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High prevalence and particular aspects of HIV-related neurological complications in a Romanian cohort of HIV-1 infected children and young adults Duiculescu D¹, Ene L¹, Radoi R¹, Ruta S², Achim CL³ ¹ “Dr. Victor Babes” Hospital for Infectious and Tropical Diseases, Bucharest, Romania ² “Stefan S. Nicolau” Institute of Virology and „Carol Davila” University of Medicine, Bucharest, Romania ³University of California at San Diego Department of Psychiatry and Pathology, La Jolla, California, USA Romanian cohort: homogenous & unique Infected with HIV-1 in the first years of life 1987-1990, with subtype F Parenteral route of HIV transmission Currently aged 20-22 years Sex ratio male/female=54/46 Common genetic background HAART starting 1998 HBV co-infection (69% HBc Ab +, 44% HBs Ag +) TB co-infection (~1/3 of patients) 1660 children (~1/4 of pediatric HIV population from Romania) followed in “Dr. Victor Babes” Hospital (VBH) from Bucharest *Ruta et al. MedGenMed. 2005 Mar 28;7(1):68. Prevalence of AIDS defining diseases in VBH Total % HIV encephalopathy 119 21.29 TB diseminated/extrapulmonary 78 13,95 Recurrent bacterial pneumonia 75 13,42 Oesophagial candidiasis 52 9,30 PCP 45 8.05 Subacute myoclonic measles encephalitis* 34 6,08 Cryptococosis 34 6.08 PML 27 4,83 Cerebral Toxoplasmosis 24 4,29 CMV diseases 15 2,68 Cryptosporidiasis + Isosporidiasis 14 2,50 Lymphoma (CDC) 12 2,15 Kaposi sarcoma 9 1,61 Other AIDS diseases (<1% each) 21 3.76 Total AIDS defining diseases 559 * Sugested to be clasified as AIDS defining disases Duiculescu et.al. WEPDB 03 - IAS Sydney 2007 Distribution by year of HIV-related neurological complications vs non-neuro AIDS defining diseases 40 35 HIVE Neuro AIDS OI Non-neuro AIDS OI 30 25 20 15 10 5 0 Prevalence of neuroAIDS OI Prevalence of HIVE •preHAART: 24,13% of AIDS defining diseases (77/319) •preHAART: 21,94% of AIDS defining diseases (70/319) •postHAART: 34.16% of AIDS defining diseases (82/240) •postHAART: 20.41% of AIDS defining diseases (49/240) •P=0.01 General characteristics of patients with HIVassociated neurological complications HIV-E TBM CNM Cerebral toxo PML SMME Total 119 35 34 24 27 34 273 Age in years (mean +/-SD, range) 11.8±4.86 (0.9-22) 10.0±4.1 (0.3-19) 12.6±5.8 (7.6-21) 13,1±3,3 (8.2-15.6) 13.5±4.4 (8.3-23) 11.7±4.1 (9.6-20) 12.1±4.8 (0.3-23) HIV infection route parenteral 100 32 32 23 27 32 246 Median CD4 count, range 64 (0-800) 45.5 (3-1030) 50 (3-187) 45 (0-375) 22 (0-131) 112 (1-294) 70 (0-1030) HIV diagnosed at time of CNS –OI 26 9 3 5 11 2 46 HAART at the moment of CNS-OI 47 10 5 5 9 16 92 No of death related to CNS-OI 13 30 20 8 15 34 120 Definitive diagnosis 119 22 28 2 2 9 182 - 13 4 smear 2 C.N. Ag. 22 20 PCR 5 pres 25 No of patients Presumptive diagnosis HIV-E – encephalopathy; TBM – TB meningitis; CNM – cryptococcal meningitis; Toxo – Toxoplasmosis; PML – progressive multifocal leucoencephalopathy ; SMME – subacute myoclonic measles encephalitis Survival probability in patients with HIV-related neurological disorders 100 90 80 HIVE 70 Tx disea 60 50 PML CNM 40 30 20 TBM 10 0 50 100 150 Time (months) 200 250 HIVE Similar prevalence pre- post HAART period Clinical diagnosis criteria Hyperreflexia 45.5% Pyramidal syndrome 39.1% Cerebellar syndrome 37.3% Behavioral disorders 24.5 % Cognitive deficit memory reduced performances 68.1% 20% 41.8% CSF study: Positive correlation between pleocytosis and CSF albumin levels (rho=0.29, p=0.02) Higher CSF HIV RNA compared to plasma Paired plasma-CSF HIV RNA values in a subgroup of 29 adolescents with HIVE 7 log10 HIV RNA (copies/ml) 6 5 4 3 2 1 0 log 10 HIV RNA plasma log10 HIV RNA CSF HIV RNA plasma HIV RNA CSF Mean =4.57 ±1.26 log10 c/ml Mean=4.60 ±.51 log10 c/ml 14 of 29 patients with HIVE and paired plasma-CSF samples had higher CSF HIV RNA levels compared to plasma (5.381.09 log10 c/ml vs. 4.561.17 log10c/ml, p<0.05) Diagnosis of neurocognitive deficit according to HAND criteria in a subgroup of adolescents and young adults evaluated with HNRC test battery* no Age mean SD (years) M/F Education Impairment rate HIV + HIV - 49 20 18.40.7 18.81.0 23/26 12/8 10.11.5 11.02.2 47% 15% Among the HIV + group 71.4% had a low nadir CD4 At the moment of neurocognitive evaluation all patients were on stable HAART 87.7% with good immunological status 81.6% with undetectable HIV RNA *supported by R21 MH0077487-01 and intramural funding from the HNRC International Core at UCSD Domain specific impairment rates in Romanian HIV+ young adults PML No of patients 27 Age in years (mean +/-SD, range) 13.51+/-4.47 (8,3-23) HIV infection route parenteral 27 Median CD4 count, range 22 (0-131) HIV diagnosed concomitant CNS –OI 11 HAART at the moment of CNS complication 9 No of death related to CNS-OI In house PCR for Polyomavirus (2000- 2005) 15 Confirmed cases 2 histo Molecular diagnosis 20 PCR 5 pres RT PCR for JCV (2009- 2010) Particular features: cerebellar and brainstem lesions Survival probability according to cART duration 100 80 60 40 without cART with cART < 6 months with cART > 6 months 20 0 0 10 20 30 40 50 60 Time (months) 11 patients with survival >6 months (40.74%) • Factors associated with survival in the group with ART • older age • HAART regimen with better CSF penetration score • Atypical MRI findings (cavitation, enhancement) 70 80 90 100 Subacute measles encephalitis (SME): SME = a rare and severe measles complication in immune suppressed patients SME occurs 2-12 months after exposure to measles (usually overlooked) 34 patients diagnosed with SME SME was observed as a cluster during 2 consecutive measles epidemics (1996-1998 and 2006-2008) All had severe immune supression (median CD4=112/mmc (range 1-294) Continuous myoclonus was the characteristic symptom (epilepsia partialis continua) Poor outcome Neuroimaging MRI –T1 MRI –T2 17 y.o patient diagnosed with SMME during Measles epidemic 2006 (FLAIR) 9 y.o. child with epilepsia partialis continua (EPC) diagnosed with SMME during measles epidemics 1997-1998 Diagnosis confirmation PCR (evaluation) Immunocytochemistry Treatment High mortality Practical issues: low protection against measles need for prophylaxis emerging diseases in poor resources settings Subacute myoclonic measles encephalitis 26 pts with +ve plasma HBs Ag 18 pts with + ve HBV DNA in plasma Median CD4 = 92 lf/mmc (1-490) HBV DNA = 6.01±2.09 log₁₀IU/ml HIV RNA plasma* = 4.38 ± 1.22 log₁₀ c/ml HIV RNA CSF = 3.27 ± 1.25 log₁₀ c/ml 11 pts with +ve HBV DNA in CSF Median CD4= 59 lf/mmc (1-490) HBV DNA plasma** = 7.25 ± 1.52 log₁₀IU/ml HBV DNA CSF = 4.06 ± 1.06 log₁₀ IU/ml HIV RNA plasma = 4.80 ± 0.99 log₁₀ c/m HIV RNA CSF =3.60 ± 1.28 log₁₀ c/ml *p<0.05 **p<0.001 8 pts – ve HBV DNA - in plasma Median CD4 = 237 lf/mmc (1-738) HBV DNA = ND HIV RNA plasma* = 2.7 ± 1.12 log₁₀ c/ml HIV RNA CSF = 2.61 ± 1.28 log₁₀ c/ml 7 pts with – ve HBV DNA in CSF Median CD4 = 306 lf/mmc (7-380) HBV DNA plasma** = 4.06 ± 1.11 log₁₀ IU/ml HBV DNA CSF = ND HIV RNA plasma = 3.71 ± 1.31 log₁₀ c/ml HIV RNA CSF = 2.75 ± 0.54 log₁₀ c/ml Investigation of HBV antiviral-resistant variants in the CSF-plasma using the reverse hybridization line probe assay (INNO LiPA HBV DR v.2, Innogenetics) with distinct genetic profile suggest compartmentalization of HBV in CSF of HBV co-infected patients Pt. DI TV L80 Plasma wt CSF wt Plasma CSF V173 L173* L180/A181 L181/T181* M180/A181** M204-WT V204** N236 wt wt wt wt wt wt wt wt wt wt wt wt wt wt wt wt wt Distinct genetic profile IF DR SI Plasma wt wt CSF wt Plasma L173 wt wt wt V204 wt wt wt wt wt V204 wt wt wt wt wt wt V204 wt CSF wt wt wt wt wt V204 wt Plasma wt wt wt wt wt CSF wt wt wt L181/T181 L181/T181 wt *possibly relevant for lamivudine compensatory mutation ** relevant for lamivudine resistance mutations wt V204 wt Summary Unique cohort of children surviving over 20 years with chronic HIV-1 infection - evolution pattern similar to adults High rate of PML, Cerebral toxo and Criptococcal meningitis Neurocognitive impairment will be one of the main challenges for the future – need for adequate evaluation What will be the impact of aging in this cohort compared with adult HIV+ population Summary As measles is still an emerging disease (pediatric HIV population has low protection antibodies) -SMME is a severe complication that has to be considered HBV in CSF Is there a neurotropism of HBV? Does HIV play a role in HBV penetration into CSF in chronic HIV/HBV coinfected patients? What is the clinical signifficance of HBV in the brain? Acknowledgements VBH team: Ruxandra Burlacu Andreea Blaglosov Petronela Ionescu Anca Luca Maria Nica Cristiana Oprea Gratiela Tardei Eugenia Ungureanu HNRC team Thomas Marcotte Ronald Ellis Terry Alexander and Donald Franklin Sarah Archibald, Christine Fennema and Terry Jernigan for the neuroimaging analyses Igor Grant Part of this work was supported by R21 MH0077487-01 and intramural funding from the HNRC International Core at UCSD