Acquired Immunodeficiency Syndrome: Delfraissy JF

Delfraissy JF, Anonymous00281. · No affiliation provided · Rev Pneumol Clin. · Pubmed #12545131 No free full text.

This publication has no abstract.

Blanc FX, Havlir DV, Onyebujoh PC, Thim S, Goldfeld AE, Delfraissy JF. · Agence Nationale de Recherches sur le Sida et les Hepatites Virales, Paris, France. · J Infect Dis. · Pubmed #17624825 No free full text.

Abstract: Currently, there are limited data to guide the management of highly active antiretroviral therapy (HAART) for human immunodeficiency virus type 1 (HIV-1)-infected patients with active tuberculosis (TB), the leading cause of death among individuals with acquired immunodeficiency syndrome (AIDS) in resource-limited areas. Four trials to take place in Southeast Asian, African, and South American countries will address the unresolved question of the optimal timing for initiation of HAART in patients with AIDS and TB: (1) Cambodian Early versus Late Introduction of Antiretrovirals (CAMELIA [ANRS 1295/NIH-CIPRA KH001]), (2) Adult AIDS Clinical Trials Group A5221, (3) START, and (4) a trial sponsored by the World Health Organization/Special Programme for Research and Training in Tropical Diseases. Two other clinical questions regarding patients with TB and HIV-1 coinfection are also undergoing evaluation: (1) the benefits of short-term HAART when CD4 cell counts are >350 cells/mm(3) (PART [NIH 1 R01 AI051219-01A2]) and (2) the efficacy of a once-daily HAART regimen in treatment-naive patients (BKVIR [ANRS 129]). Here, we present an overview of these ongoing or planned clinical studies, which are supported by international agencies.

Cunningham CK, Chaix ML, Rekacewicz C, Britto P, Rouzioux C, Gelber RD, Dorenbaum A, Delfraissy JF, Bazin B, Mofenson L, Sullivan JL. · Department of Pediatrics, State University of New York Upstate Medical University, Syracuse, Syracuse, NY 13210, USA. · J Infect Dis. · Pubmed #12134253 No free full text.

Abstract: Pediatric AIDS Clinical Trials Group protocol 316 was an international, multicenter, placebo-controlled trial comparing single-dose oral nevirapine (200 mg to mother and 2 mg/kg to infant) with placebo in human immunodeficiency virus (HIV)-infected pregnant women receiving standard antiretroviral therapy. This substudy evaluated the emergence of nevirapine-resistance mutations at 6 weeks postpartum in a subgroup of participants. Maternal risk factors for the emergence of nevirapine-resistance mutations were evaluated. Mutations associated with nevirapine resistance were detectable at delivery, prior to receipt of study drug, in 5 (2.3%) of 217 women. Fourteen (15%; 95% confidence interval, 8%-23%) of 95 women who received intrapartum nevirapine developed a nevirapine-resistance mutation 6 weeks postpartum. The most common mutation was K103N, which was present in 10 women. The risk for development of a new nevirapine-resistance mutation did not correlate with CD4 cell count or HIV-1 RNA load at delivery or with type of antepartum antiretroviral therapy. The risk of nevirapine resistance should be considered when determining the risks or benefits of intrapartum nevirapine in women receiving antepartum antiretroviral therapy.

Gasnault J, Kousignian P, Kahraman M, Rahoiljaon J, Matheron S, Delfraissy JF, Taoufik Y. · Neuro-AIDS Rehabilitation Unit, Department of Internal Medicine, INSERM E109, Faculté de Médecine Paris Sud, Le Kremlin-Bicêtre, France. · J Neurovirol. · Pubmed #11517420 No free full text.

Abstract: A monocenter observational study was conducted to determine the clinical and virological effects of cidofovir added to highly active anti-retroviral therapy (HAART) in AIDS-associated progressive multifocal leukoencephalopathy (PML). Exposure to other anti-viral drugs or late initiation of cidofovir were exclusion criteria. Of the 53 consecutive patients with virologically proven PML admitted at the NeuroAIDS Unit of Bicêtre Hospital between May 1996 and July 2000 and having received HAART with or without cidofovir, 46 met the inclusion criteria. Cidofovir was initiated in most cases on compassionate grounds. The 22 patients treated with HAART only (HAART group) were compared to the 24 patients treated with HAART and cidofovir (CDV group). Survival, neurological outcome assessed by the expanded disability status scale (EDSS), and monitoring of the JC virus (JCV) load in CSF were investigated prospectively. At baseline (date of initiation or intensification of HAART), both groups were similar regarding CD4 cell count, plasma HIV load, CSF JCV load, EDSS, and demographic features. Both groups had similar response to HAART in terms of plasma HIV load and CD4 cell count. At month 6, CSF-JCV load was below the detection level in 8 out of 24 (33%) patients from the CDV group and 7 out of 18 (39%) patients from the HAART group (P = 0.71). One-year cumulative probability of being alive was 62% in the CDV group and 53% in the HAART group (P = 0.72). However, an additional benefit with respect to survival was observed in patients who were given cidofovir after adjustment to the following baseline variables (CSF-JCV load, CD4 cell count, and EDSS). Despite the addition of cidofovir to HAART, no significant benefit had been observed in neurological outcome, particularly in patients with an early worsening.

Michelet C, Bellissant E, Ruffault A, Arvieux C, Delfraissy JF, Raffi F, Bazin C, Renard I, Sébille V, Chauvin JP, Dohin E, Cartier F. · Clinique des Maladies Infectieuses, Unité de Pharmacologie Clinique, Hôpital Universitaire, Rennes, France. · Clin Pharmacol Ther. · Pubmed #10391672 No free full text.

Abstract: BACKGROUND: Ritonavir is a potent inhibitor of cytochrome P4503A4 that strongly increases saquinavir bioavailability. In this study we assessed the safety and antiretroviral efficacy of the combination of these two compounds in patients pretreated and receiving continued treatment with zidovudine and lamivudine who were protease inhibitor naive and who had a CD4 cell counts below 200/mm3. METHODS: In this 48-week pilot study, all patients received 600 mg ritonavir and 400 mg saquinavir twice daily. Administration of zidovudine and lamivudine was continued without a change in previous doses. Viral load, CD4 cell count, and the emergence of resistance to the two protease inhibitors were evaluated repeatedly up to week 48. RESULTS: Sixteen patients were included in the study. Previous nucleoside analog treatment duration was 48+/-22 months (mean +/- SD). Two patients quit taking both protease inhibitors within 2 weeks. The ritonavir dose had to be reduced in 10 other patients because of side effects. Between inclusion and week 48, plasma viremia varied from 4.87+/-0.43 to 3.00+/-1.29 log10 copies/mL and CD4 cell counts ranged from 98+/-61 to 250+/-139/mm3. Ten patients (63%) had viral loads below 200 copies/mL and 7 (44%) had viral loads below 50 copies/mL. A single key mutation that conferred ritonavir resistance I84V and V82A/V developed in two patients. A mutation at codon 54 developed in another patient. These mutations were associated with repeated cessations of antiretroviral treatment. No lipodystrophy was observed. CONCLUSION: Ritonavir and saquinavir in combination are quite well tolerated and induce a high and sustained antiretroviral efficacy. A four-drug combination that includes these two protease inhibitors should be considered as a first line of treatment in patients with low CD4 cell counts.

Limou S, Le Clerc S, Coulonges C, Carpentier W, Dina C, Delaneau O, Labib T, Taing L, Sladek R, Deveau C, Ratsimandresy R, Montes M, Spadoni JL, Lelièvre JD, Lévy Y, Therwath A, Schächter F, Matsuda F, Gut I, Froguel P, Delfraissy JF, Hercberg S, Zagury JF, Anonymous00017. · Conservatoire National des Arts et Métiers, Université Paris 7, Paris, France. · J Infect Dis. · Pubmed #19115949 No free full text.

Abstract: To elucidate the genetic factors predisposing to AIDS progression, we analyzed a unique cohort of 275 human immunodeficiency virus (HIV) type 1-seropositive nonprogressor patients in relation to a control group of 1352 seronegative individuals in a genomewide association study (GWAS). The strongest association was obtained for HCP5 rs2395029 (P=6.79x10(-10); odds ratio, 3.47) and was possibly linked to an effect of sex. Interestingly, this single-nucleotide polymorphism (SNP) was in high linkage disequilibrium with HLA-B, MICB, TNF, and several other HLA locus SNPs and haplotypes. A meta-analysis of our genomic data combined with data from the previously conducted Euro-CHAVI (Center for HIV/AIDS Vaccine Immunology) GWAS confirmed the HCP5 signal (P=3.02x10(-19)) and identified several new associations, all of them involving HLA genes: MICB, TNF, RDBP, BAT1-5, PSORS1C1, and HLA-C. Finally, stratification by HCP5 rs2395029 genotypes emphasized an independent role for ZNRD1, also in the HLA locus, and this finding was confirmed by experimental data. The present study, the first GWAS of HIV-1 nonprogressors, underscores the potential for some HLA genes to control disease progression soon after infection.

Lambotte O, Delfraissy JF. · Service de médecine interne et maladies infectieuses, CHU de Kremlin-Bicêtre, unité Inserm U802, 78, rue du Général-Leclerc, 94275 Le-Kremlin-Bicêtre, France. · Pathol Biol (Paris). · Pubmed #17027185 No free full text.

Abstract: We identified a group of chronically HIV-1-infected patients in whom viral replication is spontaneously controlled without antiretroviral treatment. These patients account for less than 1% of HIV-infected patients. They are defined according to a virological definition: plasma viral load less than 400 copies RNA/ml in more than 90% of the samples tested and HIV positive serology known for more than 10 years. They should never have received antiretroviral therapy. The CD4 T cell count is not taken into account, which differenciate these patients from long-term non progressors. Fifteen patients HIV controllers have been studied in a preliminary work with two main results: i) the demonstration of a strong HIV-specific CD8 immune response and ii) the amount of viral DNA in PBMCs is very low and stable along the time. The aim of the ANRS EP36 study group is to precize the immunological and virological characteristics of these patients. First data seem to confirm an essential role of CD8 T cells to control viral replication, the absence of defective virus, and a normal susceptibility of the CD4 T cells from these patients to the infection with various HIV strains. This group of patients is homogeneous and its study supports physiopathological studies. To go further, a national survey of these patients has been set up to allow future study.

Delfraissy JF. · l'Agence nationale de recherches sur le sida et les hépatites virales, Paris, France. · Med Trop (Mars). · Pubmed #16999040 No free full text.

This publication has no abstract.

Goujard C, Bonarek M, Meyer L, Bonnet F, Chaix ML, Deveau C, Sinet M, Galimand J, Delfraissy JF, Venet A, Rouzioux C, Morlat P, Anonymous00160. · Service de Médecine Interne, Bicêtre Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France. · Clin Infect Dis. · Pubmed #16447119 No free full text.

Abstract: BACKGROUND: Treatment initiation at the time of primary human immunodeficiency virus (HIV) type 1 (HIV-1) infection has become less frequent in recent years. METHODS: In the French prospective PRIMO Cohort, in which patients are enrolled at the time of primary HIV-1 infection, 30% of the 552 patients recruited during 1996-2004 did not start receiving antiretroviral treatment during the first 3 months after diagnosis. We analyzed the patients' clinical and immunological outcomes and examined potential predictors of disease progression. Progression was defined as the occurrence of an acquired immunodeficiency syndrome (AIDS)-related clinical event or a CD4 cell count <350 cells/mm3. RESULTS: Fifty-six (34%) of the untreated patients experienced immunological progression during a median duration of follow-up of 24 months, and 1 of these patients had an AIDS-related event. The estimated risks of progression were 25%, 34%, and 42% at 1, 2, and 3 years after enrollment, respectively. Compared with patients who did not have progression, those with progression had significantly lower CD4 cell counts at diagnosis (455 vs. 738 cells/mm3), higher plasma HIV RNA levels (4.9 vs. 4.5 log10 copies/mL), and higher HIV DNA levels (3.3 vs. 3.0 log(10) copies/10(6) peripheral blood mononuclear cells [PBMCs]). All 3 parameters were significantly associated with progression in univariate analysis. In multivariate analysis, only the CD4 cell count and HIV DNA level were independently predictive of disease progression (relative hazard for CD4 cell count, 1.84 per decrease of 100 cells/mm3; relative hazard for HIV DNA level, 2.73 per increase of 1 log(10) copies/10(6) PBMCs). CONCLUSIONS: Both a low initial CD4 cell count and a high HIV DNA level are predictive of rapid progression of untreated primary HIV-1 infection. Affected patients may therefore benefit from close clinical and laboratory monitoring and/or early administration of treatment.

Geskus RB, Meyer L, Hubert JB, Schuitemaker H, Berkhout B, Rouzioux C, Theodorou ID, Delfraissy JF, Prins M, Coutinho RA. · Municipal Health Service, Amsterdam, The Netherlands and Leiden University Medical Center, The Netherlands. · J Acquir Immune Defic Syndr. · Pubmed #15980693 No free full text.

Abstract: OBJECTIVE: To investigate the causal pathways by which age and the CCR5-Delta32, CCR2-64I, and SDF-1 3'A alleles influence progression to AIDS. DESIGN: Analysis of follow-up data from 2 cohort studies among homosexual men (n=400), having >10 years of follow-up. METHODS: The effects of the 4 cofactors on the CD4 and HIV-1 RNA trajectories after seroconversion were modeled in a random-effects model. A proportional hazards model was used to investigate their effect on the risk of AIDS after correction for CD4 cell count and RNA level. This approach allows investigation as to whether they influence AIDS progression by affecting CD4 count and RNA level or by other pathways. RESULTS: Persons of younger age or having the CCR2-64I or SDF-1 3'A mutation have significantly higher CD4 levels. Persons with the CCR5-Delta32 deletion or CCR2-64I mutation have significantly lower RNA levels. After correction for both CD4 count and RNA level, only the SDF-1 3'A mutation significantly increases the AIDS risk. CONCLUSIONS: Age and the CCR5-Delta32 deletion and CCR2-64I mutation influence AIDS progression by affecting CD4 and HIV-1 RNA. The SDF-1 3'A allele increases the AIDS risk, but this effect is countered by its effect on CD4 and HIV-1 RNA level.

Rouzioux C, Hubert JB, Burgard M, Deveau C, Goujard C, Bary M, Séréni D, Viard JP, Delfraissy JF, Meyer L, Anonymous00362. · Laboratoire de Virologie, Paris, France. · J Infect Dis. · Pubmed #15942893 No free full text.

Abstract: BACKGROUND: The objective of this work was to assess the role of human immunodeficiency virus (HIV) reservoirs in the risk of disease progression, by studying the relationship between HIV DNA level in peripheral blood mononuclear cells (PBMCs) and progression toward acquired immunodeficiency syndrome (AIDS). METHODS: HIV-1 DNA levels in PBMCs were determined by quantitative polymerase chain reaction for 383 patients enrolled in the SEROCO Cohort Study who had experienced seroconversion and had been followed up for >8 years. We compared the predictive values of HIV DNA level, HIV RNA level, and CD4+ cell count. RESULTS: Between 6 and 24 months after seroconversion, HIV DNA level was a major predictor of progression to AIDS independently of HIV RNA level and CD4+ T cell count (adjusted relative risk [RR] for a 1-log(10) increase, 3.20 [95% confidence interval {CI}, 1.70-6.00]). HIV DNA level was also a major predictor of disease progression during the first 6 months after seroconversion (adjusted RR, 4.16 [95% CI, 1.70-10.21]), when HIV RNA level and CD4+ T cell count were less predictive. Thus, a combination of these 3 markers provides the best estimate of the risk of disease progression for each patient. CONCLUSIONS: Our results suggest that HIV DNA level could be a useful additional marker in clinical practice and could aid in helping to define the best time to initiate treatment for each patient.

Deuffic-Burban S, Wong JB, Valleron AJ, Costagliola D, Delfraissy JF, Poynard T. · Unité de Recherche Epidémiologie et Sciences de l'Information INSERM U444, Faculté de Médecine Saint-Antoine, 27 rue Chaligny, 75 571 Paris Cedex 12, France. · J Hepatol. · Pubmed #14739105 No free full text.

Abstract: BACKGROUND/AIMS: In France, the prevalence of hepatitis C virus (HCV) exceeds that of HIV, but in the absence of treatment, HIV infection progresses more rapidly than HCV. More HIV-infected patients, however, have received treatment. Using reported public health data in France and natural history models, we applied the back-calculation method to project future mortality from HCV and HIV incorporating current therapies. METHODS: The HCV model was based on literature data for the natural history of HCV and reports of hepatocellular carcinoma mortality. The HIV model used estimates from the French Hospital Database on HIV and reported AIDS cases and deaths. RESULTS: Peak annual mortality from HIV at 5000 occurred in 1994 and was 1000 in 1998, but HCV mortality likely increased through the 1990s and reached 3000 in 1998. Considering only HCV infections occurring until 1998 and currently available therapy, our model suggested that annual HCV-related mortality would continue to rise and would reach 4500 deaths in 2022. In contrast, AIDS-related deaths began to decrease in 1997. CONCLUSIONS: The public health burden of HCV is likely on the rise, while the burden of HIV, given the fairly widespread use of effective medications, may be on the decline. These results may help health policymakers in planning their responses to these epidemics.

Nakayama EE, Meyer L, Iwamoto A, Persoz A, Nagai Y, Rouzioux C, Delfraissy JF, Debre P, McIlroy D, Theodorou I, Shioda T, Anonymous00189. · Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita-shi, Osaka 565-0871, Japan. · J Infect Dis. · Pubmed #11930331 No free full text.

Abstract: The interleukin (IL)-4 -589T allele bears a single nucleotide polymorphism at position -589 upstream from the open-reading frame of the IL-4 gene. To determine the influence of this allele on human immunodeficiency virus (HIV) type 1 disease, disease progression and serum virus load were assessed by IL-4 genotype in 427 white patients with known seroconversion dates who were followed in the French SEROCO cohort between 1988 and 1996. Serum virus load was 0.20 log lower during the 6-24-month plateau phase after seroconversion in patients with IL-4 -589T than in those without this allele (P=.02). Kaplan-Meier analysis survival curves showed a slower progression to clinical AIDS in carriers of IL-4 -589T (P=.04). Adjustment for early serum virus load greatly diminished the strength of this association. These results suggest that IL-4 -589T protects against HIV-1 disease progression by reducing virus load.

Sala M, Vartanian JP, Kousignian P, Delfraissy JF, Taoufik Y, Wain-Hobson S, Gasnault J. · Unité de Rétrovirologie Moléculaire, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France. · J Gen Virol. · Pubmed #11257196 links to  free full text

Abstract: Progressive multifocal leukoencephalopathy (PML) is a rapidly fatal demyelinating disease of the central nervous system related to JC polyomavirus (JCV) replication in oligodendrocytes. PML usually occurs in immunocompromised individuals, especially in the setting of AIDS. Administration of highly active anti-retroviral therapy (HAART) may improve survival prognosis in some, but not all, patients with AIDS-related PML. This observation might be explained by the outgrowth of some JCV variants of increased fitness. To evaluate this hypothesis, two subgroups of five patients with AIDS-related PML, started on HAART after PML diagnosis, were analysed. The non-responder (NR) patients died rapidly despite HAART, while responders (R) had a positive outcome and were still alive. JCV DNA was extracted from cerebrospinal fluid biopsies and two regions of the genome were analysed, the transcriptional control region (TCR) and the major capsid protein gene (VP1). Both regions show different degrees of polymorphism and are recognized as evolving independently. Sequence analysis demonstrated that (i) extensive TCR rearrangements were present in both subgroups of patients, (ii) VP1 sequence polymorphisms could be identified in the BC loop, suggesting the absence of immune selection, and (iii) no genomic marker for JCV specific neurovirulence could be identified in the TCR and VP1 loci.

Saada M, Le Chenadec J, Berrebi A, Bongain A, Delfraissy JF, Mayaux MJ, Meyer L. · Service d'Epidémiologie and INSERM U292, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France. · AIDS. · Pubmed #11089624 No free full text.

Abstract: OBJECTIVE: To investigate whether pregnancy accelerates HIV-1 disease progression. METHOD: In two large French SEROCO and SEROGEST prospective cohorts of HIV infected patients, the progression to AIDS in 365 women with a known date of HIV-1 seroconversion was examined by comparing those who delivered after HIV infection (n = 241) with those who did not become pregnant while HIV-infected (n = 124). RESULTS: The crude relative risk of developing AIDS associated with pregnancy was 0.7 [95% confidence interval (CI), 0.4-1.2]. Adjustment for age at seroconversion, the CD4+ cell percentage at entry, and the method used to date seroconversion did not modify the results (adjusted relative risk, 0.7; 95% CI 0.4-1.2). CONCLUSIONS: No deleterious effect of pregnancy on progression from seroconversion to AIDS was found. This result has important implications for the counselling of HIV-infected women of child-bearing age.

Faure S, Meyer L, Costagliola D, Vaneensberghe C, Genin E, Autran B, Delfraissy JF, McDermott DH, Murphy PM, Debré P, Théodorou I, Combadière C. · Laboratoire d'Immunologie Cellulaire et Tissulaire, Centre National de la Recherche Scientifique UMR 7627, Hôpital Pitié-Salpétrière, Paris, France. · Science. · Pubmed #10731151 links to  free full text

Abstract: Human immunodeficiency virus (HIV) enters cells in vitro via CD4 and a coreceptor. Which of 15 known coreceptors are important in vivo is poorly defined but may be inferred from disease-modifying mutations, as for CCR5. Here two single nucleotide polymorphisms are described in Caucasians in CX3CR1, an HIV coreceptor and leukocyte chemotactic/adhesion receptor for the chemokine fractalkine. HIV-infected patients homozygous for CX3CR1-I249 M280, a variant haplotype affecting two amino acids (isoleucine-249 and methionine-280), progressed to AIDS more rapidly than those with other haplotypes. Functional CX3CR1 analysis showed that fractalkine binding is reduced among patients homozygous for this particular haplotype. Thus, CX3CR1-I249 M280 is a recessive genetic risk factor in HIV/AIDS.

Hubert JB, Burgard M, Dussaix E, Tamalet C, Deveau C, Le Chenadec J, Chaix ML, Marchadier E, Vildé JL, Delfraissy JF, Meyer L, Rouzioux. · Department of Epidemiology, INSERM U292, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France. · AIDS. · Pubmed #10708282 No free full text.

Abstract: OBJECTIVE: To describe the spontaneous course, before the introduction of highly active antiretroviral therapy (HAART), of HIV-1 RNA during the AIDS-free period of the disease. To assess the predictive value of changes in HIV-1 RNA levels. DESIGN: A total of 330 patients with a known date of infection followed in the SEROCO cohort. METHODS: HIV-1 RNA levels (threshold, 200 copies/ml) were evaluated from 2243 frozen sera obtained from enrolment until the onset of AIDS or until February 1996. Lowess curves were used to describe the variations of viraemia during follow-up. A Cox regression model was used to assess the predictive value of early and updated CD4 cell count and viral load. RESULTS: In addition to a lower early viral load, patients who remained AIDS-free had, on average, a longer period of viral load decrease after infection (36 versus 18 months), followed by a slower viral load increase compared with those who progressed to AIDS. A true plateau-phase after the seroconversion period, lasting approximately 4 years, was identified only in patients who remained AIDS-free for at least 90 months. In multivariate analysis, both early viral load and later changes were significant predictors of progression to AIDS. A decrease in the CD4 cell count to less than 200 cells/microl and the onset of a group B condition remained significant predictors of progression. CONCLUSION: Our study extends to the early post-seroconversion phase the prognostic value of extracellular HIV-1 RNA levels. Moreover, our data suggest that, in most HIV-infected individuals, a progressive loss of control of viral replication arises during the early years of HIV-1 infection.

Follézou JY, Lan NY, Lien TX, Lafon ME, Tram LT, Hung PV, Aknine X, Lowenstein W, Ngai NV, Theodorou I, Delfraissy JF, Debré P, Fleury HJ, Barré-Sinoussi F, Chi NH. · Centre Hospitalo-Universitaire Pitié-Salpêtrière, Paris, France. · Am J Trop Med Hyg. · Pubmed #10497983 links to  free full text

Abstract: To define the medical characteristics of intravascular drug users in Ho Chi Minh City, Vietnam, we examined 280 men, of whom 235 were infected with human immunodeficiency virus (HIV), being treated in a rehabilitation center. The patients used mainly opium, often in shooting galleries (50%). The prevalence of oral candidiasis (58%) and zoster infection (20%) was high in HIV-seropositive patients, whereas oral hairy leukoplasia and Kaposi's sarcoma were absent. The prevalence of acquired immunodeficiency syndrome was 24%. More than 80% of the patients had infections with hepatitis C virus, hepatitis B virus, cytomegalovirus, or human T cell lymphotropic virus type-1. The CD4+ cell counts correlated well with viral load. Only HIV-1 subtype E was detected in the 30 patients tested. A cohort study of HIV-infected subjects in this population seems feasible, and would permit introduction of anti-retroviral therapy The large number of HIV-seronegative subjects sharing the same at-risk practices as the HIV-infected subjects raises the possibility of natural protection in this population.

Meyer L, Magierowska M, Hubert JB, Mayaux MJ, Misrahi M, Le Chenadec J, Debre P, Rouzioux C, Delfraissy JF, Theodorou I. · Service d'Epidémiologie, INSERM U292, Hôpital du Kremlin-Bicêtre, 82 rue du Général Leclerc, 94276 Le Kremlin-Bicêtre Cedex, France. · J Infect Dis. · Pubmed #10438395 No free full text.

Abstract: This study attempted to determine whether the CCR5 Delta32 deletion affected progression to certain first AIDS-defining illnesses in human immunodeficiency virus type 1-infected patients enrolled in the French SEROCO/HEMOCO/SEROGEST cohorts. Toxoplasmosis onset as a first AIDS-defining illness was significantly delayed in 253 heterozygous patients, compared with 1404 wild type patients. The relative risk of toxoplasmosis associated with heterozygosity was 0. 39 (95% confidence interval, 0.16-0.96) after adjustment for age, CD4 cell count, and primary specific prophylaxis. A nonsignificant protective trend was observed with regard to the onset of mycobacterial, cytomegalovirus, and herpesvirus diseases, but these events were less frequent than toxoplasmosis. Progression to other conditions (e.g., wasting, non-Hodgkin's lymphoma, Kaposi's sarcoma) was similar in the 2 groups as was the frequency of toxoplasmosis as a subsequent AIDS-defining illness. As chemokines are involved in numerous infectious processes, the Delta32 deletion could delay progression to certain opportunistic infections such as toxoplasmosis.