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BACKGROUND: It is cost-effective to perform an HIV test in people with specific indicator conditions (IC) with an undiagnosed HIV prevalence of at least 0.1%. Our aim was to determine the HIV prevalence for 14 different conditions across 20 European countries.METHODS: Individuals aged 18-65 years presenting for care with one of 14 ICs between January 2012 and June 2014 were included and routinely offered an HIV test. Logistic regression assessed factors associated with testing HIV positive. Patients presenting with infectious mononucleosis-like syndrome (IMS) were recruited up until September 2015.RESULTS: Of 10,877 patients presenting with an IC and included in the analysis, 303 tested positive (2.8%; 95% CI 2.5-3.1%). People presenting with an IC in Southern and Eastern Europe were more likely to test HIV positive as were people presenting with IMS, lymphadenopathy and leukocytopenia/ thrombocytopenia. One third of people diagnosed with HIV after presenting with IMS reported a negative HIV test in the preceding 12 months. Of patients newly diagnosed with HIV where data was available, 92.6% were promptly linked to care; of these 10.4% were reported lost to follow up or dead 12 months after diagnosis.CONCLUSION: The study showed that 10 conditions had HIV prevalences > 0.1%. These 10 ICs should be adopted into HIV testing and IC specialty guidelines. As IMS presentation can mimic acute HIV sero-conversion and has the highest positivity rate, this IC in particular affords opportunities for earlier diagnosis and public health benefit.

Background The effect of neuraminidase inhibitor (NAI) treatment on length of stay (LoS) in patients hospitalized with influenza is unclear. Methods We conducted a one-stage individual participant data (IPD) meta-analysis exploring the association between NAI treatment and LoS in patients hospitalized with 2009 influenza A(H1N1) virus (A[H1N1]pdm09) infection. Using mixed-effects negative binomial regression and adjusting for the propensity to receive NAI, antibiotic, and corticosteroid treatment, we calculated incidence rate ratios (IRRs) and 95% confidence intervals (CIs). Patients with a LoS of, We found that neuraminidase inhibitor (NAI) treatment initiated on hospital admission to patients with clinically diagnosed or laboratory-confirmed A(H1N1)pdm09 virus infection was associated with a reduction in hospital length of stay when compared to later or no NAI treatment.

Stella G. Muthuri,1 Sudhir Venkatesan,1 Puja R. Myles,1 Jo Leonardi-Bee,1 Wei Shen Lim,2 Abdullah Al Mamun,3 Ashish P. Anovadiya,4 Wildo N. Ara ujo,5 Eduardo Azziz-Baumgartner,6 Clarisa B aez,7 Carlos Bantar,8 Mazen M. Barhoush,9 Matteo Bassetti,10 Bojana Beovic,11 Roland Bingisser,12 Isabelle Bonmarin,13 Victor H. Borja-Aburto,14 Bin Cao,15 Jordi Carratala,16 Mar ıa R. Cuezzo,17 Justin T. Denholm,18 Samuel R. Dominguez,19 Pericles A. D. Duarte,20 Gal Dubnov-Raz,21 Marcela Echavarria,22 Sergio Fanella,23 James Fraser,24 Zhancheng Gao,25 Patrick G erardin,26,27,28,29 Maddalena Giannella,30 Sophie Gubbels,31 Jethro Herberg,32 Anjarath L. Higuera Iglesias,33 Peter H. Hoeger,34 Matthias Hoffmann,35 Xiaoyun Hu,36 Quazi T. Islam,37 Mirela F. Jim enez,38 Amr Kandeel,39 Gerben Keijzers,40 Hossein Khalili,41 Gulam Khandaker,42 Marian Knight,43 Gabriela Kusznierz,44 Ilija Kuzman,45 Arthur M. C. Kwan,46 Idriss Lahlou Amine,47 Eduard Langenegger,48 Kamran B. Lankarani,49 Yee-Sin Leo,50 Rita Linko,51 Pei Liu,52 Faris Madanat,53 Toshie Manabe,54 Elga Mayo-Montero,55 Allison McGeer,56 Ziad A. Memish,57,58 Gokhan Metan,59 Dragan Miki c,60 Kristin G. I. Mohn,61,62 Ahmadreza Moradi,63,64 Pagbajabyn Nymadawa,65 Bulent Ozbay,66 Mehpare Ozkan,67 Dhruv Parekh,68 Mical Paul,69 Wolfgang Poeppl,70 Fernando P. Polack,71,72 Barbara A. Rath,73 Alejandro H. Rodr ıguez,74 Marilda M. Siqueira,75 Joanna Skre zt-Magierło,76 Ewa Talarek,77 Julian W. Tang,78,79,80 Antoni Torres,81 Selda H. T€ or€un,82 Dat Tran,83 Timothy M. Uyeki,84 Annelies van Zwol,85 Wendy Vaudry,86 Daiva Velyvyte,87 Tjasa Vidmar,88 Paul Zarogoulidis,89 PRIDE Consortium Investigators* Jonathan S. Nguyen-Van-Tam1 1Division of Epidemiology and Public Health, University of Nottingham, Nottingham, UK. 2Respiratory Medicine, Nottingham University Hospitals NHS Trust, Nottingham, UK. 3International Centre for Diarrhoeal Diseases, Research Bangladesh (ICDDRB), Dhaka, Bangladesh. 4Department of Pharmacology, Government Medical College and Sir Takhtsinhji General Hospital, Bhavnagar, Gujarat, India. 5University of Bras ılia, Bras ılia, DF, Brazil. 6Centers for Disease Control and Prevention, Atlanta, GA, USA. 7Ministerio de Salud de la Provincia de Buenos Aires, Buenos Aires, Argentina. 8Department of Infection Control, Hospital San Mart ın de Paran a, Entre R ıos, Argentina. 9Department of Medicine, King Saud Medical City, Riyadh, Saudi Arabia. 10Santa Maria Misericordia Hospital, Udine, Italy. 11Department of Infectious Diseases, University Medical Centre, Ljubljana, Slovenia. 12Department of Emergency Medicine, University Hospital Basel, Basel, Switzerland. 13Institut de Veille Sanitaire, Saint-Maurice, France. 14Instituto Mexicano del Seguro Social (IMSS), Mexico City, Mexico. 15Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China. 16Department of Infectious Diseases, Hospital Universitari de Bellvitge, Bellvitge Institute for Biomedical Research, L’Hospitalet de Llobregat, Red Espa~nola de Investigaci on en Patolog ıa Infecciosa, University of Barcelona, Barcelona, Spain. 17Ministerio de Salud de Tucum an, Tucum an, Argentina. 18Victorian Infectious Diseases Service and Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, Parkville, Vic., Australia. 19Department of Pediatric Infectious Diseases, Children’s Hospital Colorado, University of Colorado School of Medicine, Aurora, CO, USA. 20Universidade Estadual do Oeste do Parana ´, UNIOESTE, Cascavel, PR, Brazil. 21The Edmond and Lily Safra Children’s Hospital, Sheba Medical Center, Tel-Hashomer, Israel. 22Clinical Virology Laboratory, CEMIC University Hospital, Buenos Aires, Argentina. 23Section of Pediatric Infectious Diseases, University of Manitoba, Winnipeg, MB, Canada. 24Paediatric Intensive Care Unit, Bristol Children’s Hospital, Bristol, UK. 25Department of Respiratory & Critical Care Medicine, Peking University People’s Hospital, Beijing, China. 26NICU/PICU, PFME, CHU Saint Pierre, Saint Pierre, La R eunion, France. 27CIC 1410 (CHU/Inserm/University of La Re ´union/URML-OI), CHU Saint Pierre, Saint Pierre, La Réunion, France. 28UMR PIMIT (CHU/Inserm/University of La Re ´union/IRD/CNRS), CYROI, Saint Denis – Reunion Island, Saint Denis, France. 29NICU/PICU CHU of La Re ´union, Groupe Hospitalier Sud Re ´union, Saint Pierre, La Re ´union, France. 30Department of Clinical Microbiology and Infectious Diseases, Hospital General Universitario Gregorio Maran ˜o ´n, Madrid, Spain. 31Department of Infectious Disease Epidemiology, Sector for National Health Documentation and Research, Statens Serum Institut, Copenhagen, Denmark. 32Section of Paediatrics, Division of Infectious Disease, Imperial College, London, UK. 33Epidemiology Research Unit, Instituto Nacional de Enfermedades Respiratorias, Ismael Cosı ´o Villegas, Mexico City, Mexico. 34Cath. Children’s Hospital Wilhelmstift, Hamburg, Germany. 35Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland. 36Peking Union Medical College Hospital, Beijing, China. 37Dhaka Medical College Hospital, Dhaka, Bangladesh. 38Departamento de Ginecologia e Obstetrı ´cia – UFCSPA, Preceptora da Reside ˆncia Me ´dica do Hospital Fe ˆmina, Porto Alegre, Brazil. 39Ministry of Health in Egypt, Cairo, Egypt. 40Gold Coast Hospital, Gold Coast, Qld, Australia. 41Department of Clinical Pharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran. 42National Centre for Immunisation Research and Surveillance (NCIRS), The Children’s Hospital at Westmead, University of Sydney, Sydney, NSW, Australia. 43National Perinatal Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. 44National Institute of Respiratory Diseases ‘Emilio Coni’ ANLIS “C. Malbran”, Santa Fe, Argentina. 45School of Medicine, University Hospital for Infectious Diseases, University of Zagreb, Zagreb, Croatia. 46Department of Intensive Care, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong. 47Faculty of Medicine and Pharmacy, Mohammed V Military Teaching Hospital, Biosafety Level 3 and Research Laboratory, University Mohammed V-Souissi, Rabat, Morocco. 48Department of Obstetrics and Gynaecology, Stellenbosch University and Tygerberg, Stellenbosch, South Africa. 49Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. 50Department of Infectious Diseases, Tan Tock Seng Hospital, Singapore, Singapore. 51Helsinki University Hospital, Helsinki, Finland. 52Department of Infectious Diseases, The First Affiliated Hospital, China Medical University, Shenyang, China. 53Department of Pediatrics, King Hussein Cancer Center, Amman, Jordan. 54Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. 55Instituto de Medicina Preventiva de la Defensa, Capitan Medico Ramon y Cajal (IMPDEF), Ministerio de Defensa, Madrid, Spain. 56Toronto Invasive Bacterial Diseases Network, University of Toronto, Toronto, ON, Canada. 57Ministry of Health, Riyadh, Saudi Arabia. 58College of Medicine, Alfaisal University, Riyadh, Saudi Arabia. 59Department of Infectious Diseases and Clinical Microbiology, Erciyes University Faculty of Medicine, Kayseri, Turkey. 60Military Medical Academy, Clinic for Infectious and Tropical Diseases, Belgrade, Serbia. 61Section for Infectious Diseases, Medical Department, and Department of Research and Development, Haukeland University Hospital, Bergen, Norway. 62Department of Clinical Science, The Influenza Centre, University of Bergen, Bergen, Norway. 63The Division of Ocular Immunology, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 64National Research Institute for Tuberculosis and Lung Disease, Massih Daneshvari Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 65National Influenza Center, National Center of Communicable Diseases, Ministry of Health, Ulaanbaatar, Mongolia. 66Department of Pulmonary and Critical Care, Yuzuncu Yil University Medical Faculty, Van, Turkey. 67Clinic of Pediatric Neurology, Dr. Sami Ulus Research and Training Hospital of Women’s and Children’s Health and Diseases, Ankara, Turkey. 68Critical Care and Pain Perioperative, Critical Care and Trauma Trials Group, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK. 69Division of Infectious Diseases, Rambam Health Care Campus, Haifa, Israel. 70Medical University of Vienna, Vienna, Austria. 71Department of Pediatrics, Vanderbilt Vaccine Center, Vanderbilt University, Nashville, TN, USA. 72Fundacion INFANT, Buenos Aires, Argentina. 73Division of Pneumonology-Immunology, Department of Pediatrics, Charite ´ University Medical Center, Berlin, Germany. 74Critical Care Department, Hospital Joan XXIII, IISPV, URV, CIBERES, Tarragona, Spain. 75Laboratory of Respiratory Viruses, Oswaldo Cruz Institute/Fiocruz, Rio de Janeiro, Brazil. 76Uniwersytet Rzeszowski, Rzeszo ´w, Poland. 77Department of Children’s Infectious Diseases, Medical University of Warsaw, Warsaw, Poland. 78Division of Microbiology/Molecular Diagnostic Centre, Department of Laboratory Medicine, National University Hospital, Singapore, Singapore. 79Alberta Provincial Laboratory for Public Health, University of Alberta Hospital, Edmonton, Canada. 80Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB, Canada. 81Hospital Clinic, University of Barcelona, IDIBAPS, CIBERES, Barcelona, Spain. 82Department of Pediatric Infectious Diseases, Istanbul Medical Faculty, Istanbul, Turkey. 83Division of Infectious Diseases, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Canada. 84Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. 85Department of Pediatric Intensive Care, VU University Medical Center, Amsterdam, The Netherlands. 86Division of Infectious Diseases, Department of Pediatrics, Stollery Children’s Hospital, University of Alberta, Edmonton, AB, Canada. 87Lithuanian University of Health Sciences, Kaunas, Lithuania. 88General Hospital, Slovenj Gradec, Slovenia. 89Unit of Infectious Diseases, University General Hospital of Alexandroupolis, Democritus University Thrace, Dragana, Greece. Correspondence: Jonathan S. Nguyen-Van-Tam, University of Nottingham, City Hospital, DM, Room A28b, Clinical Sciences Building, Nottingham NG5 1PB, UK. E-mail: jvt@nottingham.ac.uk *List of PRIDE Consortium Investigators are in Appendix 1. For affiliations, please see Table S1. Múltipla - ver em notas Background The impact of neuraminidase inhibitors (NAIs) on influenza-related pneumonia (IRP) is not established. Our objective was to investigate the association between NAI treatment and IRP incidence and outcomes in patients hospitalised with A(H1N1) pdm09 virus infection. Methods A worldwide meta-analysis of individual participant data from 20 634 hospitalised patients with laboratory-confirmed A (H1N1)pdm09 (n = 20 021) or clinically diagnosed (n = 613) ‘pandemic influenza’. The primary outcome was radiologically confirmed IRP. Odds ratios (OR) were estimated using generalised linear mixed modelling, adjusting for NAI treatment propensity, antibiotics and corticosteroids. Results Of 20 634 included participants, 5978 (29 0%) had IRP; conversely, 3349 (16 2%) had confirmed the absence of radiographic pneumonia (the comparator). Early NAI treatment (within 2 days of symptom onset) versus no NAI was not significantly associated with IRP [adj. OR 0 83 (95% CI 0 64–1 06; P = 0 136)]. Among the 5978 patients with IRP, early NAI treatment versus none did not impact on mortality [adj. OR = 0 72 (0 44–1 17; P = 0 180)] or likelihood of requiring ventilatory support [adj. OR = 1 17 (0 71– 1 92; P = 0 537)], but early treatment versus later significantly reduced mortality [adj. OR = 0 70 (0 55–0 88; P = 0 003)] and likelihood of requiring ventilatory support [adj. OR = 0 68 (0 54– 0 85; P = 0 001)]. Conclusions Early NAI treatment of patients hospitalised with A (H1N1)pdm09 virus infection versus no treatment did not reduce the likelihood of IRP. However, in patients who developed IRP, early NAI treatment versus later reduced the likelihood of mortality and needing ventilatory support.

BACKGROUND The incidence of anal cancer is high in HIV-positive men who have sex with men (MSM). We modeled the impact of screening strategies and combination antiretroviral therapy (cART) coverage on anal cancer incidence in Switzerland. METHODS Individual-based, dynamic simulation model parameterized with Swiss HIV Cohort Study (SHCS) and literature data. We assumed all men to be HPV infected. CD4 cell count trajectories were the main predictors of anal cancer. From 2016 we modeled cART coverage either as below 100% (corresponding to 2010-2015) or as 100%, and the following four screening strategies: (i) no screening, (ii) yearly anal cytology (Pap smears), (iii) yearly anoscopy and (iv) targeted anoscopy five years after CD4 count dropped below 200 cells/μl. RESULTS Median nadir CD4 cell count of 6,411 MSM increased from 229 cells/μl during 1980-89 to 394 cells/μl during 2010-15; cART coverage increased from 0% to 83.4%. Modeled anal cancer incidence peaked at 81.7/100,000 in 2009, plateaued 2010-2015 and decreased to 58.7 by 2030 with stable cART coverage, and to 52.0 with 100% cART coverage. With yearly cytology, incidence declined to 38.2/100,000 by 2030, with yearly anoscopy to 32.8 and with CD4 count guided anoscopy to 51.3. The numbers needed to screen over 15 years to prevent one anal cancer case (NNS) were 384 for yearly cytology, 313 for yearly anoscopy and 242 for CD4 count dependent screening. CONCLUSIONS Yearly screening of HIV-positive MSM may reduce anal cancer incidence substantially, with a NNS that is comparable to other screening interventions to prevent cancer.

BACKGROUND Switzerland recommends individuals who originate from high-prevalence countries to be screened for hepatitis C virus (HCV) infection. However, not all these persons are equally at risk. We thus aimed to describe the number and characteristics of persons with HCV infection born outside of Switzerland. METHODS We compared characteristics of anti-HCV-positive individuals in the Swiss Hepatitis C Cohort Study (SCCS) and of HCV cases reported to the Federal Office of Public Health (FOPH), with those of the general population in Switzerland. Persons who inject drugs (PWID) and persons who do not inject drugs (non-PWID) were compared by age groups for different countries of origin (represented by ≥1% of participants in the SCCS or FOPH). RESULTS We included 4,199 persons from the SCCS and 26,610 cases from the FOPH. Both groups had similar characteristics. In both data sources non-PWID were more frequent in foreign-born than in Swiss-born persons (63% versus 34% in the SCCS). The only subgroup with a clearly higher proportion both in the SCCS and FOPH than in the general population were persons over 60 years from Italy and Spain, with a 3.7- and 2.8-fold increase in the SCCS. These persons were non-PWID (99%), less frequently HIV- and anti-HBc positive and more often female than PWID from Italy and Spain; cirrhosis at enrolment was frequent (31%). Their HCV genotypes were consistent with those observed in elderly non-PWID of their birth countries. In the FOPH a higher proportion than in the general population was also seen for cases from Georgia and Russia. CONCLUSION The identification of subgroups in which HCV infection is particularly frequent might allow for better targeting HCV screening among foreign-born persons in Switzerland and elsewhere.

OBJECTIVES: Inequalities and inequities in health are an important public health concern. In Switzerland, mortality in the general population varies according to the socio-economic position (SEP) of neighbourhoods. We examined the influence of neighbourhood SEP on presentation and outcomes in HIV-positive individuals in the era of combination antiretroviral therapy (cART). METHODS: The neighbourhood SEP of patients followed in the Swiss HIV Cohort Study (SHCS) 2000-2013 was obtained on the basis of 2000 census data on the 50 nearest households (education and occupation of household head, rent, mean number of persons per room). We used Cox and logistic regression models to examine the probability of late presentation, virologic response to cART, loss to follow-up and death across quintiles of neighbourhood SEP. RESULTS: A total of 4489 SHCS participants were included. Presentation with advanced disease [CD4 cell count

Although persons infected with human immunodeficiency virus (HIV), particularly men who have sex with men, are at excess risk for anal cancer, it has been difficult to disentangle the influences of anal exposure to human papillomavirus (HPV) infection, immunodeficiency, and combined antiretroviral therapy. A case-control study that included 59 anal cancer cases and 295 individually matched controls was nested in the Swiss HIV Cohort Study (1988-2011). In a subset of 41 cases and 114 controls, HPV antibodies were tested. A majority of anal cancer cases (73%) were men who have sex with men. Current smoking was significantly associated with anal cancer (odds ratio (OR) = 2.59, 95% confidence interval (CI): 1.25, 5.34), as were antibodies against L1 (OR = 4.52, 95% CI: 2.00, 10.20) and E6 (OR = ∞, 95% CI: 4.64, ∞) of HPV16, as well as low CD4+ cell counts, whether measured at nadir (OR per 100-cell/μL decrease = 1.53, 95% CI: 1.18, 2.00) or at cancer diagnosis (OR per 100-cell/μL decrease = 1.24, 95% CI: 1.08, 1.42). However, the influence of CD4+ cell counts appeared to be strongest 6-7 years prior to anal cancer diagnosis (OR for

HIV-infected women are at increased risk of cervical intra-epithelial neoplasia (CIN) and invasive cervical cancer (ICC), but it has been difficult to disentangle the influences of heavy exposure to HPV infection, inadequate screening, and immunodeficiency. A case-control study including 364 CIN2/3 and 20 ICC cases matched to 1,147 controls was nested in the Swiss HIV Cohort Study (1985-2013). CIN2/3 risk was significantly associated with low CD4+ cell counts, whether measured as nadir (odds ratio (OR) per 100-cell/μL decrease=1.15, 95% CI: 1.08, 1.22), or at CIN2/3 diagnosis (1.10, 95% CI: 1.04, 1.16). An association was evident even for nadir CD4+ 200-349 versus ≥350 cells/μL (OR=1.57, 95% CI: 1.09, 2.25). After adjustment for nadir CD4+, a protective effect of >2-year cART use was seen against CIN2/3 (OR versus never cART use=0.64, 95% CI: 0.42, 0.98). Despite low study power, similar associations were seen for ICC, notably with nadir CD4+ (OR for 50 versus >350 cells/μL= 11.10, 95% CI: 1.24, 100). HPV16-L1 antibodies were significantly associated with CIN2/3, but HPV16-E6 antibodies were nearly exclusively detected in ICC. In conclusion, worsening immunodeficiency, even at only moderately decreased CD4+ cell counts (200-349 CD4+ cells/μL), is a significant risk factor for CIN2/3 and cervical cancer. This article is protected by copyright. All rights reserved.

BACKGROUND AND AIMS Hepatitis C (HCV) is a leading cause of morbidity and mortality in people who live with HIV. In many countries, access to direct acting antiviral agents to treat HCV is restricted to individuals with advanced liver disease (METAVIR stage F3 or F4). Our goal was to estimate the long term impact of deferring HCV treatment for men who have sex with men (MSM) who are coinfected with HIV and often have multiple risk factors for liver disease progression. METHODS We developed an individual-based model of liver disease progression in HIV/HCV coinfected men who have sex with men. We estimated liver-related morbidity and mortality as well as the median time spent with replicating HCV infection when individuals were treated in liver fibrosis stages F0, F1, F2, F3 or F4 on the METAVIR scale. RESULTS The percentage of individuals who died of liver-related complications was 2% if treatment was initiated in F0 or F1. It increased to 3% if treatment was deferred until F2, 7% if it was deferred until F3 and 22% if deferred until F4. The median time individuals spent with replicating HCV increased from 5 years if treatment was initiated in F2 to almost 15 years if it was deferred until F4. CONCLUSIONS Deferring HCV therapy until advanced liver fibrosis is established could increase liver-related morbidity and mortality in HIV/HCV coinfected individuals, and substantially prolong the time individuals spend with replicating HCV infection.

Background: Neuraminidase inhibitors were widely used during the 2009-10 influenza A H1N1 pandemic, but evidence for their effectiveness in reducing mortality is uncertain. We did a meta-analysis of individual participant data to investigate the association between use of neuraminidase inhibitors and mortality in patients admitted to hospital with pandemic influenza A H1N1pdm09 virus infection. Methods: We assembled data for patients (all ages) admitted to hospital worldwide with laboratory confirmed or clinically diagnosed pandemic influenza A H1N1pdm09 virus infection. We identified potential data contributors from an earlier systematic review of reported studies addressing the same research question. In our systematic review, eligible studies were done between March 1, 2009 (Mexico), or April 1, 2009 (rest of the world), until the WHO declaration of the end of the pandemic (Aug 10, 2010); however, we continued to receive data up to March 14, 2011, from ongoing studies. We did a meta-analysis of individual participant data to assess the association between neuraminidase inhibitor treatment and mortality (primary outcome), adjusting for both treatment propensity and potential confounders, using generalised linear mixed modelling. We assessed the association with time to treatment using time-dependent Cox regression shared frailty modelling. Findings: We included data for 29234 patients from 78 studies of patients admitted to hospital between Jan 2, 2009, and March 14, 2011. Compared with no treatment, neuraminidase inhibitor treatment (irrespective of timing) was associated with a reduction in mortality risk (adjusted odds ratio [OR] 0·81; 95% CI 0·70-0·93; p=0·0024). Compared with later treatment, early treatment (within 2 days of symptom onset) was associated with a reduction in mortality risk (adjusted OR 0·48; 95% CI 0·41-0·56; p

Anal cancer is common among people infected with human immunodeficiency virus (HIV). This cancer is caused by human papillomavirus, and immunosuppression likely contributes to its development. In this issue of the Journal, Bertisch et al. (Am J Epidemiol. 2013;178(6):877–884) present the results of a case-control study of anal cancer among HIV-infected people in Switzerland. They demonstrate that anal cancer risk is increased in association with a low CD4+ cell count (a clinical measurement of immune status). In particular, HIV-induced immunosuppression was most severe among cases approximately 6–7 years prior to the diagnosis of anal cancer. A plausible biological interpretation is that immunosuppression is important at an early stage of the development of anal cancer, but that the neoplastic process becomes irreversible over time with persistent human papillomavirus infection and genetic damage. With current efforts to provide earlier combination antiretroviral therapy to HIV-infected people, anal cancer incidence may start to decline. Bertisch et al. also demonstrate a strong association between serum antibodies against the human papillomavirus type 16 protein E6 and anal cancer risk, highlighting the role of this viral oncoprotein in carcinogenesis. Additional biomarkers could help refine clinical approaches to anal cancer screening and prevention for the HIV-infected population.