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• W2107515502 abstract "Introduction There is increasing awareness of an ongoing epidemic of acute hepatitis C virus (HCV) infection in HIV-infected MSM. The epidemiology has been reviewed in this journal recently [1]; however, there is a lack of guidance on the management of acute HCV infection in HIV-infected individuals. To address this issue, the European AIDS Treatment Network (NEAT) invited members of the European AIDS Clinical Society (EACS) hepatitis group, the European Association for the Study of the Liver (EASL), the European Study Group on Viral Hepatitis of the European Society of Clinical Microbiology and Infectious Diseases, the European AIDS Treatment group and other experts to draw up a consensus statement at a conference held in Paris, France, in May 2010. Four working groups prepared draft guidelines for consideration at the conference on case definition and diagnosis; transmission risk and epidemiology; pathogenesis and natural history; and acute HCV infection management in the HIV-infected population. A literature search using the PubMed database of the National Library of Medicine and abstract databases of the Conference on Retroviruses and Opportunistic Infections, the Interscience Conference on Antimicrobial Agents and Chemotherapy, the Liver Meetings of the American Association for the Study of Liver Disease and EASL was utilized by all groups. Statements and recommendations were graded by the strength of recommendation and level of evidence (Table 1) [2]. A consensus was reached if 80% or more of the participants were in favour.Table 1: Grading strength of recommendation and level of evidence.Case definition and diagnosis of acute hepatitis C virus infection in HIV-infected patients Acute HCV infection is defined as the first 6 months after exposure to HCV. This definition is arbitrary, as there is a lack of evidence on when ‘acute’ infection becomes ‘chronic’ and determining the precise timing of infection is usually problematic. As the majority of individuals with acute HCV infection are asymptomatic [3,4], clinical diagnosis has a low sensitivity. Differentiating between acute HCV infection and an exacerbation of chronic HCV infection clinically, virologically and immunologically is difficult in the absence of recent negative HCV-RNA and antibody results. A serological test does not exist to differentiate between acute and chronic infection [5–7]. One third to a half of individuals with acute HCV infection experience symptoms attributable to an acute illness [3,4], although symptoms are nonspecific. Eighty-eight percent individuals experience elevated alanine aminotransferases (ALTs) within 3 months of infection [8] with peak ALT levels higher than five times the upper limit of normal in 55% individuals [4]. Patients in this study were sampled at 1–3 month intervals, so the rate of ALT elevation could be an underestimation. HIV-infected patients with chronic HCV develop hepatic flares with a rise of ALT higher than five times the upper limits of normal (ULN) in less than 2% [9], minimizing the possibility of classifying ‘chronic’ HCV infection as ‘acute’. The first marker of HCV infection is serum or plasma HCV-RNA detected through nucleic acid test (NAT) as early as 1 week postinfection [10]. HCV antibody responses may be delayed or absent in HIV-infected individuals with two-thirds positive at 3 months and 5% remaining negative up to 1 year after infection [8]. Fluctuations in HCV-RNA levels during the acute phase of HCV infection are characteristic in HIV-uninfected individuals and may be of value in suggesting a diagnosis of acute hepatitis C [11]. A definitive diagnosis of acute hepatitis C can be made by documented seroconversion from negative to positive in a test for HCV antibodies. Owing to the asymptomatic nature of the illness, seroconversion often occurs prior to diagnosis. Even if annual antibody screening is performed, a prior HCV antibody test may not have been performed within the previous 6 months. Owing to delayed and occasionally absent HCV antibody seroconversion, the window period in which HCV-RNA will be detectable in peripheral blood without the presence of anti-HCV antibodies cannot be used with accuracy to diagnose acute hepatitis C. Advanced serologic assays for HCV including HCV antigen tests improve the sensitivity of serological testing [12,13], but are inferior to testing for HCV-RNA (Table 2) [8,12].Table 2: Sensitivity of serum-based assays for the detection of hepatitis C virus compared with hepatitis C virus RNA.Consensus recommendation: case definition acute hepatitis C virus infection Preferred criteria (grade A, level II) Positive anti-HCV immunoglobulin G (IgG) in the presence or absence of a positive HCV-RNA and a documented negative anti-HCV IgG in the previous 12 months. Positive HCV-RNA and a documented negative HCV-RNA and negative anti-HCV IgG in the previous 12 months. Alternative criteria (Grade B, Level III) If historical data is lacking and relevant test results within the past year unavailable, acute hepatitis C may be diagnosed if the following criteria are met: Positive HCV-RNA regardless of anti-HCV IgG with any of the following two conditions: An acute rise in ALT greater than 10 times the ULN. An acute rise in ALT greater than five times the ULN, with documented normal ALT within 12 months. In individuals with a previously high ALT, an acute rise to 3.5 times their previous ALT is acceptable [14]. Antihepatitis A virus IgM negative and antihepatitis B core IgM antibody negative, and exclusion of other causes of acute hepatitis. No consensus (20 in favour, six against with three abstentions) was reached to include a history of transmission risk factors for acute HCV in the alternative case definition. Epidemiology and transmission Prevalence of hepatitis C virus infection The prevalence of HCV infection in the HIV-infected is higher than in the uninfected population [15]. Within the HIV-infected population, the highest prevalence is in those with a history of intravenous drug use (IVDU) or haemophilia and other bleeding disorders. The European AIDS cohort (EuroSIDA) reported a prevalence of anti-HCV antibody or HCV-RNA positivity of 33%, ranging from 6.6% in MSM to 75% in IVDUs [16]. This is similar to other cohorts and cross-sectional studies in HIV-infected populations [17–26]. Incidence of acute hepatitis C The most efficient means of HCV transmission is through parenteral exposure in IVDUs who share needles, syringes or other paraphernalia for drug use. Cases of sexual transmission of HCV infection in heterosexuals remain uncommon [27,28]. Since 2000, there have been reports from Europe, Australia and the USA of an increasing incidence of acute hepatitis C infection in HIV-infected MSM (Table 3) [22,23,26,29–32]. In Amsterdam, incidence has risen 10-fold from an estimated 0.08 per 100 person-years in 1984–1999 to 0.87 in 2000–2003 in HIV-infected MSM attending a sexually transmitted infection (STI) clinic [29].Table 3: Hepatitis C virus incidence among people who are HIV infected.Hepatitis C virus transmission in MSM Studies in MSM have shown HIV infection and IVDU to be independently associated with the presence of HCV antibodies [29,33–35]. In early reports, evidence for sexual transmission was weak with conflicting evidence of an association with sexual risk behaviour [33–39]. Recent studies investigating factors underlying HCV transmission in HIV-infected MSM have provided further evidence for an association with certain sexual practices including fisting, using sex toys and group sex [29,36,37]. Noninjecting drug use is also associated, probably because of the influence on sexual behaviour, but transmission through sharing contaminated devices may also contribute. There is an association with bacterial STIs, notably syphilis and lymphogranuloma venereum. The mechanism of sexual transmission remains uncertain, but the association with traumatic sexual practices and ulcerative STIs affecting the mucosa of the rectum provides some clues. HCV-RNA has been detected in semen and more often in the HIV-infected individuals [38], although one study failed to detect HCV-RNA in the semen of most HIV-infected men even during acute HCV infection [39]. Group sex may facilitate transfer of infected material [36]. Other causes of disruption of the anorectal mucosa, including surgery, may contribute to the risk [36]. There is no evidence that HIV-infected men are more susceptible to HCV infection due to immunological deficits, or that a more virulent HCV strain is being selected. Phylogenetic analyses of transmitted HCV strains show clustering consistent with transmission among a social and sexual network of HIV-infected MSM which extends nationally and internationally [40]. Although the majority of patients present with two or more risk factors described above, cases of acute HCV infection are seen in MSM who report only unprotected anal intercourse. Although current outbreaks have been largely confined to HIV-infected MSM, cases have also been reported in HIV-uninfected individuals. Public health implications The recognition of ongoing transmission of HCV requires measures to reduce rates of transmission. This involves identification of undiagnosed HCV infection and ensuring appropriate risk-reduction advice is provided to the infected and those at risk. Although unselected screening for acute hepatitis C in HIV-infected individuals may not be cost-effective in regions with a low prevalence [41], annual testing in populations at high risk may detect seroconversions in those with normal transaminases and permit improved estimation of the time of infection. Liver transaminases at routine visits with subsequent HCV-RNA testing in suspected patients will identify 90% of those with acute HCV [8]. HIV-infected individuals with severe immunodeficiency may lose anti-HCV antibodies, but may regenerate antibodies after initiation of HIV therapy with subsequent immune reconstitution. Consensus recommendation screening for acute HCV infection (grade A, level II, *grade C, level II) All newly diagnosed HIV individuals should be screened for anti-HCV antibody [42]. HIV-infected MSM at risk for contracting acute hepatitis C infection should be screened at 6-month interval with ALT and annually with anti-HCV antibody. HIV-infected patients with newly diagnosed STI or continued IVDU should be screened 3 months after diagnosis/last exposure. A NAT test for HCV-RNA should be performed if a diagnosis of acute HCV infection is suspected. The management of those diagnosed with acute HCV infection should include encouraging partner notification to identify potential sources of infection and those at risk of exposure. Screening for other sexually transmitted diseases is required. Consensus recommendation risk-reduction advice (grade B, level II) Although the mode of HCV transmission remains unclear, epidemiological studies suggest that the following risk behaviours be considered in risk-reduction advice: fisting, recreational drug use, group sex, use of sex toys, unprotected anal sex, sharing of paraphernalia (for IVDU and permucosal drug use) and sexual practices with risk for blood–blood contact or mucosal damage. Information regarding risk of HCV transmission should be given to all HIV-infected individuals after HIV diagnosis and on an ongoing basis. Advice regarding risk factors for transmission must be given to all those newly diagnosed with HCV infection including risk-reduction. Pathogenesis, natural history and implications for treatment of acute hepatitis C Innate and adaptive immune responses The immune response in acute hepatitis C, and correlates of spontaneous clearance, has been studied predominantly in HCV-monoinfected individuals and in chimpanzees. Acute hepatitis C infection induces a range of innate and adaptive immune responses. Single nucleotide polymorphisms near the interleukin (IL28B) gene, encoding for interferon-λ (IFNλ), provide strong evidence for an important role of the innate immune system in the natural defence against HCV [43–45]. Individuals with the rs12979860 CC genotype were more than three times likely to clear HCV-RNA compared with individuals with C/T and T/T genotypes [43]. A similar association is observed in HIV/HCV-coinfected individuals [44]. The frequency of the protective allele varies across ethnic groups with a lower frequency in those of African origin compared with European patients which could explain observed differences in spontaneous clearance between races [43]. The cellular immune response is important for the outcome of acute hepatitis C. Clearance in HIV-uninfected individuals is associated with a broad, vigorous and sustained memory CD4+ and CD8+ T-cell response [46,47]. In one study, memory T-cell responses to nonstructural (NS4) protein correlated with HCV clearance [48], whereas in a comparative study of HIV-infected and uninfected individuals, HIV-infected patients had CD4+ T-cell IFNγ ELISpot responses against NS3-5 proteins, but were reduced in frequency, breadth and magnitude [49]. Successful antiretroviral therapy can restore HCV-specific cellular immune responses [50]. The importance of CD4/CD8 HCV antigen-specific responses in determining spontaneous clearance and patterns of viraemia after HCV acquisition has been demonstrated in HIV-negative [51] and HIV-coinfected individuals [52,53]. A lack of antigen-specific responses early in the course of acute infection determines progression to chronic HCV and may be associated with the pattern of viraemia observed [51]. Spontaneous clearance was associated with early antigen-specific responses and rapid HCV clearance. The role of humoral immune responses in acute hepatitis C is not well defined [52–58]. Evoked cellular and humoral immune responses after first acute HCV infection diminish following spontaneous resolution or successful antiviral therapy [58], although data are inconsistent. Rates and predictors of spontaneous hepatitis C virus RNA clearance The rate of and factors associated with spontaneous viral clearance in HIV-infected patients with acute hepatitis C have been studied in prospective cohorts. In the Johns Hopkins cohort [59] of predominantly black men with prior or current IVDU, HCV-RNA clearance was observed in 14% of HIV-uninfected and 7% of HIV-infected individuals with the lowest rate (5%) associated with CD4+ cell counts less than 200 cells/μl. Viral clearance was associated with nonblack ethnicity, younger age (<45 years) and hepatitis B surface antigen (HBsAg) positivity [59]. In the EuroSIDA cohort, spontaneous HCV-RNA clearance was 23% in 1940 HCV antibody-positive individuals [60]. Factors associated with spontaneous viral clearance were female sex, mode of transmission (sexual vs. IVDU), HBsAg positivity and region (other European regions vs. southern Europe/Argentina). Viral clearance was not associated with age, ethnicity or HIV-related variables [60]. Rates of spontaneous viral clearance in those with established HIV infection range from 0 to 40%, but due to small sample sizes, and the majority being MSM, factors associated with spontaneous viral clearance are not well defined [49,61–63]. Gilleece et al.[62] reported lower HCV-RNA titers and CD4+ T-cell count higher than 500 cells/μl were predictive of spontaneous clearance. Consensus statement on the natural history of acute hepatitis C infection Acute hepatitis C takes a chronic course more frequently in HIV-infected individuals (II). Spontaneous clearance of acute HCV in HIV patients occurs in 0–40% (III) and is associated with the following factors: Host genetic factors (e.g. IL28b-CC genotype*) and stronger adaptive immune responses (II). Female sex, exposure group (sexual transmission vs. IVDU), HBsAg positivity, jaundice and higher peak ALT (II). Early decline of HCV-RNA 4–8 weeks after presentation (III) *using the rs12979860 SNP. Selection for early antiviral therapy Ideally, only those who will not clear HCV spontaneously would be candidates for early antiviral treatment. However, delays in treatment could reduce efficacy. A positive HCV-RNA 12 weeks into acute hepatitis is associated with transition to chronic infection. Thus, treatment has been recommended in those with persistent HCV-RNA reactivity 12 weeks after onset of symptoms or 12 weeks after putative exposure, although there may be as much as 8 weeks difference between these time points. Low-level viraemia and viral load fluctuations are common in acute HCV and are incorporated in standard diagnostic criteria [11]. The definition of 12-week HCV-RNA reactivity as a predictor of chronicity is supported by Gerlach et al.[64]. In this study in HIV-negative patients, two of 24 cases that resolved still had HCV-RNA detectable 12 weeks after onset of hepatitis and none after 16 weeks. A limitation of this study was that the HCV-RNA assay used (Amplicor Monitor; Hoffmann–La Roche, Basel, Switzerland) had a sensitivity of 600 IU/ml, more than a log higher than currently available tests. In a recent study of acute posttransfusion hepatitis C [65] utilizing a more sensitive HCV-RNA assay (transcription-mediated amplification), 48% with resolved infection had HCV-RNA detectable at 12 weeks and 32% at 16 weeks after ALT elevation. However, 16% of patients progressing to chronic HCV had a negative HCV-RNA assay result 12 and 16 weeks after occurrence of hypertransaminasemia. In a European cohort of 92 HIV-positive patients with acute HCV, the sensitivity and specificity of HCV-RNA determination at 4 and 12 weeks to predict the outcome of acute HCV was similarly strong [66]. Eighty-five percent of individuals who did not reduce HCV-RNA by more than 2 log, 4 weeks after diagnosis, progressed to chronic hepatitis C defined as a positive HCV-RNA 24 weeks after the first positive HCV-RNA. Ninety-two percent of individuals who were HCV-RNA positive 12 weeks after diagnosis developed chronic hepatitis C. The observational setting and high cut-off of HCV-RNA assay used limits generalization of these data. The studies are summarized in Table 4[64–66]. A robust study utilizing highly sensitive NAT assays is required to provide stronger conclusions on the predictive value of HCV-RNA measurements during acute hepatitis C.Table 4: Predictability of week 4 and 12 hepatitis C virus RNA in determining spontaneous viral clearance.Optimum interval between the onset of hepatitis and treatment initiation If initiation of anti-HCV treatment is delayed for more than 1 year after onset, rates of sustained virological response (SVR) in HIV-uninfected persons are halved [67]. A shorter delay (12 weeks) did not impair outcome in the HEPNET III cohort [68]. In studies of acute HCV treatment in the HIV-infected individuals, most initiated treatment between 12 and 24 weeks into acute hepatitis and the length of time between the start of acute hepatitis and treatment initiation did not influence treatment response. This is exemplified in the Australian Trial in Acute HCV (ATAHC) in which SVR of greater than 75% was achieved in coinfected individuals with 24 weeks of combination therapy, with a median estimated duration of HCV infection before the start of therapy of 30 weeks, and greater than 24 weeks in over 80% [3]. Consensus recommendation on the monitoring and initiation of treatment in the course of acute hepatitis C infection HCV-RNA levels should be measured at initial presentation and 4 weeks later (BII). Treatment should be offered to the following individuals: Patients without a decrease of 2 log10 of HCV-RNA at 4 weeks compared with initial HCV-RNA (BII). Patients with persistent serum HCV-RNA 12 weeks after diagnosis of acute HCV (AII). Patients showing spontaneous HCV-RNA clearance before and after 12 weeks should undergo serial HCV-RNA measurement for 48 weeks to confirm resolution (AIII). Testing of retrospective samples may be useful to assess duration of viral infection. In cases of persistent HCV infection of duration greater than 12 weeks, initiation of treatment is recommended. Management of acute hepatitis C in HIV-infected patients In monoinfected acute hepatitis C, early therapy with standard IFNα or pegylated IFNα alone for up to 24 weeks is sufficient to obtain high rates of SVR (ranging from 71 to 98%) [64,69,70]. HIV-infected patients may be different due to a number of factors including high HCV viral loads, the proportion of genotype 1/4 infection and possible adverse impact of HIV-associated immune suppression. There are several reports of cohorts studying treatment of acute hepatitis C in HIV-infected persons (Table 5) [3,48,62,63,71–75].Table 5: Acute hepatitis C virus treatment in HIV-infected patients.In these studies, patients were treated with pegylated IFNs at standard doses (α-2b, 1.5 μg/kg per week and α-2a, 180 μg/week). Ribavirin was used in 145 of 170 individuals: weight-adjusted dosing in 122 and fixed dose in 23 (800 mg/day in 19 and 1000 mg/day in four patients). Twelve of 25 individuals (48%) treated with pegylated IFN monotherapy showed an SVR compared with 96 of 159 (60%) with combination therapy (P > 0.05). Although the cumulative results of these studies do not establish the role of ribavirin, other evidence of breakthrough and nonresponse in patients treated with pegylated IFN alone are also suggestive [3,76]. In a report of a study of acute hepatitis C genotype 1 and 4, in HIV-infected patients, six of 12 (50%) stopped therapy due to lack of early virological response (EVR, fall in HCV-RNA of more than 2 log or undetectability by 12 weeks after start of antiviral therapy) when treated with pegylated IFN alone [77]. The role of ribavirin in improving viral kinetic response has been demonstrated in the ATAHC study in which greater reductions in HCV-RNA were seen between weeks 8 and 12 of treatment in HIV/HCV-coinfected patients receiving combination therapy compared with pegylated IFN alone in monoinfected patients [78]. This translated into comparable rapid virological response (RVR, undetectable HCV-RNA 4 weeks after start of therapy) and SVR (undetectable HCV-RNA 24 weeks after the end of antiviral therapy) rates. Another treatment strategy suggested for acute hepatitis C is to start pegylated IFN and ribavirin, but then to discontinue the ribavirin in those with a fast decay of HCV-RNA (in this study defined as confirmed negative HCV-RNA at week 8 and 12). This treatment strategy may allow synergistic antiviral therapy in the beginning, yet limiting ribavirin-associated toxicities. Even though no disadvantages of this strategy have been reported thus far, SVR data are not yet available [79]. Although 48 weeks of therapy for acute HCV in HIV-infected patients appeared more efficacious than 24 weeks in a single study [71], a preliminary report [80] in mostly genotype 1/4 acute infections showed SVR rates of greater than 70% with no statistically significant difference by length of therapy. Furthermore, as seen in Table 5, 24 weeks of therapy is associated with SVR rates of over 60% overall. A lack of RVR predicting relapse is apparent from a study in monoinfected patients [81]. Evidence for the use of viral kinetics in determining the chance of SVR and potentially the optimal length of therapy comes from the European Collaborative Cohort Study [82] in which 111 HIV-infected men with acute HCV achieved an overall SVR of 62%. Ninety-three percent of those with an RVR achieved a SVR, whereas only 9% not achieving complete EVR reached a SVR. Response rates were defined by an HCV-RNA below 615 IU/ml. It would be reasonable to aim for 24 weeks of therapy, with a longer duration of therapy reserved for those without RVR but having EVR. Consensus recommendation on treatment of acute hepatitis C infection Pegylated IFN and weight-based ribavirin is recommended for the treatment of acute hepatitis C in HIV-infected patients (grade A, level II). Duration of treatment should be based on RVR [negative HCV-RNA at week 4 (evidence based on using a 615 IU/ml cut-off to define negative HCV-RNA)], regardless of HCV genotype. In patients with RVR, treatment duration should be 24 weeks (AII). In patients without RVR, treatment duration of 48 weeks should be considered (BIII). In non-RVR patients not achieving a 2 log10 drop in HCV-RNA at week 12, treatment can be discontinued (BIII). When and which antiretroviral therapy to use in HIV-infected patients with acute hepatitis C virus For information on CD4 strata for commencement of therapy and which antiretroviral components to use in HIV patients with acute hepatitis C commencing pegylated IFN and ribavirin therapy, the EACS guidelines should be consulted [83]. Consensus recommendation on the use of antiretroviral therapy in the setting of acute hepatitis C virus infection In those with acute HCV and CD4 cell count higher than 350 cells/μl, HCV therapy can be commenced before starting HIV therapy (BIII). Acknowledgements Panel members and conflict of interest: The development of guidelines demanded commercial independence and avoidance of potential conflict of interests, which could influence statements and recommendations made. The organization and related expenses of the conference were therefore solely funded through NEAT. NEAT is a project funded by the European Union under the 6th Framework programme, contract “acronym: NEAT, number: LSHP-CT-2006-037570”. All conference participants were asked to declare any conflict of interest of themselves or their families. The NEAT AHC panelists who were able to participate at the conference and vote on the statements/recommendations were: Matthieu Albert, Institut Pasteur, France, no conflict of interest; Jose Benito, Hospital Carlos III, Madrid, Spain, no conflict of interest; Sanjay Bhagani Group leader “Management” (EACS), Royal Free Hospital, London, United Kingdom, no conflict of interest; Christoph Boesecke, Bonn University Hospital, Bonn, Germany, no conflict of interest; Katja Deterding (EASL), Medizinische Hochschule Hannover, Hannover, Germany, no conflict of interest; Stephanie Dominguez, Hôpital de la Pitié-Salpétière, Paris, France, no conflict of interest; Martin Fisher Group leader “Epidemiology and transmission risk factors”, Royal Sussex County Hospital, Brighton, United Kingdom, no conflict of interest; Arnaud Fontanet, Institut Pasteur, Paris, France, no conflict of interest; Diego Garcia (EATG)/(EACS), Foro Español Activistas en Tratamientos, Sevilla, Spain, no conflict of interest; Richard Gilson Group leader “Epidemiology and transmission risk factors”, University College London, London, United Kingdom, no conflict of interest; Marguerite Guiguet INSERM-UPMC UMR S943, Paris, France, no conflict of interest; Andy I.M. Hoepelman, University Medical Center, Utrecht, The Netherlands, educational grant Roche; Andrzej Horban, Centrum Diagnostyki i Terapii AIDS, Warsaw, Poland, no conflict of interest; Christine Katlama, Hôpital de la Pitié-Salpétière, Paris, France, no conflict of interest; Josep Mallolas, Hospital Clínic, Barcelona, Spain, no conflict of interest; Emma Page Group leader “Case definition and diagnosis”, Chelsea and Westminster Hospital, London, United Kingdom, no conflict of interest; Lars Peters Group leader “Natural history and pathogenesis” (EACS), Copenhagen HIV Programme, Copenhagen, Denmark, no conflict of interest; Anton Pozniak, Chelsea and Westminster Hospital, London, United Kingdom, no conflict of interest; Maria Prins, Public Health Service, Amsterdam, the Netherlands, no conflict of interest; Massimo Puoti Group leader “Management” (EACS), A.O. Niguarda Cà Granda, Milan, Italy, no conflict of interest; Andri Rauch, University Hospital Berne and University of Berne, Inselspital, Bern, Switzerland, no conflict of interest; Alison Rodger, University College London, London, United Kingdom, no conflict of interest; Jürgen K. Rockstroh (EACS) Co-chair, Bonn University Hospital, Bonn, Germany, advisor of Essex and Roche pharmaceuticals; Vincent Soriano Group leader “Natural history and pathogenesis” (EACS), Hospital Carlos III, Madrid, Spain, no conflict of interest; Christoph Stephan, J. W. Goethe University Hospital, Frankfurt, Germany, no conflict of interest; Vincent Thibault, Hôpital de la Pitié-Salpétière, Paris, France, no conflict of interest; Cristina Tural (EACS), Hospital Germans Trias i Pujol, Badalona, Spain, no conflict of interest; Marc-Antoine Valantin, Hôpital de la Pitié-Salpétière, Paris, France, no conflict of interest; Thijs van de Laar, Public Health Service, Amsterdam, the Netherlands, no conflict of interest; Jan van der Meer, Academic Medical Center University of Amsterdam, Amsterdam, the Netherlands, no conflict of interest; Stefano Vella, Istituto Superiore di Sanita, Rome, Italy, no conflict of interest; Martin Vogel Group leader “Case definition and diagnosis”, Bonn University Hospital, Bonn, Germany, travel grants and speaker honoraria Roche and Essex pharmaceuticals; Stéphane de Wit, St. Pierre University Hospital, Brussels, Belgium, no conflict of interest. The following NEAT AHC panelists were not able to participate at the conference and vote on the statements/recommendations. They were still involved in drafting statements/recommendations and reviewed and commented the final version of the manuscript: Brigitte Autran, Hôpital Pitié-Salpêtrière, Paris, France, no conflict of interest; Bonaventura Clotet, Hospital Germans Trias i Pujol, Badalona, Spain, no conflict of interest; Mark Danta, UNSW St Vincent's Clinical School, Sidney, Australia, no conflict of interest; Maxime Journiac (EATG), EATG Brussels, Belgium, no conflict of interest; Gail Matthews, UNSW National Centre in HIV Epidemiology and Clinical Research, Sidney, Australia, no conflict of interest; Dirk Meyer-Olson, Medizinische Hochschule Hannover, Hannover, Germany, no conflict of interest; Mark Nelson Co-chair, Chelsea and Westminster Hospital, London, United Kingdom, no conflict of interest; Reinhold Schmidt, Medizinische Hochschule Hannover, Hannover, Germany, no conflict of interest; Heiner Wedemeyer (EASL), Medizinische Hochschule Hannover, Hannover, Germany, grant support for research, fees for lectures and consultancy: Roche, Merck, Transgene, Gilead, BMS, Novartis." @default.
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• W2107515502 title "Acute hepatitis C in HIV-infected individuals: recommendations from the European AIDS Treatment Network (NEAT) consensus conference" @default.
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