Publications
343 results found
Lycett SJ, Baillie G, Coulter E, et al., 2012, Estimating reassortment rates in co-circulating Eurasian swine influenza viruses, JOURNAL OF GENERAL VIROLOGY, Vol: 93, Pages: 2326-2336, ISSN: 0022-1317
Swine have often been considered as a mixing vessel for different influenza strains. In order to assess their role in more detail, we undertook a retrospective sequencing study to detect and characterize the reassortants present in European swine and to estimate the rate of reassortment between H1N1, H1N2 and H3N2 subtypes with Eurasian (avian-like) internal protein-coding segments. We analysed 69 newly obtained whole genome sequences of subtypes H1N1–H3N2 from swine influenza viruses sampled between 1982 and 2008, using Illumina and 454 platforms. Analyses of these genomes, together with previously published genomes, revealed a large monophyletic clade of Eurasian swine-lineage polymerase segments containing H1N1, H1N2 and H3N2 subtypes. We subsequently examined reassortments between the haemagglutinin and neuraminidase segments and estimated the reassortment rates between lineages using a recently developed evolutionary analysis method. High rates of reassortment between H1N2 and H1N1 Eurasian swine lineages were detected in European strains, with an average of one reassortment every 2–3 years. This rapid reassortment results from co-circulating lineages in swine, and in consequence we should expect further reassortments between currently circulating swine strains and the recent swine-origin H1N1v pandemic strain.
Wash R, Calabressi S, Franz S, et al., 2012, Permissive and restricted virus infection of murine embryonic stem cells., Journal of General Virology, Vol: 93, Pages: 2118-2130, ISSN: 1465-2099
Recent RNA interference (RNAi) studies have identified many host proteins that modulate virus infection, but small interfering RNA 'off-target' effects and the use of transformed cell lines limit their conclusiveness. As murine embryonic stem (mES) cells can be genetically modified and resources exist where many and eventually all known mouse genes are insertionally inactivated, it was reasoned that mES cells would provide a useful alternative to RNAi screens. Beyond allowing investigation of host-pathogen interactions in vitro, mES cells have the potential to differentiate into other primary cell types, as well as being used to generate knockout mice for in vivo studies. However, mES cells are poorly characterized for virus infection. To investigate whether ES cells can be used to explore host-virus interactions, this study characterized the responses of mES cells following infection by herpes simplex virus type 1 (HSV-1) and influenza A virus. HSV-1 replicated lytically in mES cells, although mES cells were less permissive than most other cell types tested. Influenza virus was able to enter mES cells and express some viral proteins, but the replication cycle was incomplete and no infectious virus was produced. Knockdown of the host protein AHCYL1 in mES cells reduced HSV-1 replication, showing the potential for using mES cells to study host-virus interactions. Transcriptional profiling, however, indicated the lack of an efficient innate immune response in these cells. mES cells may thus be useful to identify host proteins that play a role in virus replication, but they are not suitable to determine factors that are involved in innate host defence.
Williamson SM, Tucker AW, McCrone IS, et al., 2012, Descriptive clinical and epidemiological characteristics of influenza A H1N1 2009 virus infections in pigs in England, VETERINARY RECORD, Vol: 171, Pages: 271-U47, ISSN: 0042-4900
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- Citations: 20
Dolling D, Sabin C, Delpech V, et al., 2012, Time trends in drug resistant HIV-1 infections in the United Kingdom up to 2009: multicentre observational study, BMJ-BRITISH MEDICAL JOURNAL, Vol: 345, ISSN: 1756-1833
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- Citations: 40
Wright DW, Hall BA, Kellam P, et al., 2012, Global conformational dynamics of HIV-1 reverse transcriptase bound to non-nucleoside inhibitors, Biology, Vol: 1, Pages: 222-244, ISSN: 2079-7737
HIV-1 Reverse Transcriptase (RT) is a multifunctional enzyme responsible for the transcription of the RNA genome of the HIV virus into DNA suitable for incorporation within the DNA of human host cells. Its crucial role in the viral life cycle has made it one of the major targets for antiretroviral drug therapy. The Non-Nucleoside RT Inhibitor (NNRTI) class of drugs binds allosterically to the enzyme, affecting many aspects of its activity. We use both coarse grained network models and atomistic molecular dynamics to explore the changes in protein dynamics induced by NNRTI binding. We identify changes in the flexibility and conformation of residue Glu396 in the RNaseH primer grip which could provide an explanation for the acceleration in RNaseH cleavage rate observed experimentally in NNRTI bound HIV-1 RT. We further suggest a plausible path for conformational and dynamic changes to be communicated from the vicinity of the NNRTI binding pocket to the RNaseH at the other end of the enzyme.
Everitt A, Clare S, Pertel T, et al., 2012, IFITM3 restricts the morbidity and mortality associated with influenza, INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES, Vol: 16, Pages: E79-E79, ISSN: 1201-9712
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- Citations: 4
Murcia PR, Hughes J, Battista P, et al., 2012, Evolution of an Eurasian avian-like influenza virus in naïve and vaccinated pigs., PLoS Pathogens, Vol: 8, Pages: e1002730-e1002730, ISSN: 1553-7366
Influenza viruses are characterized by an ability to cross species boundaries and evade host immunity, sometimes with devastating consequences. The 2009 pandemic of H1N1 influenza A virus highlights the importance of pigs in influenza emergence, particularly as intermediate hosts by which avian viruses adapt to mammals before emerging in humans. Although segment reassortment has commonly been associated with influenza emergence, an expanded host-range is also likely to be associated with the accumulation of specific beneficial point mutations. To better understand the mechanisms that shape the genetic diversity of avian-like viruses in pigs, we studied the evolutionary dynamics of an Eurasian Avian-like swine influenza virus (EA-SIV) in naïve and vaccinated pigs linked by natural transmission. We analyzed multiple clones of the hemagglutinin 1 (HA1) gene derived from consecutive daily viral populations. Strikingly, we observed both transient and fixed changes in the consensus sequence along the transmission chain. Hence, the mutational spectrum of intra-host EA-SIV populations is highly dynamic and allele fixation can occur with extreme rapidity. In addition, mutations that could potentially alter host-range and antigenicity were transmitted between animals and mixed infections were commonplace, even in vaccinated pigs. Finally, we repeatedly detected distinct stop codons in virus samples from co-housed pigs, suggesting that they persisted within hosts and were transmitted among them. This implies that mutations that reduce viral fitness in one host, but which could lead to fitness benefits in a novel host, can circulate at low frequencies.
Everitt AR, Clare S, Pertel T, et al., 2012, IFITM3 restricts the morbidity and mortality associated with influenza., Nature, Vol: 484, Pages: 519-523
The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses1, 2, 3, 4, 5, 6, 7. Both the magnitude and breadth of the IFITM proteins’ in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model8, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 ‘Spanish’ influenza9, 10. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.
Barber TJ, Harrison L, Asboe D, et al., 2012, Frequency and patterns of protease gene resistance mutations in HIV-infected patients treated with lopinavir/ritonavir as their first protease inhibitor, JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, Vol: 67, Pages: 995-1000, ISSN: 0305-7453
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- Citations: 22
Archer J, Baillie G, Watson SJ, et al., 2012, Analysis of high-depth sequence data for studying viral diversity: a comparison of next generation sequencing platforms using Segminator II., BMC Bioinformatics, Vol: 13, ISSN: 1471-2105
BACKGROUND: Next generation sequencing provides detailed insight into the variation present within viral populations, introducing the possibility of treatment strategies that are both reactive and predictive. Current software tools, however, need to be scaled up to accommodate for high-depth viral data sets, which are often temporally or spatially linked. In addition, due to the development of novel sequencing platforms and chemistries, each with implicit strengths and weaknesses, it will be helpful for researchers to be able to routinely compare and combine data sets from different platforms/chemistries. In particular, error associated with a specific sequencing process must be quantified so that true biological variation may be identified. RESULTS: Segminator II was developed to allow for the efficient comparison of data sets derived from different sources. We demonstrate its usage by comparing large data sets from 12 influenza H1N1 samples sequenced on both the 454 Life Sciences and Illumina platforms, permitting quantification of platform error. For mismatches median error rates at 0.10 and 0.12%, respectively, suggested that both platforms performed similarly. For insertions and deletions median error rates within the 454 data (at 0.3 and 0.2%, respectively) were significantly higher than those within the Illumina data (0.004 and 0.006%, respectively). In agreement with previous observations these higher rates were strongly associated with homopolymeric stretches on the 454 platform. Outside of such regions both platforms had similar indel error profiles. Additionally, we apply our software to the identification of low frequency variants. CONCLUSION: We have demonstrated, using Segminator II, that it is possible to distinguish platform specific error from biological variation using data derived from two different platforms. We have used this approach to quantify the amount of error present within the 454 and Illumina platforms in relation to genomic location as
Castro H, Pillay D, Sabin C, et al., 2012, Effect of misclassification of antiretroviral treatment status on the prevalence of transmitted HIV-1 drug resistance, BMC Medical Research Methodology, Vol: 12, ISSN: 1471-2288
BackgroundEstimates of the prevalence of transmitted HIV drug resistance (TDR) in a population are derived from resistance tests performed on samples from patients thought to be naïve to antiretroviral treatment (ART). Much of the debate over reliability of estimates of the prevalence of TDR has focused on whether the sample population is representative. However estimates of the prevalence of TDR will also be distorted if some ART-experienced patients are misclassified as ART-naïve.MethodsThe impact of misclassification bias on the rate of TDR was examined. We developed methods to obtain adjusted estimates of the prevalence of TDR for different misclassification rates, and conducted sensitivity analyses of trends in the prevalence of TDR over time using data from the UK HIV Drug Resistance Database. Logistic regression was used to examine trends in the prevalence of TDR over time.ResultsThe observed rate of TDR was higher than true TDR when misclassification was present and increased as the proportion of misclassification increased. As the number of naïve patients with a resistance test relative to the number of experienced patients with a test increased, the difference between true and observed TDR decreased. The observed prevalence of TDR in the UK reached a peak of 11.3% in 2002 (odds of TDR increased by 1.10 (95% CI 1.02, 1.19, p(linear trend) = 0.02) per year 1997-2002) before decreasing to 7.0% in 2007 (odds of TDR decreased by 0.90 (95% CI 0.87, 0.94, p(linear trend) < 0.001) per year 2002-2007. Trends in adjusted TDR were altered as the misclassification rate increased; the significant downward trend between 2002-2007 was lost when the misclassification increased to over 4%.ConclusionThe effect of misclassification of ART on estimates of the prevalence of TDR may be appreciable, and depends on the number of naïve tests relative to the number of experienced tests. Researchers can examine the effect of ART misclassification on their esti
Lefevre EA, Carr BV, Inman CF, et al., 2012, Immune Responses in Pigs Vaccinated with Adjuvanted and Non-Adjuvanted A(H1N1)pdm/09 Influenza Vaccines Used in Human Immunization Programmes, PLOS One, Vol: 7, ISSN: 1932-6203
Following the emergence and global spread of a novel H1N1 influenza virus in 2009, two A(H1N1)pdm/09 influenza vaccines produced from the A/California/07/09 H1N1 strain were selected and used for the national immunisation programme in the United Kingdom: an adjuvanted split virion vaccine and a non-adjuvanted whole virion vaccine. In this study, we assessed the immune responses generated in inbred large white pigs (Babraham line) following vaccination with these vaccines and after challenge with A(H1N1)pdm/09 virus three months post-vaccination. Both vaccines elicited strong antibody responses, which included high levels of influenza-specific IgG1 and haemagglutination inhibition titres to H1 virus. Immunisation with the adjuvanted split vaccine induced significantly higher interferon gamma production, increased frequency of interferon gamma-producing cells and proliferation of CD4−CD8+ (cytotoxic) and CD4+CD8+ (helper) T cells, after in vitro re-stimulation. Despite significant differences in the magnitude and breadth of immune responses in the two vaccinated and mock treated groups, similar quantities of viral RNA were detected from the nasal cavity in all pigs after live virus challenge. The present study provides support for the use of the pig as a valid experimental model for influenza infections in humans, including the assessment of protective efficacy of therapeutic interventions.
Baillie GJ, Galiano M, Agapow P-M, et al., 2012, Evolutionary Dynamics of Local Pandemic H1N1/2009 Influenza Virus Lineages Revealed by Whole-Genome Analysis, JOURNAL OF VIROLOGY, Vol: 86, Pages: 11-18, ISSN: 0022-538X
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- Citations: 81
Reperant LA, van de Bildt MWG, van Amerongen G, et al., 2012, Marked Endotheliotropism of Highly Pathogenic Avian Influenza Virus H5N1 following Intestinal Inoculation in Cats, JOURNAL OF VIROLOGY, Vol: 86, Pages: 1158-1165, ISSN: 0022-538X
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- Citations: 28
Depledge DP, Palser AL, Watson SJ, et al., 2012, Correction: specific capture and whole-genome sequencing of viruses from clinical samples., PLoS One, Vol: 7
[This corrects the article on p. e27805 in vol. 6.].
Donegan KL, Walker AS, Dunn D, et al., 2012, The prevalence of darunavir-associated mutations in HIV-1-infected children in the UK, ANTIVIRAL THERAPY, Vol: 17, Pages: 599-603, ISSN: 1359-6535
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- Citations: 7
Daly GM, Bexfield N, Heaney J, et al., 2011, A viral discovery methodology for clinical biopsy samples utilising massively parallel next generation sequencing., PLoS One, Vol: 6, Pages: e28879-e28879, ISSN: 1932-6203
Here we describe a virus discovery protocol for a range of different virus genera, that can be applied to biopsy-sized tissue samples. Our viral enrichment procedure, validated using canine and human liver samples, significantly improves viral read copy number and increases the length of viral contigs that can be generated by de novo assembly. This in turn enables the Illumina next generation sequencing (NGS) platform to be used as an effective tool for viral discovery from tissue samples.
Depledge DP, Palser AL, Watson SJ, et al., 2011, Specific Capture and Whole-Genome Sequencing of Viruses from Clinical Samples, PLOS ONE, Vol: 6, ISSN: 1932-6203
Whole genome sequencing of viruses directly from clinical samples is integral for understanding the genetics of host-virus interactions. Here, we report the use of sample sparing target enrichment (by hybridisation) for viral nucleic acid separation and deep-sequencing of herpesvirus genomes directly from a range of clinical samples including saliva, blood, virus vesicles, cerebrospinal fluid, and tumour cell lines. We demonstrate the effectiveness of the method by deep-sequencing 13 highly cell-associated human herpesvirus genomes and generating full length genome alignments at high read depth. Moreover, we show the specificity of the method enables the study of viral population structures and their diversity within a range of clinical samples types.
Bexfield N, Kellam P, 2011, Metagenomics and the molecular identification of novel viruses, Equine Veterinary Journal, Vol: 190, Pages: 191-198, ISSN: 0425-1644
There have been rapid recent developments in establishing methods for identifying and characterising viruses associated with animal and human diseases. These methodologies, commonly based on hybridisation or PCR techniques, are combined with advanced sequencing techniques termed ‘next generation sequencing’. Allied advances in data analysis, including the use of computational transcriptome subtraction, have also impacted the field of viral pathogen discovery. This review details these molecular detection techniques, discusses their application in viral discovery, and provides an overview of some of the novel viruses discovered. The problems encountered in attributing disease causality to a newly identified virus are also considered.
Caporale M, Wash R, Pini A, et al., 2011, Determinants of Bluetongue Virus Virulence in Murine Models of Disease, JOURNAL OF VIROLOGY, Vol: 85, Pages: 11479-11489, ISSN: 0022-538X
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- Citations: 43
Katzourakis A, Hue S, Kellam P, et al., 2011, Phylogenetic Analysis of Murine Leukemia Virus Sequences from Longitudinally Sampled Chronic Fatigue Syndrome Patients Suggests PCR Contamination Rather than Viral Evolution, JOURNAL OF VIROLOGY, Vol: 85, Pages: 10909-10913, ISSN: 0022-538X
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- Citations: 13
Prosperi MCF, Mackie N, Di Giambenedetto S, et al., 2011, Detection of drug resistance mutations at low plasma HIV-1 RNA load in a European multicentre cohort study, JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, Vol: 66, Pages: 1886-1896, ISSN: 0305-7453
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- Citations: 34
Frampton D, Kerr J, Harrison TJ, et al., 2011, Assessment of a 44 gene classifier for the evaluation of chronic fatigue syndrome from peripheral blood mononuclear cell gene expression., PLoS One, Vol: 6, ISSN: 1932-6203
Chronic fatigue syndrome (CFS) is a clinically defined illness estimated to affect millions of people worldwide causing significant morbidity and an annual cost of billions of dollars. Currently there are no laboratory-based diagnostic methods for CFS. However, differences in gene expression profiles between CFS patients and healthy persons have been reported in the literature. Using mRNA relative quantities for 44 previously identified reporter genes taken from a large dataset comprising both CFS patients and healthy volunteers, we derived a gene profile scoring metric to accurately classify CFS and healthy samples. This metric out-performed any of the reporter genes used individually as a classifier of CFS.To determine whether the reporter genes were robust across populations, we applied this metric to classify a separate blind dataset of mRNA relative quantities from a new population of CFS patients and healthy persons with limited success. Although the metric was able to successfully classify roughly two-thirds of both CFS and healthy samples correctly, the level of misclassification was high. We conclude many of the previously identified reporter genes are study-specific and thus cannot be used as a broad CFS diagnostic.
Gray ER, Garson JA, Breuer J, et al., 2011, No evidence of XMRV or related retroviruses in a London HIV-1-positive patient cohort., PLoS One, Vol: 6, Pages: e18096-e18096, ISSN: 1932-6203
BACKGROUND: Several studies have implicated a recently discovered gammaretrovirus, XMRV (Xenotropic murine leukaemia virus-related virus), in chronic fatigue syndrome and prostate cancer, though whether as causative agent or opportunistic infection is unclear. It has also been suggested that the virus can be found circulating amongst the general population. The discovery has been controversial, with conflicting results from attempts to reproduce the original studies. METHODOLOGY/PRINCIPAL FINDINGS: We extracted peripheral blood DNA from a cohort of 540 HIV-1-positive patients (approximately 20% of whom have never been on anti-retroviral treatment) and determined the presence of XMRV and related viruses using TaqMan PCR. While we were able to amplify as few as 5 copies of positive control DNA, we did not find any positive samples in the patient cohort. CONCLUSIONS/SIGNIFICANCE: In view of these negative findings in this highly susceptible group, we conclude that it is unlikely that XMRV or related viruses are circulating at a significant level, if at all, in HIV-1-positive patients in London or in the general population.
Garson JA, Kellam P, Towers GJ, 2011, Analysis of XMRV integration sites from human prostate cancer tissues suggests PCR contamination rather than genuine human infection., Retrovirology, Vol: 8, Pages: 13-13, ISSN: 1742-4690
XMRV is a gammaretrovirus associated in some studies with human prostate cancer and chronic fatigue syndrome. Central to the hypothesis of XMRV as a human pathogen is the description of integration sites in DNA from prostate tumour tissues. Here we demonstrate that 2 of 14 patient-derived sites are identical to sites cloned in the same laboratory from experimentally infected DU145 cells. Identical integration sites have never previously been described in any retrovirus infection. We propose that the patient-derived sites are the result of PCR contamination. This observation further undermines the notion that XMRV is a genuine human pathogen.
Lai IY-C, Farrell PJ, Kellam P, 2011, X-box binding protein 1 induces the expression of the lytic cycle transactivator of Kaposi's sarcoma-associated herpesvirus but not Epstein Barr virus in co-infected primary effusion lymphoma, Journal of General Virology, Vol: 92, Pages: 421-431, ISSN: 1465-2099
Cells of primary effusion lymphoma (PEL), a B-cell non-Hodgkin's lymphoma, are latently infected by Kaposi's sarcoma-associated herpesvirus (KSHV), with about 80 % of PEL also co-infected with Epstein–Barr virus (EBV). Both viruses can be reactivated into their lytic replication cycle in PEL by chemical inducers. However, simultaneous activation of both lytic cascades leads to mutual lytic cycle co-repression. The plasma cell-differentiation factor X-box binding protein 1 (XBP-1) transactivates the KSHV immediate–early promoter leading to the production of the replication and transcription activator protein (RTA), and reactivation of KSHV from latency. XBP-1 has been reported to act similarly on the EBV immediate–early promoter Zp, leading to the production of the lytic-cycle transactivator protein BZLF1. Here we show that activated B-cell terminal-differentiation transcription factor X-box binding protein 1 (XBP-1s) does not induce EBV BZLF1 and BRLF1 expression in PEL and BL cell lines, despite inducing lytic reactivation of KSHV in PEL. We show that XBP-1s transactivates the KSHV RTA promoter but does not transactivate the EBV BZLF1 promoter in non-B-cells by using a luciferase assay. Co-expression of activated protein kinase D, which can phosphorylate and inactivate class II histone deacetylases (HDACs), does not rescue XBP-1 activity on Zp nor does it induce BZLF1 and BRLF1 expression in PEL. Finally, chemical inducers of KSHV and EBV lytic replication in PEL, including HDAC inhibitors, do not lead to XBP-1 activation. We conclude that XBP-1 specifically reactivates the KSHV lytic cycle in dually infected PELs.
Baker K, Kellam P, Suu-Ire R, et al., 2011, Next Generation Surveillance? A metaviromic Study of a West African Bat Population Using Next Generation Sequencing, Publisher: SPRINGER, Pages: S41-S42, ISSN: 1612-9202
Hué S, Gray ER, Gall A, et al., 2010, Disease-associated XMRV sequences are consistent with laboratory contamination., Retrovirology, Vol: 7, ISSN: 1742-4690
BACKGROUND: Xenotropic murine leukaemia viruses (MLV-X) are endogenous gammaretroviruses that infect cells from many species, including humans. Xenotropic murine leukaemia virus-related virus (XMRV) is a retrovirus that has been the subject of intense debate since its detection in samples from humans with prostate cancer (PC) and chronic fatigue syndrome (CFS). Controversy has arisen from the failure of some studies to detect XMRV in PC or CFS patients and from inconsistent detection of XMRV in healthy controls. RESULTS: Here we demonstrate that Taqman PCR primers previously described as XMRV-specific can amplify common murine endogenous viral sequences from mouse suggesting that mouse DNA can contaminate patient samples and confound specific XMRV detection. To consider the provenance of XMRV we sequenced XMRV from the cell line 22Rv1, which is infected with an MLV-X that is indistinguishable from patient derived XMRV. Bayesian phylogenies clearly show that XMRV sequences reportedly derived from unlinked patients form a monophyletic clade with interspersed 22Rv1 clones (posterior probability >0.99). The cell line-derived sequences are ancestral to the patient-derived sequences (posterior probability >0.99). Furthermore, pol sequences apparently amplified from PC patient material (VP29 and VP184) are recombinants of XMRV and Moloney MLV (MoMLV) a virus with an envelope that lacks tropism for human cells. Considering the diversity of XMRV we show that the mean pairwise genetic distance among env and pol 22Rv1-derived sequences exceeds that of patient-associated sequences (Wilcoxon rank sum test: p = 0.005 and p < 0.001 for pol and env, respectively). Thus XMRV sequences acquire diversity in a cell line but not in patient samples. These observations are difficult to reconcile with the hypothesis that published XMRV sequences are related by a process of infectious transmission. CONCLUSIONS: We provide several independent lines of evidence that XMRV detected by
Kellam P, Coulter E, Frampton D, et al., 2010, Human herpesviruses, tumours and miRNAs; new points of host and pathogen interactions, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL PUBLISHING, INC, Pages: 17-17, ISSN: 0019-2805
Fox J, Castro H, Kaye S, et al., 2010, Epidemiology of non-B clade forms of HIV-1 in men who have sex with men in the UK, AIDS, Vol: 24, Pages: 2397-2401, ISSN: 0269-9370
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- Citations: 31
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