1 and 3 months later (M1 and M3) and every 3 months as long as possible. In the 3 groups of treatment modifications a decrease in plasma viral load was observed. A statistically significant increase in CD4 counts was only observed in the group treated with the association of 2 nucleoside analogues and 1 proteinase inhibitor. This group demonstrated the most important decrease in plasma viral load (> 0.7 log 10 Eq Cop/ml). This leads us to propose to the "ANRS" a protocol study for the treatment of all vertically HIV-1 infected children by the association of 3 nucleoside analogues and 1 proteinase inhibitor as early as 8 weeks post natal when the HIV infection is confirmed.

Acquired Immunodeficiency Syndrome↗

Expression of CD69 on T-cells from HIV-1-infected children and adolescents increases with increasing viral load.

We evaluated the use of a whole-blood assay that measures spontaneous and activation-induced CD69 expression on peripheral blood T-cells in vitro for assessment of T-cell function in HIV-1-infected paediatric patients. Heparinized venous blood from 28 HIV-1 positive children and adolescents and 23 healthy controls was incubated for 4 h with or without 5 microg/ml phytohaemagglutinin (PHA). Thereafter, analysis of CD69 expression on CD4+ and CD8+ T-cells was done by flow cytometry; simultaneously we determined CD4+ T-cell counts and plasma HIV-1 viral load. Neither spontaneous nor PHA-induced CD69 expression differed significantly between HIV-1 positive patients and healthy controls. However, T-cells from HIV-1 positive patients with plasma HIV-1 viral load levels above 70x10(3) copies/ml showed a higher spontaneous CD69 expression than T-cells from patients with lower plasma viral load levels in different stages of the disease. Antiretroviral treatment in four patients reduced spontaneous CD69 expression in CD4+ T-cells and PHA-induced CD69 expression in CD4+ and CD8+ T-cells significantly after 8 weeks of therapy. Conclusion Spontaneous and activation-induced expression of the early (activation) antigen CD69 on peripheral blood T-cells does not distinguish HIV-1 positive patients from HIV-1 negative healthy controls and is not correlated with peripheral blood CD4+ T-cell counts. This test may not be a reliable marker for functional T-cell deficiency during early stages of HIV disease. Increased spontaneous as well as PHA-induced CD69 expression on T-cells from HIV-1-infected children and adolescents in vitro may rather reflect HIV-induced pre-activation of T-cells in vivo.

Adolescent↗