OBJECTIVES: To assess whether JC virus (JCV) DNA is frequently harboured by peripheral blood leukocytes (PBL) in HIV-positive patients, before the onset of progressive multifocal leukoencephalopathy (PML). DESIGN: The polyomavirus JCV induces PML in immunocompromised persons and particularly AIDS patients. Leukocytes may play a central part in the onset of PML, but their precise role in JCV latency and reactivation still remains hypothetical. The controversial presence of JCV DNA in PBL has been, until now, investigated only among small groups of patients. We therefore studied 157 HIV-positive persons and compared them with 65 HIV-negative immunocompromised patients. METHODS: DNA was extracted from PBL. The presence of JCV DNA was demonstrated by the polymerase chain reaction (PCR) alone or combined with a molecular hybridization assay. RESULTS. The presence of JCV DNA was ascertained by PCR and hybridization in 28.9% of 135 HIV-infected persons at all stages of HIV infection and only 16.4% of 61 HIV-negative immunocompromised patients. No correlation could be drawn between the detection of JCV DNA and the clinical or biological status of the HIV-positive patients. CONCLUSIONS: JCV DNA is detectable in the PBL of 28.9% of HIV-infected persons, even in the early stages of infection. JCV is more seldomly amplified in HIV-negative immunocompromised patients. Further work is in progress to determine the prognostic value of the presence of JCV DNA in the blood of HIV-positive patients.
OBJECTIVES: To assess whether JC virus (JCV) DNA is frequently harboured by peripheral blood leukocytes (PBL) in HIV-positive patients, before the onset of progressive multifocal leukoencephalopathy (PML). DESIGN: The polyomavirusJCV induces PML in immunocompromised persons and particularly AIDSpatients. Leukocytes may play a central part in the onset of PML, but their precise role in JCV latency and reactivation still remains hypothetical. The controversial presence of JCV DNA in PBL has been, until now, investigated only among small groups of patients. We therefore studied 157 HIV-positive persons and compared them with 65 HIV-negative immunocompromised patients. METHODS: DNA was extracted from PBL. The presence of JCV DNA was demonstrated by the polymerase chain reaction (PCR) alone or combined with a molecular hybridization assay. RESULTS. The presence of JCV DNA was ascertained by PCR and hybridization in 28.9% of 135 HIV-infectedpersons at all stages of HIV infection and only 16.4% of 61 HIV-negative immunocompromised patients. No correlation could be drawn between the detection of JCV DNA and the clinical or biological status of the HIV-positive patients. CONCLUSIONS:JCV DNA is detectable in the PBL of 28.9% of HIV-infectedpersons, even in the early stages of infection. JCV is more seldomly amplified in HIV-negative immunocompromised patients. Further work is in progress to determine the prognostic value of the presence of JCV DNA in the blood of HIV-positive patients.
Authors: V Dubois; H Dutronc; M E Lafon; V Poinsot; J L Pellegrin; J M Ragnaud; A M Ferrer; H J Fleury Journal: J Clin Microbiol Date: 1997-09 Impact factor: 5.948
Authors: D García de Viedma; R Alonso; P Miralles; J Berenguer; M Rodriguez-Créixems; E Bouza Journal: J Clin Microbiol Date: 1999-03 Impact factor: 5.948
Authors: Sylvia Eash; Rosemarie Tavares; Edward G Stopa; Scott H Robbins; Laurent Brossay; Walter J Atwood Journal: Am J Pathol Date: 2004-02 Impact factor: 4.307