[Measuring the HIV viral load with LCx (Abbott): importance for the therapeutic follow-up of 3 patients infected by type O HIV].
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Biomedical subjects
Publications and source records attributed to J Loison.
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The clearance of human cytomegalovirus (HCMV) was evaluated in infected patients under Ganciclovir (GCV) treatment, using a novel HCMV DNA quantitation assay (HCMV DNA hybrid capture system, Murex Diagnostics). Peripheral white blood cells (WBC) from whole blood specimens of seven AIDS patients, three kidney and two allogeneic bone marrow transplant (BMT) recipients suffering from HCMV disease, were assessed by this method. HCMV DNA 50 and 90% mean clearances were observed at 2.11 +/- 1.97 and 6.22 +/- 4.31 days, respectively, after initial GCV treatment. The viral DNA kinetics were correlated with positive and negative pp65 antigenaemia and viral blood culture. Two-fold higher clearances and initial DNA levels were observed in the AIDS group compared to the transplant group. Neither clinical nor virological relapses were observed under GCV treatment. HCMV DNA quantitation in WBC appears well adapted for a therapeutic follow up of patients with HCMV disease.
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Fifty patients in stage IV of HIV infection (including 41 AIDS patients) were prospectively studied by echocardiography. Thirteen of them showed abnormalities: 4 had pericardial effusion, 1 endocarditis, 7 myocardial disorders and 1 primary pulmonary arterial hypertension. Pericardial effusion, also present in patients who had pleuropulmonary Kaposi's sarcoma, was not specific. Myocardial disorders concerned the diastolic function in 1 case, the segmental kinetics in 2 cases and the whole systolic function in 4 cases (3 had congestive myocardiopathy and 1 had transient systole alteration without left ventricular dilatation). The mechanism of global left ventricular disorders was multifactorial, and several hypotheses were discussed: infectious myocarditis, adrenergic or nutritional deficiency myocarditis, cardiotoxicity of antiviral drugs, common pathology with HIV encephalopathy. The prognosis of congestive myocardiopathy was poor in AIDS patients and undetermined in stage IV non-AIDS patients. Echocardiography is capable of detecting these lesions, and its use may contribute to a better care of these patients.
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We have studied the evolution of the avidity of anti-HIV antibodies, in 14 infected patients with Aids, including 11 patients with severe immunodeficiency at Aids stage and under active antiretroviral therapy (HAART), and 3 non-treated patients with moderate immunodeficiency. These patients have been followed up to 4 years, every 4 months the first year and every 6 months the three others, with HIV1 RNA viral load, CD4 and CD8 cells dosages and anti-HIV avidity measurements (Axsym HIV-1/2), using 1 M guanidine denaturation. A rapid decrease of the viral load was observed under Haart, inducing immune restoration with CD4 and CD8 cells increases (10 and 2-fold respectively). The decrease of anti-HIV avidity (- 20%) has been observed after 5 to 8 months under Haart, with a return to baseline value (84%). The quick restoration of CD4 cells with a persistence of viral antigens at the beginning of treatment has facilitated the selection of novel naive B lymphocytes producing low-affinity antibodies, measured by the decrease of global anti-HIV avidity. The reduction or even clearance of viral antigens under Haart could secondarily induce the selection of B lymphocytes with higher antibody affinity and therefore higher anti-HIV avidity. Thus, this avidity measurement could be used to assess the functional activity of CD4 cells restoration in HIV infected patients under Haart.
Determination of IgG avidity is useful to distinguish primary infection from reactivation or reinfection in viral, parasitic or bacterial infections. For diagnosis of HIV type 1 primary infection, the detection of IgM antibodies is often useless since they are also found in chronic infection. The usual serology (Elisa, western-blot, p24 antigen) may present no interest if done too late (more than 2 or 3 months after infection). Therefore, we have developed a test to determine the avidity of anti-HIV1 antibodies, using 1 M guanidine as denaturing agent. We have adapted the measurement of avidity to the Axsym automatic system for a routine use. Indeed, since requests for avidity determinations are sporadic, the use of microplates is not convenient. Using this assay, we found a low avidity (less than 50%) in immunocompetent and recent infected patients (less than 6 months), compared to old infected patients (more than 12 months) who had high avidity (80 to 100%). However, early treated patients (in the 6 months after contamination) had also low avidities but with a slower development of antibody maturation (8 to 27 months versus 2 to 8 months in non treated patients). To conclude, the determination of the anti-HIV1 avidity, according to the proper procedures explained here (notion of treatment and/or serious immunodepression), may help the physician to date the infection in each new infected patient who might benefit from an early treatment.