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1. The global spread of HIV-1 subtype B epidemic.

Author

Magiorkinis G, Angelis K, Mamais I, Katzourakis A, Hatzakis A, Albert J, Lawyer G, Hamouda O, Struck D, Vercauteren J, Wensing A, Alexiev I, Åsjö B, Balotta C, Gomes P, Camacho RJ, Coughlan S, Griskevicius A, Grossman Z, Horban A, Kostrikis LG, Lepej SJ, Liitsola K, Linka M, Nielsen C, Otelea D, Paredes R, Poljak M, Puchhammer-Stöckl E, Schmit JC, Sönnerborg A, Staneková D, Stanojevic M, Stylianou DC, Boucher CAB, Nikolopoulos G, Vasylyeva T, Friedman SR, van de Vijver D, Angarano G, Chaix ML, de Luca A, Korn K, Loveday C, Soriano V, Yerly S, Zazzi M, Vandamme AM, and Paraskevis D

Subjects
Cluster Analysis, HIV Infections transmission, Human Activities, Humans, Phylogeography, Epidemics statistics & numerical data, HIV Infections epidemiology, HIV Infections virology, HIV-1
Abstract

Human immunodeficiency virus type 1 (HIV-1) was discovered in the early 1980s when the virus had already established a pandemic. For at least three decades the epidemic in the Western World has been dominated by subtype B infections, as part of a sub-epidemic that traveled from Africa through Haiti to United States. However, the pattern of the subsequent spread still remains poorly understood. Here we analyze a large dataset of globally representative HIV-1 subtype B strains to map their spread around the world over the last 50years and describe significant spread patterns. We show that subtype B travelled from North America to Western Europe in different occasions, while Central/Eastern Europe remained isolated for the most part of the early epidemic. Looking with more detail in European countries we see that the United Kingdom, France and Switzerland exchanged viral isolates with non-European countries than with European ones. The observed pattern is likely to mirror geopolitical landmarks in the post-World War II era, namely the rise and the fall of the Iron Curtain and the European colonialism. In conclusion, HIV-1 spread through specific migration routes which are consistent with geopolitical factors that affected human activities during the last 50years, such as migration, tourism and trade. Our findings support the argument that epidemic control policies should be global and incorporate political and socioeconomic factors., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)

Published
2016
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2. Transmission of HIV Drug Resistance and the Predicted Effect on Current First-line Regimens in Europe.

Author

Hofstra LM, Sauvageot N, Albert J, Alexiev I, Garcia F, Struck D, Van de Vijver DAMC, Åsjö B, Beshkov D, Coughlan S, Descamps D, Griskevicius A, Hamouda O, Horban A, Van Kasteren M, Kolupajeva T, Kostrikis LG, Liitsola K, Linka M, Mor O, Nielsen C, Otelea D, Paraskevis D, Paredes R, Poljak M, Puchhammer-Stöckl E, Sönnerborg A, Staneková D, Stanojevic M, Van Laethem K, Zazzi M, Zidovec Lepej S, Boucher CAB, Schmit JC, Wensing AMJ, Puchhammer-Stockl E, Sarcletti M, Schmied B, Geit M, Balluch G, Vandamme AM, Vercauteren J, Derdelinckx I, Sasse A, Bogaert M, Ceunen H, De Roo A, De Wit S, Echahidi F, Fransen K, Goffard JC, Goubau P, Goudeseune E, Yombi JC, Lacor P, Liesnard C, Moutschen M, Pierard D, Rens R, Schrooten Y, Vaira D, Vandekerckhove LPR, Van den Heuvel A, Van Der Gucht B, Van Ranst M, Van Wijngaerden E, Vandercam B, Vekemans M, Verhofstede C, Clumeck N, Van Laethem K, Beshkov D, Alexiev I, Lepej SZ, Begovac J, Kostrikis L, Demetriades I, Kousiappa I, Demetriou V, Hezka J, Linka M, Maly M, Machala L, Nielsen C, Jørgensen LB, Gerstoft J, Mathiesen L, Pedersen C, Nielsen H, Laursen A, Kvinesdal B, Liitsola K, Ristola M, Suni J, Sutinen J, Descamps D, Assoumou L, Castor G, Grude M, Flandre P, Storto A, Hamouda O, Kücherer C, Berg T, Braun P, Poggensee G, Däumer M, Eberle J, Heiken H, Kaiser R, Knechten H, Korn K, Müller H, Neifer S, Schmidt B, Walter H, Gunsenheimer-Bartmeyer B, Harrer T, Paraskevis D, Hatzakis A, Zavitsanou A, Vassilakis A, Lazanas M, Chini M, Lioni A, Sakka V, Kourkounti S, Paparizos V, Antoniadou A, Papadopoulos A, Poulakou G, Katsarolis I, Protopapas K, Chryssos G, Drimis S, Gargalianos P, Xylomenos G, Lourida G, Psichogiou M, Daikos GL, Sipsas NV, Kontos A, Gamaletsou MN, Koratzanis G, Sambatakou H, Mariolis H, Skoutelis A, Papastamopoulos V, Georgiou O, Panagopoulos P, Maltezos E, Coughlan S, De Gascun C, Byrne C, Duffy M, Bergin C, Reidy D, Farrell G, Lambert J, O'Connor E, Rochford A, Low J, Coakely P, O'Dea S, Hall W, Mor O, Levi I, Chemtob D, Grossman Z, Zazzi M, de Luca A, Balotta C, Riva C, Mussini C, Caramma I, Capetti A, Colombo MC, Rossi C, Prati F, Tramuto F, Vitale F, Ciccozzi M, Angarano G, Rezza G, Kolupajeva T, Vasins O, Griskevicius A, Lipnickiene V, Schmit JC, Struck D, Sauvageot N, Hemmer R, Arendt V, Michaux C, Staub T, Sequin-Devaux C, Wensing AMJ, Boucher CAB, van de Vijver DAMC, van Kessel A, van Bentum PHM, Brinkman K, Connell BJ, van der Ende ME, Hoepelman IM, van Kasteren M, Kuipers M, Langebeek N, Richter C, Santegoets RMWJ, Schrijnders-Gudde L, Schuurman R, van de Ven BJM, Åsjö B, Kran AB, Ormaasen V, Aavitsland P, Horban A, Stanczak JJ, Stanczak GP, Firlag-Burkacka E, Wiercinska-Drapalo A, Jablonowska E, Maolepsza E, Leszczyszyn-Pynka M, Szata W, Camacho R, Palma C, Borges F, Paixão T, Duque V, Araújo F, Otelea D, Paraschiv S, Tudor AM, Cernat R, Chiriac C, Dumitrescu F, Prisecariu LJ, Stanojevic M, Jevtovic D, Salemovic D, Stanekova D, Habekova M, Chabadová Z, Drobkova T, Bukovinova P, Shunnar A, Truska P, Poljak M, Lunar M, Babic D, Tomazic J, Vidmar L, Vovko T, Karner P, Garcia F, Paredes R, Monge S, Moreno S, Del Amo J, Asensi V, Sirvent JL, de Mendoza C, Delgado R, Gutiérrez F, Berenguer J, Garcia-Bujalance S, Stella N, de Los Santos I, Blanco JR, Dalmau D, Rivero M, Segura F, Elías MJP, Alvarez M, Chueca N, Rodríguez-Martín C, Vidal C, Palomares JC, Viciana I, Viciana P, Cordoba J, Aguilera A, Domingo P, Galindo MJ, Miralles C, Del Pozo MA, Ribera E, Iribarren JA, Ruiz L, de la Torre J, Vidal F, Clotet B, Albert J, Heidarian A, Aperia-Peipke K, Axelsson M, Mild M, Karlsson A, Sönnerborg A, Thalme A, Navér L, Bratt G, Karlsson A, Blaxhult A, Gisslén M, Svennerholm B, Bergbrant I, Björkman P, Säll C, Mellgren Å, Lindholm A, Kuylenstierna N, Montelius R, Azimi F, Johansson B, Carlsson M, Johansson E, Ljungberg B, Ekvall H, Strand A, Mäkitalo S, Öberg S, Holmblad P, Höfer M, Holmberg H, Josefson P, and Ryding U

Subjects
Adult, Europe, Female, HIV Infections drug therapy, HIV Protease Inhibitors pharmacology, HIV-1 genetics, Humans, Male, Microbial Sensitivity Tests, Middle Aged, Mutation, Prevalence, Reverse Transcriptase Inhibitors pharmacology, Anti-HIV Agents pharmacology, Drug Resistance, Viral genetics, HIV Infections virology, HIV-1 drug effects
Abstract

Background: Numerous studies have shown that baseline drug resistance patterns may influence the outcome of antiretroviral therapy. Therefore, guidelines recommend drug resistance testing to guide the choice of initial regimen. In addition to optimizing individual patient management, these baseline resistance data enable transmitted drug resistance (TDR) to be surveyed for public health purposes. The SPREAD program systematically collects data to gain insight into TDR occurring in Europe since 2001., Methods: Demographic, clinical, and virological data from 4140 antiretroviral-naive human immunodeficiency virus (HIV)-infected individuals from 26 countries who were newly diagnosed between 2008 and 2010 were analyzed. Evidence of TDR was defined using the WHO list for surveillance of drug resistance mutations. Prevalence of TDR was assessed over time by comparing the results to SPREAD data from 2002 to 2007. Baseline susceptibility to antiretroviral drugs was predicted using the Stanford HIVdb program version 7.0., Results: The overall prevalence of TDR did not change significantly over time and was 8.3% (95% confidence interval, 7.2%-9.5%) in 2008-2010. The most frequent indicators of TDR were nucleoside reverse transcriptase inhibitor (NRTI) mutations (4.5%), followed by nonnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations (2.0%). Baseline mutations were most predictive of reduced susceptibility to initial NNRTI-based regimens: 4.5% and 6.5% of patient isolates were predicted to have resistance to regimens containing efavirenz or rilpivirine, respectively, independent of current NRTI backbones., Conclusions: Although TDR was highest for NRTIs, the impact of baseline drug resistance patterns on susceptibility was largest for NNRTIs. The prevalence of TDR assessed by epidemiological surveys does not clearly indicate to what degree susceptibility to different drug classes is affected., (© The Author 2015. Published by Oxford University Press for the Infectious Diseases Society of America.)

Published
2016
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3. Global Dispersal Pattern of HIV Type 1 Subtype CRF01_AE: A Genetic Trace of Human Mobility Related to Heterosexual Sexual Activities Centralized in Southeast Asia.

Author

Angelis K, Albert J, Mamais I, Magiorkinis G, Hatzakis A, Hamouda O, Struck D, Vercauteren J, Wensing AM, Alexiev I, Åsjö B, Balotta C, Camacho RJ, Coughlan S, Griskevicius A, Grossman Z, Horban A, Kostrikis LG, Lepej S, Liitsola K, Linka M, Nielsen C, Otelea D, Paredes R, Poljak M, Puchhammer-Stöckl E, Schmit JC, Sönnerborg A, Staneková D, Stanojevic M, Boucher CA, Kaplan L, Vandamme AM, and Paraskevis D

Subjects
Asia, Southeastern, Cluster Analysis, Databases, Factual, Europe, Humans, Phylogeny, HIV Infections transmission, HIV Infections virology, HIV-1 classification, HIV-1 genetics, Heterosexuality, Phylogeography, Population Dynamics
Abstract

Background: Human immunodeficiency virus type 1 (HIV-1) subtype CRF01_AE originated in Africa and then passed to Thailand, where it established a major epidemic. Despite the global presence of CRF01_AE, little is known about its subsequent dispersal pattern., Methods: We assembled a global data set of 2736 CRF01_AE sequences by pooling sequences from public databases and patient-cohort studies. We estimated viral dispersal patterns, using statistical phylogeographic analysis run over bootstrap trees estimated by the maximum likelihood method., Results: We show that Thailand has been the source of viral dispersal to most areas worldwide, including 17 of 20 sampled countries in Europe. Japan, Singapore, Vietnam, and other Asian countries have played a secondary role in the viral dissemination. In contrast, China and Taiwan have mainly imported strains from neighboring Asian countries, North America, and Africa without any significant viral exportation., Discussion: The central role of Thailand in the global spread of CRF01_AE can be probably explained by the popularity of Thailand as a vacation destination characterized by sex tourism and by Thai emigration to the Western world. Our study highlights the unique case of CRF01_AE, the only globally distributed non-B clade whose global dispersal did not originate in Africa., (© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Published
2015
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4. Increase in transmitted resistance to non-nucleoside reverse transcriptase inhibitors among newly diagnosed HIV-1 infections in Europe.

Author

Frentz D, Van de Vijver DA, Abecasis AB, Albert J, Hamouda O, Jørgensen LB, Kücherer C, Struck D, Schmit JC, Vercauteren J, Åsjö B, Balotta C, Beshkov D, Camacho RJ, Clotet B, Coughlan S, Griskevicius A, Grossman Z, Horban A, Kolupajeva T, Korn K, Kostrikis LG, Liitsola K, Linka M, Nielsen C, Otelea D, Paraskevis D, Paredes R, Poljak M, Puchhammer-Stöckl E, Sönnerborg A, Stanekova D, Stanojevic M, Van Wijngaerden E, Wensing AM, and Boucher CA

Subjects
Adult, Europe epidemiology, Female, Genotype, HIV Infections epidemiology, HIV Infections transmission, HIV-1 classification, HIV-1 drug effects, HIV-1 isolation & purification, Humans, Male, Mutation, Phylogeny, Prevalence, Anti-HIV Agents therapeutic use, Drug Resistance, Viral, HIV Infections drug therapy, HIV Infections virology, HIV-1 genetics
Abstract

Background: One out of ten newly diagnosed patients in Europe was infected with a virus carrying a drug resistant mutation. We analysed the patterns over time for transmitted drug resistance mutations (TDRM) using data from the European Spread program., Methods: Clinical, epidemiological and virological data from 4317 patients newly diagnosed with HIV-1 infection between 2002 and 2007 were analysed. Patients were enrolled using a pre-defined sampling strategy., Results: The overall prevalence of TDRM in this period was 8.9% (95% CI: 8.1-9.8). Interestingly, significant changes over time in TDRM caused by the different drug classes were found. Whereas nucleoside resistance mutations remained constant at 5%, a significant decline in protease inhibitors resistance mutations was observed, from 3.9% in 2002 to 1.6% in 2007 (p = 0.001). In contrast, resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) doubled from 2.0% in 2002 to 4.1% in 2007 (p = 0.004) with 58% of viral strains carrying a K103N mutation. Phylogenetic analysis showed that these temporal changes could not be explained by large clusters of TDRM., Conclusion: During the years 2002 to 2007 transmitted resistance to NNRTI has doubled to 4% in Europe. The frequent use of NNRTI in first-line regimens and the clinical impact of NNRTI mutations warrants continued monitoring.

Published
2014
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5. Limited cross-border infections in patients newly diagnosed with HIV in Europe.

Author

Frentz D, Wensing AM, Albert J, Paraskevis D, Abecasis AB, Hamouda O, Jørgensen LB, Kücherer C, Struck D, Schmit JC, Åsjö B, Balotta C, Beshkov D, Camacho RJ, Clotet B, Coughlan S, De Wit S, Griskevicius A, Grossman Z, Horban A, Kolupajeva T, Korn K, Kostrikis LG, Liitsola K, Linka M, Nielsen C, Otelea D, Paredes R, Poljak M, Puchhammer-Stöckl E, Sönnerborg A, Stanekova D, Stanojevic M, Vandamme AM, Boucher CA, and Van de Vijver DA

Subjects
Adult, Cluster Analysis, Europe epidemiology, HIV Infections transmission, HIV-1 isolation & purification, Humans, Male, Molecular Epidemiology, Molecular Sequence Data, Phylogeny, Sequence Analysis, DNA, Travel, HIV Infections epidemiology, HIV Infections virology, HIV-1 classification, HIV-1 genetics, RNA, Viral genetics
Abstract

Background: International travel plays a role in the spread of HIV-1 across Europe. It is, however, not known whether international travel is more important for spread of the epidemic as compared to endogenous infections within single countries. In this study, phylogenetic associations among HIV of newly diagnosed patients were determined across Europe., Results: Data came from the SPREAD programme which collects samples of newly diagnosed patients that are representative for national HIV epidemics. 4260 pol sequences from 25 European countries and Israel collected in 2002-2007 were included.We identified 457 clusters including 1330 persons (31.2% of all patients). The cluster size ranged between 2 and 28. A number of 987 patients (74.2%) were part of a cluster that consisted only of patients originating from the same country. In addition, 135 patients (10.2%) were in a cluster including only individuals from neighboring countries. Finally, 208 patients (15.6%) clustered with individuals from countries without a common border. Clustering with patients from the same country was less prevalent in patients being infected with B subtype (P-value <0.0001), in men who have sex with men (P-value <0.0001), and in recently infected patients (P-value =0.045)., Conclusions: Our findings indicate that the transmission of HIV-1 in Europe is predominantly occurring between patients from the same country. This could have implications for HIV-1 transmission prevention programmes. Because infections through travelling between countries is not frequently observed it is important to have good surveillance of the national HIV-1 epidemics.

Published
2013
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6. HIV-1 drug-resistance patterns among patients on failing treatment in a large number of European countries.

Author

van de Vijver DA, Wensing AM, Åsjö B, Bruckova M, Jorgensen LB, Camacho R, Horban A, Linka M, Lazanas M, Loveday C, MacRae E, Nielsen C, Paraskevis D, Poljak M, Puchhammer-Stöckl E, Ruiz L, Schmit JC, Stanczak G, Stanojevic M, Vandamme AM, Vercauteren J, Zazzi M, Bacheler L, Lecocq P, Villacian J, and Boucher CA

Subjects
Adult, Amino Acid Substitution, Europe, Female, Genotype, HIV Infections virology, HIV Protease genetics, HIV Protease Inhibitors therapeutic use, HIV Reverse Transcriptase genetics, Humans, Male, Middle Aged, Mutation, Sequence Analysis, Protein, Treatment Failure, Drug Resistance, Viral genetics, HIV Infections drug therapy, HIV-1 genetics
Abstract

Background: Information about patterns of HIV-1 drug resistance among treatment-exposed patients is crucial for the development of novel effective drugs. Currently no system exists that monitors patterns of resistance in patients failing therapy., Methods: The study included 1,988 HIV-1 sequences from patients experiencing therapy failure collected between 2000 and 2004 in 15 European countries. Genotypic resistance was interpreted using the ANRS algorithm. Phenotypic resistance was predicted using the Virco geno- to phenotype system., Results: 80.7% of the sequences included at least one drug-resistance mutation. Mutations were found for NRTIs (73.5%), NNRTIs (48.5%), and protease inhibitors (35.8%). Ninety percent of sequences with genotypic resistance harbored M184V, M41L, K103N, D67N, and/or T215Y. Among NRTIs, resistance was most frequently predicted for lamivudine. About half of all sequences had reduced susceptibility for NNRTIs. Resistance to most boosted protease inhibitors was found in < 25%. No sequence had resistance to all currently available drugs., Conclusion: Levels of resistance among patients with therapy failure were high. The patterns of resistance reflect resistance to drugs available for a longer time. Fully suppressive regimens can be designed even for the most mutated HIV because boosted protease inhibitors have remained active against most circulating viruses and new drug classes have become available.

Published
2010

7. Transmission of drug-resistant HIV-1 in Europe remains limited to single classes

Author

Wensing, A, Vercauteren, J, Van De Vijver, D, Albert, J, Åsjö, B, Balotta, C, Camacho, R, Coughlan, S, Grossman, Z, Horban, A, Kücherer, C, Nielsen, C, Paraskevis, D, Loke, W, Poggensee, G, Puchhammer Stöckl, E, Riva, C, Ruiz, L, Schmit, J, Schuurman, R, Salminen, M, Sonnerborg, A, Stanojevic, M, Struck, D, Vandamme, A, Boucher, C, TRAMUTO, Fabio, VITALE, Francesco, Wensing, A, Vercauteren, J, Van De Vijver, D, Albert, J, Åsjö, B, Balotta, C, Camacho, R, Coughlan, S, Grossman, Z, Horban, A, Kücherer, C, Nielsen, C, Paraskevis, D, Loke, W, Poggensee, G, Puchhammer Stöckl, E, Riva, C, Ruiz, L, Schmit, J, Schuurman, R, Salminen, M, Sonnerborg, A, Stanojevic, M, Struck, D, Vandamme, A, Boucher, C, Tramuto, F, Vitale, F, and Internal Medicine

Subjects
Male, Genes, Viral, medicine.medical_treatment, Resistance, Human immunodeficiency virus (HIV), hiv-1, HIV Infections, Drug resistance, Settore MED/42 - Igiene Generale E Applicata, medicine.disease_cause, Nucleoside Reverse Transcriptase Inhibitor, Genotype, Prevalence, Immunology and Allergy, HIV Infection, Israel, risk, immunodeficiency-virus type-1, Transmission (medicine), transmission, persistence, Middle Aged, Reverse Transcriptase Inhibitor, Europe, Infectious Diseases, primary infection, Reverse Transcriptase Inhibitors, Female, europe, Human, Adult, Risk, Logistic Model, prevalence, Immunology, Biology, resistance, SDG 3 - Good Health and Well-being, Drug Resistance, Viral, Disease Transmission, Infectious, medicine, Humans, Transmission, HIV Protease Inhibitor, time trends, therapy, Chi-Square Distribution, Protease, HIV Protease Inhibitors, load, mutations, Virology, Confidence interval, Reverse transcriptase, Logistic Models, Disease Transmission, Infectiou, Mutation, HIV-1
Abstract

BACKGROUND: The spread of drug-resistant HIV-1 might compromise the future success of current first-line regimens. OBJECTIVE: To analyse the extent and impact of transmission of drug-resistant HIV-1 variants in Europe. DESIGN AND METHODS: The European prospective programme (SPREAD) collected demographic, clinical and virological data from 1245 HIV-1-infected individuals in 17 countries diagnosed in 2002-2003. The potential impact of transmitted drug resistance mutations (TDRMs) on therapy response was determined by using genotypic interpretation algorithms. RESULTS: The overall prevalence of viruses with drug-resistance mutations was 9.1% [96/1050; 95% confidence interval: 7.5-11.1]. The majority (71%) harboured only a single amino acid substitution with limited effect on predicted drug susceptibility. Mutations associated with resistance to nucleoside reverse transcriptase inhibitors were observed most frequently [57/1050 (5.4%)], followed by mutations related to protease inhibitors [32/1050 (3.0%)] and mutations related to non-nucleoside reverse transcriptase inhibitors (NNRTIs) [27/1050 (2.6%)].In some cases, however, resistance was quite extensive. Four individuals were infected with viruses with reduced susceptibility to all nucleoside reverse transcriptase inhibitors, 3 to all protease inhibitors and 20 to both NNRTIs. Remarkably, in one individual, the resistance pattern was so extensive that none of the available current antiretroviral drugs was predicted to be fully active. CONCLUSION: The prevalence of TDRM-HIV is quite prominent (9.1%) but did not increase in comparison with a large retrospective European study. Particularly the presence of single NNRTI mutations may impact the efficacy of the first-line regimens. Continuous prospective monitoring remains indicated to explore the patterns and factors contributing to the transmission of TDRMs as well as the potential clinical consequences. © 2008 Lippincott Williams & Wilkins, Inc.

Published
2008
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8. HIV Induces both a Down-Regulation of IRAK-4 that Impairs TLR Signalling and an Up-regulation of the Antibiotic Peptide Dermcidin in Monocytic Cells.

Author

Pathak, S., De Souza, G. A., Salte, T., Wiker, H. G., and Åsjö, B.

Subjects
HIV infections, BIOMOLECULES, PATHOGENIC microorganisms, NATURAL immunity, LENTIVIRUS diseases
Abstract

HIV-infected individuals have an increased risk of invasive bacterial infections, even at early clinical stages with relatively normal CD4+ T-cell counts. The pathogenic mechanisms behind this are not fully understood. However, an increasing number of studies indicate that HIV may impair the innate immunity to bacteria by infecting key cells of the monocyte/macrophage lineage. In this study, the effects of HIV infection on the protein profile of undifferentiated monocyte-like THP-1 cells were examined by a mass spectrometric approach based on stable isotope labelling with amino acid in cell culture (SILAC). We identified 651 proteins, of which nine proteins were down-regulated and 17 proteins were up-regulated in HIV-infected THP-1 cells as compared to uninfected controls. Most remarkably, the IL-1 receptor associated kinase 4 (IRAK-4), which is essential for virtually all TLR signalling, was suppressed, whereas the precursor for the antibiotic peptide Dermcidin was up-regulated in HIV-infected cells. Upon stimulation of either TLR2 or TLR4, the HIV-infected THP-1 cells displayed reduced TNF-α secretion. The HIV-induced down-regulation of IRAK-4 was reconfirmed in monocyte-derived macrophage cell cultures. These data suggests that HIV may impair the TLR signalling cascade for pathogen recognition in cells of the monocyte/macrophage lineage and thus, may reduce the ability of the innate immune system to sense invading pathogens and initiate appropriate responses. [ABSTRACT FROM AUTHOR]

Published
2009
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9. Dynamics of HIV-1 replication following influenza vaccination of HIV+ individuals.

Author

Røsok, B., Voltersvik, P., Bjerknes, R., Axelsson, M., Haaheim, L. R., and Åsjö, B.

Subjects
HIV infections, VACCINATION, IMMUNIZATION, INFLUENZA, RNA, VIRUS diseases
Abstract

Levels of HIV-1 have been reported lo increase in peripheral blood after influenza vaccination of HIV+ individuals. In this study we have evaluated the dynamics of these changes. Ten HIV-I+ individuals classified in revised CDC clinical categories B and C as well as five seronegative healthy controls were vaccinated with the recommended influenza strains. HIV viral RNA and proviral DNA were sequentially quantified in serum and blood lymphocytes, respectively. Nine of the 10 HIV+ individuals had an increase in the frequency of infected CD4 cells 2 weeks after influenza vaccination. Individuals with low viral load had a rapid increase in viraemia and a small increase in frequency of infected cells in peripheral blood. In contrast, individuals with high viral load had a small drop in viraemia followed by a significant rise in the rate of infected cells. The observed changes may resemble those taking place during intercurrent infections in HIV+ individuals. The effects of the relative increases in infectious virus after the transient viraemic phase should be further investigated to evaluate potential risks of vaccination. [ABSTRACT FROM AUTHOR]

Published
1996
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10. HIV-1 drug-resistance patterns among patients on failing treatment in a large number of European countries

Author

Da, Vijver, Am, Wensing, Åsjö B, Bruckova M, Lb, Jorgensen, Camacho R, Horban A, Linka M, Lazanas M, Loveday C, MacRae E, Nielsen C, Paraskevis D, Poljak M, Puchhammer-Stöckl E, Ruiz L, Jc, Schmit, Stanczak G, Stanojevic M, Anne-Mieke Vandamme, Vercauteren J, Zazzi M, Bacheler L, Lecocq P, Villacian J, Ca, Boucher, and Virology

Subjects
Adult, Male, Genotype, HIV Infections, HIV Protease Inhibitors, Middle Aged, HIV Reverse Transcriptase, Europe, Amino Acid Substitution, HIV Protease, SDG 3 - Good Health and Well-being, Sequence Analysis, Protein, Drug Resistance, Viral, Mutation, HIV-1, Humans, Female, Treatment Failure
Abstract

Background : Information about patterns of HIV-1 drug resistance among treatment-exposed patients is crucial for the development of novel effective drugs. Currently no system exists that monitors patterns of resistance in patients failing therapy. Methods : The study included 1,988 HIV-1 sequences from patients experiencing therapy failure collected between 2000 and 2004 in 15 European countries. Genotypic resistance was interpreted using the ANRS algorithm. Phenotypic resistance was predicted using the Virco geno- to phenotype system. Results : 80.7% of the sequences included at least one drug-resistance mutation. Mutations were found for NRTIs (73.5%), NNRTIs (48.5%), and protease inhibitors (35.8%). Ninety percent of sequences with genotypic resistance harbored M184V, M41L, K103N, D67N, and/or T215Y. Among NRTIs, resistance was most frequently predicted for lamivudine. About half of all sequences had reduced susceptibility for NNRTIs. Resistance to most boosted protease inhibitors was found in < 25%. No sequence had resistance to all currently available drugs. Conclusion : Levels of resistance among patients with therapy failure were high. The patterns of resistance reflect resistance to drugs available for a longer time. Fully suppressive regimens can be designed even for the most mutated HIV because boosted protease inhibitors have remained active against most circulating viruses and new drug classes have become available.

11. Transmission of HIV Drug Resistance and the Predicted Effect on Current First-line Regimens in Europe

Author

Moutschen, M., Hofstra, Laura Marije Arije, Sauvageot, Nicolas, Albert, Jan, Alexiev, Ivailo, Garcia, Federico, Struck, Daniel, Van, de Vijver, Åsjö, Birgitta, Beshkov, Danail, Coughlan, Suzie, Descamps, Diane, Griskevicius, Algirdas, Hamouda, Osamah, Horban, Andrzej, Van Kasteren, Marjo, Kolupajeva, Tatjana, Kostrikis, Leontios G., Liitsola, Kirsi, Linka, Marek, Mor, Orna, Nielsen, Claus, Otelea, Dan, Paraskevis, Dimitrios N., Paredes, Roger, Poljak, Mario, Puchhammer-Stöckl, Elisabeth, Sönnerborg, Anders, Staneková, Danica, Stanojevic, Maja, Van Laethem, Kristel, Zazzi, Maurizio, Zidovec Lepej, Snjezana, Boucher, Charles A. B., Schmit, Jean-Claude, Wensing, Annemarie M. J., Puchhammer-Stockl, E., Sarcletti, M., Schmied, B., Geit, M., Balluch, G., Vandamme, A. M., Vercauteren, J., Derdelinckx, I., Sasse, A., Bogaert, M., Ceunen, H., De Roo, A., De Wit, S., Echahidi, F., Fransen, K., Goffard, J. -C, Goubau, P., Goudeseune, E., Yombi, J. -C, Lacor, P., Liesnard, C., Pierard, D., Rens, R., Schrooten, Y., Vaira, D., Vandekerckhove, L. P. R., Van, den Heuvel, Van, Der Gucht, Van Ranst, M., Van Wijngaerden, E., Vandercam, B., Vekemans, M., Verhofstede, C., Clumeck, N., Van Laethem, K., Lepej, S. Z., Begovac, J., Demetriades, Ioannis, Kousiappa, Ioanna, Demetriou, Victoria L., Hezka, Johana, Linka, M., Maly, M., Machala, L., Nielsen, C., Jørgensen, L. B., Gerstoft, J., Mathiesen, L., Pedersen, C., Nielsen, H., Laursen, A., Kvinesdal, B., Liitsola, K., Ristola, M., Suni, J., Sutinen, J., Descamps, D., Assoumou, L., Castor, G., Grude, M., Flandre, P., Storto, A., Hamouda, O., Kücherer, C., Berg, T., Braun, P., Poggensee, G., Däumer, M., Eberle, J., Heiken, H., Kaiser, R., Knechten, H., Korn, K., Müller, H., Neifer, S., Schmidt, B., Walter, H., Gunsenheimer-Bartmeyer, B., Harrer, T., Hatzakis, Angelos E., Zavitsanou, Assimina, Vassilakis, A., Lazanas, Marios C., Chini, Maria C., Lioni, A., Sakka, V., Kourkounti, Sofia, Paparizos, Vassilios A., Antoniadou, Anastasia C., Papadopoulos, Antonios I., Poulakou, Garyphallia G., Katsarolis, I., Protopapas, K., Chryssos, Georgios, Drimis, Stylianos, Gargalianos, Panagiotis, Xylomenos, Georgios, Lourida, G., Psichogiou, Mina A., Daikos, George L., Sipsas, N. V., Kontos, Athanasios N., Gamaletsou, M. N., Koratzanis, Georgios, Sambatakou, H., Mariolis, H., Skoutelis, A., Papastamopoulos, V., Georgiou, O., Panagopoulos, Periklis, Maltezos, E., Coughlan, S., De Gascun, C., Byrne, C., Duffy, M., Bergin, C., Reidy, D., Farrell, G., Lambert, J., O'Connor, E., Rochford, A., Low, J., Coakely, P., O'Dea, S., Hall, W., Mor, O., Levi, I., Chemtob, D., Grossman, Z., Zazzi, M., de Luca, A., Balotta, Claudia, Riva, C., Mussini, C., Caramma, I., Capetti, A., Colombo, M. C., Rossi, C., Prati, F., Tramuto, F., Vitale, F., Ciccozzi, M., Angarano, G., Rezza, G., Kolupajeva, T., Vasins, O., Griskevicius, A., Lipnickiene, V., Schmit, J. C., Struck, D., Hemmer, R., Arendt, V., Michaux, C., Staub, T., Sequin-Devaux, C., Wensing, A. M. J., Boucher, C. A. B., van, de Vijver, van Kessel, A., van Bentum, P. H. M., Brinkman, K., Connell, B. J., van, der Ende, Hoepelman, I. M., van Kasteren, M., Kuipers, M., Langebeek, N., Richter, C., Santegoets, R. M. W. J., Schrijnders-Gudde, L., Schuurman, R., van, de Ven, Kran, A. -M B., Ormaasen, V., Aavitsland, P., Horban, A., Stanczak, J. J., Stanczak, G. P., Firlag-Burkacka, E., Wiercinska-Drapalo, A., Jablonowska, E., Maolepsza, E., Leszczyszyn-Pynka, M., Szata, W., Camacho, Ricardo J., Palma, C., Borges, F., Paixão, T., Duque, V., Araújo, F., Otelea, D., Paraschiv, S., Tudor, A. M., Cernat, R., Chiriac, C., Dumitrescu, F., Prisecariu, L. J., Stanojevic, M., Jevtovic, Dj, Salemovic, D., Stanekova, D., Habekova, M., Chabadová, Z., Drobkova, T., Bukovinova, P., Shunnar, A., Truska, P., Poljak, M., Lunar, M., Babic, Dunja Z., Tomazic, J., Vidmar, L., Vovko, T., Karner, P., Garcia, F., Paredes, R., Monge, S., Moreno, S., del Amo, J., Asensi, V., Sirvent, J. L., de Mendoza, C., Delgado, R., Gutiérrez, F., Berenguer, J., Garcia-Bujalance, S., Stella, Natalia C., de, los Santos, Blanco, J. R., Dalmau, D., Rivero, M., Segura, F., Elıás, Marıá Jesús Pérez, Alvarez, M., Chueca, N., Rodríguez-Martín, C., Vidal, C., Palomares, J. C., Viciana, I., Viciana, P., Cordoba, J., Aguilera, A., Domingo, P., Galindo, M. J., Miralles, C., del Pozo, M. A., Ribera, E., Iribarren, J. A., Ruiz, L., de, la Torre, Vidal, F., Clotet, B., Heidarian, A., Aperia-Peipke, K., Axelsson, M., Mild, M., Karlsson, A., Sönnerborg, A., Thalme, A., Navér, L., Bratt, G., Blaxhult, A., Gisslén, M., Svennerholm, B., Bergbrant, I., Björkman, Per, Säll, C., Mellgren, Å., Lindholm, A., Kuylenstierna, N., Montelius, R., Azimi, F., Johansson, B., Carlsson, M., Johansson, E., Ljungberg, B., Ekvall, H., Strand, A., Mäkitalo, S., Öberg, S., Holmblad, P., Höfer, M., Holmberg, H., Josefson, P., Ryding, U., Van Kessel, A., Clinical sciences, Microbiology and Infection Control, Supporting clinical sciences, Clinicum, Department of Medicine, Virology, Cohorte de Adultos de la Red de Investigación en SIDA, Spain., SPREAD Program, [Hofstra,LM, Sauvageot,N, Struck,D, Schmit,JC ] Luxembourg Institute of Health, Luxembourg. [Hofstra,LM, Wensing,AMJ] Department of Virology, University Medical Center Utrecht, The Netherlands. [Albert,J, Sönnerborg,A] Karolinska Institute, Solna. Karolinska University Hospital, Stockholm, Sweden. [Alexiev,I, Beshkov,D] National Center of Infectious and Parasitic Diseases, Sofia, Bulgaria. [Garcia,F] Complejo Hospitalario Universitario de Granada. Instituto de Investigación IBS Granada, Spain. [Van de Vijver,DAMC, Boucher,CAB] Erasmus MC, University Medical Center, Rotterdam, The Netherlands. [Åsjö,B] University of Bergen, Norway. [Coughlan,S] University College Dublin, Ireland. [Descamps,D] AP-HP Groupe hospitalier Bichat-Claude Bernard. IAME INSERM UMR 1137. Université Paris Diderot Sorbonne Paris Cité, Paris, France. [Griskevicius,A] Lithuanian AIDS Center, Vilnius, Lithuania. [Hamouda,O] Robert Koch Institute, Berlin, Germany. [Horban,A] Hospital of Infectious Diseases, Warsaw, Poland. [Van Kasteren,M] St Elisabeth Hospital, Tilburg, The Netherlands. [Kolupajeva,T] Infectiology Center of Latvia, Riga. [Kostrikis,LG] University of Cyprus, Nicosia. [Liitsola,K] Department of Infectious Diseases, National Institute for Health and Welfare, Helsinki, Finland. [Linka,M] National Reference Laboratory for HIV/AIDS, National Institute of Public Health, Prague, Czech Republic. [Mor,O] National HIV Reference Laboratory, Chaim Sheba Medical Center, Tel-Hashomer, Israel. [Nielsen,C] Statens Serum Institut, Copenhagen, Denmark. [Otelea,D] National Institute for Infectious Diseases 'Prof. dr. Matei Bals', Bucharest, Romania. [Paraskevis,D] National Retrovirus Reference Center, University of Athens, Greece. [Paredes,R] IrsiCaixa Foundation, Badalona, Spain. [Poljak,M] Faculty of Medicine, Slovenian HIV/AIDS Reference Centre, University of Ljubljana, Slovenia. [Puchhammer-Stöckl,E] Medical University Vienna, Austria. [Staneková,D] Slovak Medical University, Bratislava, Slovakia. [Stanojevic,M] Faculty of Medicine, University of Belgrade, Serbia. [Van Laethem,K] Rega Institute for Medical Research, KU Leuven, Belgium. [Zazzi,M] University of Siena, Italy. [Zidovec Lepej,S] University Hospital for Infectious Diseases 'Dr. Fran Mihaljevic', Zagreb, Croatia., This work was supported by a CORE grant of Fond National de la Recherche Luxembourg (grant number C12/BM/4011111–HIV molecular epidemiology in Europe). This work has been partially supported by the European Commission (fifth framework, grant number QLK2-CT-2001-01344, sixth framework, grant number LSHP-CT-2006-518211, DynaNets grant number 233847, seventh framework, CHAIN grant number 223131), Belgium: Belgian AIDS Reference Laboratory Fund, Belgian Fonds voor Wetenschappelijk Onderzoek (grant number G.0692.14), Cyprus: Cyprus Research Promotion Foundation (grant number Health/0104/22), Denmark: Danish AIDS Foundation, France: Agence Nationale de Recherches sur le SIDA et les Hepatites Virales, Germany: Ministry of Health (grant number 1502-686-18), Ministry of Education and Research (grant number 01KI501), Italy: Fifth National Program on HIV/AIDS, Instituto Superiore di Sanità (grant numbers 40F.56 and 20D.1.6), Luxembourg: Fondation Recherche sur le SiDA and Ministry of Health, Republic of Serbia: Ministry of Education and Science (grant number 175024), Slovakia: project 'Center of Excellence of Environmental Health,' ITMS number 26240120033, based on supporting operational research and development program financed from the European Regional Development Fund, and Sweden: Swedish Research Council and Swedish Civil Contingencies Agency., APH - Health Behaviors & Chronic Diseases, Graduate School, Hofstra, LM, Sauvageot, N, Albert, J, Alexiev, I, Garcia, F, Struck, D, Van de Vijver, DA, Åsjö, B, Beshkov, D, Coughlan, S, Descamps, D, Griskevicius, A, Hamouda, O, Horban, A, Van Kasteren, M, Kolupajeva, T, Kostrikis, LG, Liitsola, K, Linka, M, Mor, O, Nielsen, C, Otelea, D, Paraskevis, D, Paredes, R, Poljak, M, Puchhammer-Stöckl, E, Sönnerborg, A, Staneková, D, Stanojevic, M, Van Laethem, K, Zazzi, M, Lepej, SZ, Boucher, CA, Schmit, JC, Wensing, AM, SPREAD program investigators, including Vitale F and Tramuto, F, Vandamme, Annemie, Vercauteren, Jurgen, Schrooten, Yoeri, Van Ranst, Marc, Van Wijngaerden, Eric, Derdelinckx, Inge, Camacho, Ricardo Jorge, Kostrikis, Leontios G. [0000-0002-5340-7109], and Paraskevis, Dimitrios [0000-0001-6167-7152]

Subjects
Male, Human immunodeficiency virus 1, Etravirine, RNA directed DNA polymerase inhibitor, darunavir, HIV Infections, Settore MED/42 - Igiene Generale E Applicata, Disciplines and Occupations::Health Occupations::Medicine::Public Health [Medical Subject Headings], Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings], Salud pública, genetics, Inhibidores de proteasas, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Data Collection::Vital Statistics::Morbidity::Prevalence [Medical Subject Headings], atazanavir, media_common, transmission, Geographicals::Geographic Locations::Europe [Medical Subject Headings], 3. Good health, microbial sensitivity test, priority journal, Europe, HIV-1, antiretroviral therapy, drug resistance, HIV/AIDS, lamivudine, Reverse Transcriptase Inhibitors/pharmacology, anti human immunodeficiency virus agent, Drug, Microbiology (medical), medicine.medical_specialty, antiviral susceptibility, Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation [Medical Subject Headings], media_common.quotation_subject, 030106 microbiology, HIV Infections/drug therapy, Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Anti-Infective Agents::Antiviral Agents::Anti-Retroviral Agents::Reverse Transcriptase Inhibitors [Medical Subject Headings], Microbial Sensitivity Tests, RILPIVIRINE, Article, EFAVIRENZ, 03 medical and health sciences, transmitted drug resistance, SDG 3 - Good Health and Well-being, Humans, Transmission, human, Phenomena and Processes::Physiological Phenomena::Pharmacological Phenomena::Drug Resistance [Medical Subject Headings], REVERSE-TRANSCRIPTASE INHIBITORS, Rilpivirina, INTEGRASE, MUTATIONS, abacavir, major clinical study, Virology, Infecciones por VIH, Regimen, Antiretroviral therapy, Drug resistance, Medicine (all), Infectious Diseases, chemistry, Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds, 1-Ring::Oxazines::Benzoxazines [Medical Subject Headings], Mutation, 0301 basic medicine, nevirapine, Communicable diseases, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Confidence Intervals [Medical Subject Headings], chemistry.chemical_compound, antiviral therapy, INFECTION, Medicine and Health Sciences, Prevalence, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Data Collection::Surveys and Questionnaires [Medical Subject Headings], Viral, Non-U.S. Gov't, Reverse-transcriptase inhibitor, antiretrovirus agent, Research Support, Non-U.S. Gov't, Human immunodeficiency virus infected patient, Middle Aged, virology, PREVALENCE, Encuestas y Cuestionarios, ANTIRETROVIRAL TREATMENT, HIV-1/drug effects, HIV Protease Inhibitors/pharmacology, Rilpivirine, Reverse Transcriptase Inhibitors, Diseases::Immune System Diseases::Immunologic Deficiency Syndromes::HIV Infections [Medical Subject Headings], Female, HIV drug resistance, medicine.drug, Adult, Human immunodeficiency virus proteinase inhibitor, Chemicals and Drugs::Organic Chemicals::Nitriles::Rilpivirine [Medical Subject Headings], Efavirenz, Anti-HIV Agents, Research Support, Resistencia a medicamentos, Settore MED/17 - MALATTIE INFETTIVE, antiviral resistance, Internal medicine, Anti-HIV Agents/pharmacology, Drug Resistance, Viral, Journal Article, medicine, Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors::Protease Inhibitors [Medical Subject Headings], abacavir plus lamivudine, Europa (Continente), HIV Protease Inhibitors, emtricitabine, nonhuman, Intervalos de confianza, Mutación, business.industry, HIV, prediction, Inhibidores de la transcriptasa inversa, Human immunodeficiency virus 1 infection, tenofovir, INDIVIDUALS, Drug Resistance, Viral/genetics, Benzoxazinas, ETRAVIRINE, drug effects, 3121 General medicine, internal medicine and other clinical medicine, Prevalencia, business
Abstract

Transmitted human immunodeficiency virus drug resistance in Europe is stable at around 8%. The impact of baseline mutation patterns on susceptibility to antiretroviral drugs should be addressed using clinical guidelines. The impact on baseline susceptibility is largest for nonnucleoside reverse transcriptase inhibitors., Background. Numerous studies have shown that baseline drug resistance patterns may influence the outcome of antiretroviral therapy. Therefore, guidelines recommend drug resistance testing to guide the choice of initial regimen. In addition to optimizing individual patient management, these baseline resistance data enable transmitted drug resistance (TDR) to be surveyed for public health purposes. The SPREAD program systematically collects data to gain insight into TDR occurring in Europe since 2001. Methods. Demographic, clinical, and virological data from 4140 antiretroviral-naive human immunodeficiency virus (HIV)–infected individuals from 26 countries who were newly diagnosed between 2008 and 2010 were analyzed. Evidence of TDR was defined using the WHO list for surveillance of drug resistance mutations. Prevalence of TDR was assessed over time by comparing the results to SPREAD data from 2002 to 2007. Baseline susceptibility to antiretroviral drugs was predicted using the Stanford HIVdb program version 7.0. Results. The overall prevalence of TDR did not change significantly over time and was 8.3% (95% confidence interval, 7.2%–9.5%) in 2008–2010. The most frequent indicators of TDR were nucleoside reverse transcriptase inhibitor (NRTI) mutations (4.5%), followed by nonnucleoside reverse transcriptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations (2.0%). Baseline mutations were most predictive of reduced susceptibility to initial NNRTI-based regimens: 4.5% and 6.5% of patient isolates were predicted to have resistance to regimens containing efavirenz or rilpivirine, respectively, independent of current NRTI backbones. Conclusions. Although TDR was highest for NRTIs, the impact of baseline drug resistance patterns on susceptibility was largest for NNRTIs. The prevalence of TDR assessed by epidemiological surveys does not clearly indicate to what degree susceptibility to different drug classes is affected.

Published
2016
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12. Limited cross-border infections in patients newly diagnosed with HIV in Europe

Author

Moutschen, M., Frentz, D., Wensing, A. M. J., Albert, Jan, Paraskevis, Dimitrios N., Abecasis, A. B., Hamouda, O., Jørgensen, L. B., Kücherer, C., Struck, D., Schmit, J. -C, Åsjö, Birgitta, Balotta, Claudia, Beshkov, Danail, Camacho, Ricardo J., Clotet, B., Coughlan, S., De Wit, S., Griskevicius, A., Grossman, Z., Horban, A., Kolupajeva, T., Korn, K., Kostrikis, Leontios G., Liitsola, K., Linka, M., Nielsen, C., Otelea, D., Paredes, R., Poljak, M., Puchhammer-Stöckl, E., Sönnerborg, A., Stanekova, D., Stanojevic, M., Vandamme, A. -M, Boucher, C. A. B., Van de Vijver, D. A. M. C., Balluch, G., Vercauteren, J., Derdelinckx, I., Sasse, A., Bogaert, M., Ceunen, H., De Roo, A., Echahidi, F., Fransen, K., Goffard, J. -C, Goubau, P., Goudeseune, E., Yombi, J. -C, Lacor, P., Liesnard, C., Pierard, D., Rens, R., Schrooten, Y., Vaira, D., Vandekerckhove, L. P. R., Van den Heuvel, A., Van Der Gucht, B., Van Ranst, M., Van Wijngaerden, E., Vandercam, B., Vekemans, M., Verhofstede, C., Clumeck, N., Van Laethem, K., Demetriades, Ioannis, Kousiappa, Ioanna, Demetriou, Victoria L., Hezka, Johana, Bruckova, M., Machala, L., Gerstoft, J., Mathiesen, L., Pedersen, C., Nielsen, H., Laursen, A., Kvinesdal, B., Salminen, M., Ristola, M., Suni, J., Sutinen, J., Berg, T., Braun, P., Poggensee, G., Däumer, M., Eberle, J., Heiken, H., Kaiser, R., Knechten, H., Müller, H., Neifer, S., Schmidt, B., Walter, H., Gunsenheimer-Bartmeyer, B., Harrer, T., Hatzakis, Angelos E., Magiorkinis, Emmanouil N., Hatzitheodorou, Eleni, Haida, Catherine, Zavitsanou, Assimina, Magiorkinis, Gkikas, Lazanas, Marios C., Chini, Maria C., Magafas, N., Tsogas, Nickolaos, Paparizos, Vassilios A., Kourkounti, Sofia, Antoniadou, Anastasia C., Papadopoulos, Antonios I., Panagopoulos, Periklis, Poulakou, Garyphallia G., Sakka, V., Chryssos, Georgios, Drimis, Stylianos, Gargalianos, Panagiotis, Lelekis, Moyssis I., Chilomenos, G., Psichogiou, Mina A., Daikos, George L., Panos, George, Haratsis, G., Kordossis, Theodore, Kontos, Athanasios N., Koratzanis, Georgios, Theodoridou, Maria C., Mostrou, Glykeria J., Spoulou, Vana I., De Gascun, C., Byrne, C., Duffy, M., Bergin, C., Reidy, D., Farrell, G., Lambert, J., O'Connor, E., Rochford, A., Low, J., Coakely, P., O'Dea, S., Hall, W., Levi, I., Chemtob, D., Franzetti, M., Lai, A., Binda, F., Tramuto, F., Ciccozzi, M., Mussini, C., Angarano, G., Rezza, G., Schmit, J. C., Hemmer, R., Arendt, V., Staub, T., Schneider, F., Roman, F., van Kessel, A., van Bentum, P. H. M., Brinkman, K., de Coul, E. L., van der Ende, M. E., Hoepelman, I. M., van Kasteren, M., Juttmann, J., Kuipers, M., Langebeek, N., Richter, C., Santegoets, R. M. W. J., Schrijnders-Gudde, L., Schuurman, R., van de Ven, B. J. M., Ormaasen, V., Aavitsland, P., Stanczak, J. J., Stanczak, G. P., Firlag-Burkacka, E., Wiercinska-Drapalo, A., Jablonowska, E., Malolepsza, E., Leszczyszyn-Pynka, M., Szata, W., Palma, C., Borges, F., Paixão, T., Duque, V., Araújo, F., Jevtovic, D., Salemovic, D., Habekova, M., Mokráš, Miloš, Truska, P., Lunar, M., Babic, Dunja Z., Tomazic, J., Vidmar, L., Vovko, T., Karner, P., Domingo, P., Galindo, M. J., Miralles, C., del Pozo, M. A., Ribera, E., Iribarren, J. A., Ruiz, L., de la Torre, J., Vidal, F., Garcia, F., Heidarian, A., Aperia-Peipke, K., Axelsson, M., Mild, M., Karlsson, A., Thalme, A., Navér, L., Bratt, G., Blaxhult, A., Gisslén, M., Svennerholm, B., Bergbrant, I., Björkman, Per, Säll, C., Mellgren, Å., Lindholm, A., Kuylenstierna, N., Montelius, R., Azimi, F., Johansson, B., Carlsson, M., Johansson, E., Ljungberg, B., Ekvall, H., Strand, A., Mäkitalo, S., öberg, S., Holmblad, P., Höfer, M., Holmberg, H., Josefson, P., Ryding, U., Van Kessel, A., Instituto de Higiene e Medicina Tropical (IHMT), Centro de Malária e outras Doenças Tropicais (CMDT), Clinicum, Department of Medicine, Infektiosairauksien yksikkö, Frentz, D, Wensing, AMJ, Albert, J, Paraskevis, D, Abecasis, AB, Hamouda, O, Jørgensen, LB, Kücherer, C, Struck, D, Schmit, JC, Åsjö, B, Balotta, C, Beshkov, D, Camacho, RJ, Clotet, B, Coughlan, S, De Wit, S, Griskevicius, A, Grossman, Z, Horban, A, Kolupajeva, T, Korn, K, Kostrikis, LG, Liitsola, K, Linka, M, Nielsen, C, Otelea, D, Paredes, R, Poljak, M, Puchhammer-Stöckl, E, Sönnerborg, A, Stanekova, D, Stanojevic, M, Vandamme, AM, Boucher, CAB, Van de Vijver, DAMC, Tramuto, F, Van Wijngaerden, Eric, Van Ranst, Marc, Van Laethem, Kristel, Derdelinckx, Inge, Kostrikis, Leontios G. [0000-0002-5340-7109], Paraskevis, Dimitrios [0000-0001-6167-7152], Virology, and Graduate School

Subjects
Male, Epidemiology, Human immunodeficiency virus (HIV), Human immunodeficiency virus 1, HIV Infections, medicine.disease_cause, Virologie générale, phylogeny, Settore MED/42 - Igiene Generale E Applicata, Men who have sex with men, EMERGENCE, 0302 clinical medicine, Medicine and Health Sciences, Medicine, Infection control, Cluster Analysis, 030212 general & internal medicine, Israel, Pathologie maladies infectieuses, travel, Phylogeny, 0303 health sciences, Molecular Epidemiology, Travel, Transmission (medicine), article, virus transmission, IMMUNODEFICIENCY-VIRUS TYPE-1, 3. Good health, Europe, female, Infectious Diseases, SUBTYPE B, DRUG-RESISTANT HIV-1, RNA, Viral, male homosexual, Adult, structural gene, Molecular Sequence Data, Newly diagnosed, Clusters, 03 medical and health sciences, male, SDG 3 - Good Health and Well-being, MOLECULAR EPIDEMIOLOGY, SWITZERLAND, Virology, geographic distribution, Humans, Transmission, In patient, human, 030304 developmental biology, nonhuman, Molecular epidemiology, business.industry, Research, high risk population, Virologie médicale, nucleotide sequence, Sequence Analysis, DNA, Human immunodeficiency virus 1 infection, major clinical study, unindexed sequence, 3121 General medicine, internal medicine and other clinical medicine, HIV-1, business, Europe, HIV-1, Transmission, Clusters, Demography, cluster analysis
Abstract

Background: International travel plays a role in the spread of HIV-1 across Europe. It is, however, not known whether international travel is more important for spread of the epidemic as compared to endogenous infections within single countries. In this study, phylogenetic associations among HIV of newly diagnosed patients were determined across Europe.Results: Data came from the SPREAD programme which collects samples of newly diagnosed patients that are representative for national HIV epidemics. 4260 pol sequences from 25 European countries and Israel collected in 2002-2007 were included.We identified 457 clusters including 1330 persons (31.2% of all patients). The cluster size ranged between 2 and 28. A number of 987 patients (74.2%) were part of a cluster that consisted only of patients originating from the same country. In addition, 135 patients (10.2%) were in a cluster including only individuals from neighboring countries. Finally, 208 patients (15.6%) clustered with individuals from countries without a common border. Clustering with patients from the same country was less prevalent in patients being infected with B subtype (P-value, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2013

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