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HBV co–infected teenagers from Romania
Hepatitis C virus P1893 Changing of hepatitis C virus genotypes patterns in HIV-positive and -negative patients in Northern Spain M. Basaras, M.J. Fern´andez, M. Sota, P. Liendo, R. Cisterna (Bilbao, ES) Hepatitis C virus (HCV) genotypes show specific geographic distribution and association with particular risk factors. Nevertheless, differences in genotype distribution can be observed in different areas of the same region as well as different areas within a country. The aim of the present study was to analyse differential distribution of HCV genotypes in Northern Spain along a six-year period in HIVnegative and -positive patients. Patients and Methods: a retrospective analysis was carried out in 2301 serum samples from HCV RNA-positive patients during a six-year period (from 2000 to 2005). HCV genotyping was determined by reverse hybridisation of PCR amplicons (Versant HCV Genotype Assay, LIPA). Human immunodeficiency virus antigen was detected by INNOTEST and hepatitis B virus HBsAg and anti-HBs were detected by ADVIA Centaur (Bayer). Results: More than a half of the study group (1248 serum samples, 54.23%) were HIV-negative patients. Of them, the predominant genotype was 1 (71.39%), followed by 3 (16.98%) and 4 (9.13%), being the most prevalent subtype 1b (50.64%). On the other hand, 1053 (45.76%) of serum samples were HCV-HIV co-infected. In that group, the most frequent HCV genotype was 1 (48.71%), followed by 3 (29.25%) and 4 (19.56%); however, subtype 3a was the most prevalent (29.15%). Coinfection with several genotypes was infrequent (1.61%). There was a decline in subtype 1a over time and conversely an increase in subtype 4c/d. In all the study group, subtype 1b was detected preferentially in patients with history of blood transfusion or no known exposure to risk factors, whereas subtypes 1a, 3a and genotype 4 are related with injection drug users. Year after year, subtype 4c/d was detected in younger patients than subtype 3a. On the other hand, genotype 2 was almost imperceptible (1.76% in HIV-negative and 0.85% in HIV-positive). Moreover, HBsAg was detected in 0.7% of serum samples and anti-HBs in 1.34%. Conclusions: HCV-HIV co-infection was very frequent in the study group due to these viruses share similar transmission routes. Although genotype 1 is the most frequent HCV variant, subtype 1a has declined over time and subtype 4c/d has increased. This last subtype and subtype 3a were related with injection drug use. Subtype 1b was introduced before than subtype 1a or 3a and is related with history of blood transfusion or no known exposure to risk factors. Subtype 1a and 3a, and more recently 4 c/d, are related with HIV co-infection. P1894 Therapeutical aspects and predictors of outcome for HIV/HCV co-infected patients treated with pegylated interferon plus ribavirin. Survey in an Italian university hospital E. Righi, M. Bassetti, A. Di Biagio, C. Dentone, R. Rosso, A. Beltrame, G. Mazzarello, S. Ratto, C. Viscoli (Genoa, IT) Introduction: One third of HIV-infected individuals worldwide suffers from chronic hepatitis C virus (HCV) infection. HCV therapy is a priority in coinfected patients because they have faster liver disease progression. We assess the impact of interferon and ribavirin combination therapy in a cohort of coinfected patients analysing specifically prognostic factors for outcome. Methods: Patients enrolled in the study were all HIV/HCV patients who received HCV treatment between 2002 and 2006. Clinical data included: demographical data, HAART sitauation, HCV genotype and viral load (considering high rates >800,000 UI/mL). Primary outcome were early virological response (EVR) at week 12 and sustained virological response (SVR) 6 months after stopping treatment. Results: Forty-four patients were treated for chronic hepatitis C during the four years period. Mean age was 41 years (SD±6.7) and 74% were males. Risk factors for co-infection were mainly related to intravenous drug abusers 32/43 (74%). Regarding immuno-virological situation, 51% had T-CD4+ count >500/mm3 at baseline, 79% showed no more than four HAART changes and only 19% had a CD4 nadir <200 cells/mm3 .
S543 Genotype 3a represented 51%, while 40% were infected by genotype 1 and 9% by genotype 4. Only 16/43 (37%) were on HAART at baseline and half of the patients showed high HCV-RNA levels. Liver steatosis was present in 14/43 (33%) patients. Mean T-CD4+ count reduction was 175 cells/mm3 (33%), compared a T-CD4+ percentage reduction of 11%. High rates of HCV treatment discontinuation were present (63%), due to voluntary interruptions (52%), virological failure (26%), adverse events as cytopenia (11%) and others. Total EVR was 51%. The SVR was 30% in total, 38% and 24% for genotypes 3a and 1, respectively. Positive and negative predicting values of EVR were 60% and 90%. SVR was significantly lower in high HCV-RNA viral load group (c2 = 6, P < 0.0025), CD4 nadir <350 cells/mm3 (c2 = 3.26, P < 0.01) and <500 cells/mm3 (c2 = 3.94, P < 0.005) and in patients with genotype 1 and high viral load (c2 = 4.8, P < 0.005). Conclusions: Factors as HCV viral load rates and genotype 1 have been confirmed to threaten the response to therapy. Patients with no EVR did not have any probability of SVR. There is a significant response rate if patients have a history of nadir >350 T-CD4+/mm3 . High dropouts rates reported due to adverse event and voluntary discontinuations complicate HIV/HCV therapeutic management. P1895 Low prevalence of HCV co-infection in HIV/HBV co-infected teenagers from Romania L. Manolescu, C. Sultana, P. Marinescu, S. Ruta (Bucharest, Giurgiu, RO) Objectives: In Romania there was the biggest paediatric HIV infection acquired by parenteral route. The prevalence of HBV markers at these children was of 78.3% at HIV infected versus 21.8% in HIV negative controls. The teenagers acquired HIV and HBV infection horizontally. This study was performed to examine the impact of HCV co infection in HIV/HBV co infected teenagers from Romania. Methods: Two groups of patients with HIV infection, from different Romanian regions (161 from Constanta, 198 from Giurgiu), average age 13.8±1.3, were retrospectively analysed 2 years for clinical and virological parameters. Clinical liver function parameters (AST, ALT, total bilirubin, albumin), CD4 count, and virological parameters (HCV, HBV and HIV viral load by Roche Amplicor), HBsAg, HBeAg, HBsAb, HBcAb were performed twice a year. Results: Prevalence of HCV antibodies was low and similar in both groups 2.04% respectively 2.5%. All HCV/HIV co infected patients were also HBV infected and treated with potent antiretroviral therapy (HAART), but never experienced specific antiviral anti HCV treatment. We noticed in both groups similar correlations. HBV/HCV/HIV co infection with active HBV replication revealed through the presence of HBeAg and DNA-HBV high titer (40.000.000 copies DNA-HBV/mL) in both groups: 33.3% respectively 40%, was associated with worsened HIV-related parameters (CD4 count under 100 cell/microL, average HIV titer above 750.000 copies RNA HIV/mL), and increased transaminase (average values 156 mg/dl) but undetectable HCV titers, compared to patients without active HBV replication that presented detectable HCV titers (average of 11550 copies RNA-HCV/mL) and undetectable HIV and HBV titers and transaminase. Patients co infected with HIV/HCV and without HBeAg appeared to have a good response to HAART in terms of CD4 count changes, with a CD4 count average of 532 cells/microL. Conclusions: A surprisingly low prevalence of HCV co infection was found in HIV/HBV co infected patients despite the commune route of transmition. HIV disease outcomes following HAART do not appear to be adversely affected by HCV co infection and reveal good CD4 count responses. Active chronic HBV co infection in HCV/HIV co infected patients is associated with worsened liver disease and worsened HIV condition.
S543 Genotype 3a represented 51%, while 40% were infected by genotype 1 and 9% by genotype 4. Only 16/43 (37%) were on HAART at baseline and half of the patients showed high HCV-RNA levels. Liver steatosis was present in 14/43 (33%) patients. Mean T-CD4+ count reduction was 175 cells/mm3 (33%), compared a T-CD4+ percentage reduction of 11%. High rates of HCV treatment discontinuation were present (63%), due to voluntary interruptions (52%), virological failure (26%), adverse events as cytopenia (11%) and others. Total EVR was 51%. The SVR was 30% in total, 38% and 24% for genotypes 3a and 1, respectively. Positive and negative predicting values of EVR were 60% and 90%. SVR was significantly lower in high HCV-RNA viral load group (c2 = 6, P < 0.0025), CD4 nadir <350 cells/mm3 (c2 = 3.26, P < 0.01) and <500 cells/mm3 (c2 = 3.94, P < 0.005) and in patients with genotype 1 and high viral load (c2 = 4.8, P < 0.005). Conclusions: Factors as HCV viral load rates and genotype 1 have been confirmed to threaten the response to therapy. Patients with no EVR did not have any probability of SVR. There is a significant response rate if patients have a history of nadir >350 T-CD4+/mm3 . High dropouts rates reported due to adverse event and voluntary discontinuations complicate HIV/HCV therapeutic management. P1895 Low prevalence of HCV co-infection in HIV/HBV co-infected teenagers from Romania L. Manolescu, C. Sultana, P. Marinescu, S. Ruta (Bucharest, Giurgiu, RO) Objectives: In Romania there was the biggest paediatric HIV infection acquired by parenteral route. The prevalence of HBV markers at these children was of 78.3% at HIV infected versus 21.8% in HIV negative controls. The teenagers acquired HIV and HBV infection horizontally. This study was performed to examine the impact of HCV co infection in HIV/HBV co infected teenagers from Romania. Methods: Two groups of patients with HIV infection, from different Romanian regions (161 from Constanta, 198 from Giurgiu), average age 13.8±1.3, were retrospectively analysed 2 years for clinical and virological parameters. Clinical liver function parameters (AST, ALT, total bilirubin, albumin), CD4 count, and virological parameters (HCV, HBV and HIV viral load by Roche Amplicor), HBsAg, HBeAg, HBsAb, HBcAb were performed twice a year. Results: Prevalence of HCV antibodies was low and similar in both groups 2.04% respectively 2.5%. All HCV/HIV co infected patients were also HBV infected and treated with potent antiretroviral therapy (HAART), but never experienced specific antiviral anti HCV treatment. We noticed in both groups similar correlations. HBV/HCV/HIV co infection with active HBV replication revealed through the presence of HBeAg and DNA-HBV high titer (40.000.000 copies DNA-HBV/mL) in both groups: 33.3% respectively 40%, was associated with worsened HIV-related parameters (CD4 count under 100 cell/microL, average HIV titer above 750.000 copies RNA HIV/mL), and increased transaminase (average values 156 mg/dl) but undetectable HCV titers, compared to patients without active HBV replication that presented detectable HCV titers (average of 11550 copies RNA-HCV/mL) and undetectable HIV and HBV titers and transaminase. Patients co infected with HIV/HCV and without HBeAg appeared to have a good response to HAART in terms of CD4 count changes, with a CD4 count average of 532 cells/microL. Conclusions: A surprisingly low prevalence of HCV co infection was found in HIV/HBV co infected patients despite the commune route of transmition. HIV disease outcomes following HAART do not appear to be adversely affected by HCV co infection and reveal good CD4 count responses. Active chronic HBV co infection in HCV/HIV co infected patients is associated with worsened liver disease and worsened HIV condition.