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1.  New Introductions of Enterovirus 71 Subgenogroup C4 Strains, France, 2012 
Emerging Infectious Diseases  2014;20(8):1343-1346.
In France during 2012, human enterovirus 71 (EV-A71) subgenogroup C4 strains were detected in 4 children hospitalized for neonatal fever or meningitis. Phylogenetic analysis showed novel and independent EV-A71 introductions, presumably from China, and suggested circulation of C4 strains throughout France. This observation emphasizes the need for monitoring EV-A71 infections in Europe.
doi:10.3201/eid2008.131858
PMCID: PMC4111202  PMID: 25061698
enterovirus 71; enterovirus species A; subgenogroup C4; Picornaviridae; France; viruses; humans; neonatal fever; meningitis; meningoencephalitis; rhomboencephalitis; phylogenetic analyses; herpangina; hand; foot and mouth disease
2.  Multicenter Quality Control of Hepatitis C Virus Protease Inhibitor Resistance Genotyping 
Journal of Clinical Microbiology  2013;51(5):1428-1433.
Hepatitis C virus (HCV) protease inhibitor resistance-associated substitutions are selected during triple-therapy breakthrough. This multicenter quality control study evaluated the expertise of 23 French laboratories in HCV protease inhibitor resistance genotyping. A panel of 12 well-defined blinded samples comprising two wild-type HCV strains, nine transcripts from synthetic NS3 mutant samples or from clinical strains, and one HCV RNA-negative sample was provided to the participating laboratories. The results showed that any laboratory with expertise in sequencing techniques should be able to provide reliable HCV protease inhibitor resistance genotyping. Only a 0.7% error rate was reported for the amino acid sites studied. The accuracy of substitution identification ranged from 75% to 100%, depending on the laboratory. Incorrect results were mainly related to the methodology used. The results could be improved by changing the primers and modifying the process in order to avoid cross-contamination. This study underlines the value of quality control programs for viral resistance genotyping, which is required prior to launching observational collaborative multicenter studies on HCV resistance to direct-acting antiviral agents.
doi:10.1128/JCM.03032-12
PMCID: PMC3647889  PMID: 23426922
3.  Evaluation of an Enzyme Immunoassay for Detection of Dengue Virus NS1 Antigen in Human Serum▿  
Clinical and Vaccine Immunology  2006;13(11):1185-1189.
We evaluated a one-step sandwich-format microplate enzyme immunoassay for detecting dengue virus NS1 antigen (Ag) in human serum by use of Platelia Dengue NS1 Ag kits (Bio-Rad Laboratories, Marnes La Coquette, France). We collected 299 serum samples from patients with dengue disease and 50 serum samples from patients not infected with dengue virus. For the 239 serum samples from patients with acute infections testing positive by reverse transcription-PCR and/or virus isolation for one of the four dengue virus serotypes, the sensitivity of the Platelia Dengue NS1 Ag kit was 88.7% (95% confidence interval, 84.0% to 92.4%). None of the serum samples from patients not infected with dengue virus tested positive with the Platelia Dengue NS1 Ag kit. A diagnostic strategy combining the Platelia Dengue NS1 Ag test for acute-phase sera and immunoglobulin M capture enzyme-linked immunosorbent assay for early-convalescent-phase sera increased sensitivity only from 88.7% to 91.9%. Thus, NS1 antigen detection with the Platelia Dengue NS1 Ag kit could be used for first-line testing for acute dengue virus infection in clinical diagnostic laboratories.
doi:10.1128/CVI.00229-06
PMCID: PMC1656554  PMID: 16988003
4.  Reemergence of Dengue Virus Type 4, French Antilles and French Guiana, 2004–2005 
Emerging Infectious Diseases  2006;12(11):1748-1751.
After 10 years of absence, dengue virus type 4 (DENV-4) has recently reemerged in Martinique, Guadeloupe, and French Guiana. Phylogenetic analyses of strains isolated from 2004 to 2005 showed that they belong to DENV-4 genotype II, but to a different cluster than strains isolated from 1993 to 1995.
doi:10.3201/eid1211.060339
PMCID: PMC3372336  PMID: 17283628
Dengue-4; phylogeny; French Antilles; French Guiana; dispatch
5.  Increased proviral load in HTLV-1-infected patients with rheumatoid arthritis or connective tissue disease 
Retrovirology  2005;2:4.
Background
Human T-lymphotropic virus type 1 (HTLV-1) proviral load is related to the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and has also been shown to be elevated in the peripheral blood in HTLV-1-infected patients with uveitis or alveolitis. Increased proliferation of HTLV-1-infected cells in, or migration of such cells into, the central nervous system is also seen in HAM/TSP. In the present study, we evaluated the proviral load in a cohort of HTLV-1-infected patients with arthritic conditions.
Results
HTLV-1 proviral load in the peripheral blood from 12 patients with RA and 6 patients with connective tissue disease was significantly higher than that in matched asymptomatic HTLV-1 carriers, but similar to that in matched HAM/TSP controls. HAM/TSP was seen in one-third of the HTLV-1-infected patients with RA or connective tissue disease, but did not account for the higher proviral load compared to the asymptomatic carrier group. The proviral load was increased in the synovial fluid and tissue from an HTLV-1-infected patient with RA, the values suggesting that the majority of infiltrated cells were HTLV-1-infected. In the peripheral blood from HTLV-1-infected patients with RA or connective tissue disease, HTLV-1 proviral load correlated with the percentages of memory CD4+ T cells and activated T cells, and these percentages were shown to be markedly higher in the synovial fluid than in the peripheral blood in an HTLV-1-infected patient with RA.
Conclusions
These biological findings are consistent with a role of the retrovirus in the development of arthritis in HTLV-1-infected patients. A high level of HTLV-1-infected lymphocytes in the peripheral blood and their accumulation in situ might play a central role in the pathogenesis of HTLV-1-associated inflammatory disorders. Alternatively, the autoimmune arthritis, its etiological factors or treatments might secondarily enhance HTLV-1 proviral load.
doi:10.1186/1742-4690-2-4
PMCID: PMC549050  PMID: 15686595

Results 1-5 (5)