Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80003-X
P. Bossi, A. Yvon, M. Mouroux, J.-M. Huraux, H. Agut, V. Calvez
{"title":"Mutations in the human immunodeficiency virus type 1 reverse transcriptase gene observed in stavudine and didanosine strains obtained by in vitro passages","authors":"P. Bossi, A. Yvon, M. Mouroux, J.-M. Huraux, H. Agut, V. Calvez","doi":"10.1016/S0923-2516(99)80003-X","DOIUrl":"10.1016/S0923-2516(99)80003-X","url":null,"abstract":"<div><p>We have selected a human immunodeficiency virus type 1 (HIV1) using the technique of <em>in vitro</em> selection to generate variants that are resistant to didanosine and/or stavudine. After serial passages of the Lai strain of HIV1 in MT-2 cells in increased concentrations of didanosine-stavudine association, 2 novel mutations in reverse transcriptase at codon 57 (Asp→His) and at codon 98 (Ala→Val) were observed. These mutations were associated with an 11.5-fold increase in the didanosine and a 4.5-fold increase in the stavudine 50% inhibitory concentration.</p></div><div><p>Nous avons sélectionné <em>in vitro</em> des souches de VIH1 résistantes à la didanosine et/ou à la stavudine. Après passages de la souche Lai sur cellules MT-2 à concentrations croissantes de l'association didanosine-stavudine, 2 nouvelles mutations dans le gène de la transcriptase inverse ont été observées au niveau des codons 57 (Asp→His) et 98 (Ala→Val). Ces mutations sont associées à une élévation de 11,5 fois la CI<sub>50</sub> de la didanosine et de 4,5 fois la CI<sub>50</sub> de la stavudine.</p></div>","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 355-361"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80003-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20828455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80018-1
{"title":"Index of key-words","authors":"","doi":"10.1016/S0923-2516(99)80018-1","DOIUrl":"https://doi.org/10.1016/S0923-2516(99)80018-1","url":null,"abstract":"","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 469-471"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80018-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136816423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80019-3
{"title":"Index of articles published","authors":"","doi":"10.1016/S0923-2516(99)80019-3","DOIUrl":"https://doi.org/10.1016/S0923-2516(99)80019-3","url":null,"abstract":"","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 471-472"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80019-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136816424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80009-0
T.F. Schwarz , S. Gilch , H.M. Schätzl
{"title":"A recombinant Toscana virus nucleoprotein in a diagnostic immunoblot test system","authors":"T.F. Schwarz , S. Gilch , H.M. Schätzl","doi":"10.1016/S0923-2516(99)80009-0","DOIUrl":"10.1016/S0923-2516(99)80009-0","url":null,"abstract":"<div><p>Sandfly fever, a vector-borne disease endemic in the Mediterranean region, is caused by Toscana virus (TOS). The disease is increasingly important as a travel-related infection. Serological diagnosis is currently dependent on viral antigens derived from TOS-infected cell cultures. In this study, we report the cloning and expression of the TOS nucleoprotein (N) in <em>Escherichia coli</em> and evaluation of the recombinant (r) TOS N protein as an antigen for immunoblot assays. The TOS N gene was amplified by reversetranscriptase polymerase chain reaction and cloned into the bacterial expression vector pTrcHis-A. Sera with known TOS antibody status were used to evaluate the immunoblot assay. The expressed rTOS N protein was purified and used as antigen for immunobiots. By recombinant immunoblot, the TOS antibody status (IgM and/or IgG) of the test panel was correctly identified. No cross-reactivity was detected. The rTOS N protein is useful as an antigen for immunoblot assays, and will enable more laboratories to perform TOS antibody diagnosis.</p></div><div><p>La fièvre à phlébotomes, maladie transmise par vecteur et endémique dans le bassin méditerranéen, est provoquée par le virus Toscana (TOS) et son incidence croissante est liée aux voyages. Le diagnostic sérologique dépend actuellement des antigènes viraux extraits des cultures cellulaires infectées par TOS. Dans cette étude nous rapportons le clonage et l'expression de la nucléoprotéine (N) de TOS chez <em>Escherichia coli</em>, et l'évaluation de la N recombinante (Nr-TOS) comme antigène dans des dosages par immunotransfert. Le gène de la N-TOS a été amplifié par PCR (polymerase chain reaction) et a été clone dans le vecteur d'expression bactérienne pTrcHis-A. Des sérums contenant des anticorps anti-TOS connus ont été utilisés pour l'évaluation des dosages par immunotransfert. La Nr-TOS exprimée a été purifiée et utilisée comme antigène dans des immunotransferts qui ont permis d'identifier correctement la classe des anticorps anti-TOS (IgM et/ou IgG). Aucune réactivité croisée n'a été détectée. La Nr-TOS s'avère efficace comme antigène dans des dosages par immunotransfert: elle devra permettre à de nombreux laboratoires de diagnostiquer la présence d'anticorps anti-TOS.</p></div>","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 413-418"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80009-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20829049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80017-X
{"title":"Index of authors","authors":"","doi":"10.1016/S0923-2516(99)80017-X","DOIUrl":"https://doi.org/10.1016/S0923-2516(99)80017-X","url":null,"abstract":"","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 467-469"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80017-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136816422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80002-8
L. Gigout, B. Vaslin, F. Matheux, P. Caufour, O. Neildez, A. Chéret, S. Lebel-Binay, F. Théodoro, P. Dilda, O. Benveniste, P. Clayette, R. Le Grand, D. Dormont
{"title":"Consequences of ddI-induced reduction of acute SIVmac251 virus load on cytokine profiles in cynomolgus macaques","authors":"L. Gigout, B. Vaslin, F. Matheux, P. Caufour, O. Neildez, A. Chéret, S. Lebel-Binay, F. Théodoro, P. Dilda, O. Benveniste, P. Clayette, R. Le Grand, D. Dormont","doi":"10.1016/S0923-2516(99)80002-8","DOIUrl":"10.1016/S0923-2516(99)80002-8","url":null,"abstract":"<div><p>This study evaluates the consequences of antiretroviral treatment of the acute simian immunodeficiency virus (SIV) primary infection on virus load and cytokine responses. Four cynomolgus macaques were inoculated intravenously with a pathogenic primary isolate (SIVmac251). Animals were pretreated with 10.8 mg/kg/day of dideoxyinosine (ddl) from 4 days before inoculation, and treatment was continued for 28 days. Proinflammatory (IL6, IL1β and TNFα) and antiinflammatory (IL10) cytokine and lymphokine (IL2, IL4 and IFNγ) polymerase chain reaction (PCR) ratios were monitored in unmanipulated peripheral blood mononuclear cells (PBMCs) during acute infection by using a semiquantitative reverse transcription (RT)-PCR method. PBMC-associated virus loads were dramatically reduced compared to those of placebo-treated macaques. Nevertheless, a transient rise in IL6, IL1β, TNFα and IL10 mRNA expression was observed in PBMCs. IL2, IL4 and IFNγ mRNAs were either undetectable or weakly detectable throughout the study, with no major changes. Despite a dramatic reduction in the acute viral loads in ddl-treated monkeys, early cytokine mRNA profiles were comparable to those of untreated SIVmac251-infected monkeys. Contrary to what was previously evidenced during primary infection with an attenuated SIV clone, no increase in IL2 and IL4 mRNA was detected in PBMCs of the ddl-treated monkeys, although these monkeys exhibited virus loads similar to those evidenced in macaques infected by attenuated SIV. These data indicate that differential lymphokine expression patterns found in pathogenic and Nef-truncated SIV-infected monkeys may not be strictly dependent on virus load levels.</p></div><div><p>Le but de cette étude était de déterminer les conséquences d'une réduction précoce de la charge virale périphérique sur la réponse cytokinique durant la primo-infection de macaques par le SIV-mac. Pour cela, quatre macaques cynomolgus ont été inoculés par voie veineuse avec l'isolat pathogène SIVmac251. Ces animaux ont, par ailleurs, reçu par voie sous-cutanée de la didanosine (ddl) à la dose de 10,8 mg/kg/jour du jour -4 au jour 28 post-inoculation. L'expression constitutive précoce des ARNms codant des monokines proinflammatoires (IL6, IL1β et TNFα), des lymphokines (IL2, IL4 et IFNγ) et de l'IL10 a été mesurée à l'aide d'une technique de RT-PCR semi-quantitative. La charge virale périphérique des animaux traités par la ddI, a été considérablement réduite par rapport à celle des animaux témoins infectés non traités. Une augmentation transitoire des ARNms codant l'IL6, le TNFα, l'IL1β et l'IL10 a été observée dans les CMSPs (cellules mononucléaires du sang périphérique) des animaux infectés et traités. En revanche, le niveau d'expression des ARNms codant l'IL2 et l'IL4 est resté indétectable ou très faible tout au long de l'étude. Bien que la charge virale ait été considérablement réduite chez les animaux traités par la ddI, les profils cytokiniques précoces étaient co","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 341-354"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80002-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20827964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80006-5
D.-X. Fu, Y. Haraguchi, A. Jinno, D. Yang, H. Hoshino
{"title":"Identification of membrane antigens important for adsorption of human T-cell leukaemia virus type I","authors":"D.-X. Fu, Y. Haraguchi, A. Jinno, D. Yang, H. Hoshino","doi":"10.1016/S0923-2516(99)80006-5","DOIUrl":"10.1016/S0923-2516(99)80006-5","url":null,"abstract":"<div><p>We isolated three monoclonal antibodies (mAbs), H3e, H11b and H16h, which were capable of inhibiting syncytium formation induced in a human T-cell line MOLT-4 or a human glioma line U2S1 MG by coculture with human T-cell leukaemia virus type I (HTLV-I)-positive human T-cell lines. The mAbs partially inhibited the plating of pseudotypes of vesicular stomatitis virus (VSV) bearing envelope antigens of HTLV-I. Formation of proviral DNA was also inhibited when indicator cells were treated with the mAbs before adsorption of HTLV-I, but not after its adsorption. They did not inhibit syncytium formation induced by human immunodeficiency virus type 1. Flow cytometry revealed that H16h hardly reacted with various HTLV-I-positive T cells, while H3e and H11b reacted with HTLV-I-positive human cells as well as HTLV-I-negative human cells. H11b and H16h immunoprecipitated the membrane antigen with a molecular weight of 20 and 110–130 kDa, respectively. Western blot analysis showed that H3e, H11b and H16h bound to the protein of 20, 20 and 110–130 kDa, respectively. Thus, these findings suggest that the 20- and 110–130-kDa cell surface proteins may play a role at the early stage of HTLV-I infection.</p></div><div><p>Nous avons isolé trois anticorps monoclonaux (mAbs), H3e, H11b et H16h, capables d'inhiber la formation de syncytium induit, sur des lymphocytes T humains ou sur une lignée de gliome humain U251 MG, par coculture avec des lignées de cellules T humaines HTLV-I positives. Les mAbs inhibent partiellement la constitution de pseudotypes de VSV porteurs d'antigènes d'enveloppe de HTLV-I. La formation d'ADN proviral est également inhibée quand les cellules ≪indicatrices≫ sont traitées par les mAbs avant l'adsorption de HTLV-I et non après son adsorption. Ils n'inhibent pas la formation de syncytium induite par HIV1. Une analyse cytométrique révèle que H16h réagit fortement avec diverses cellules T HTLV-I positives alors que H3e et H11b réagissent avec des cellules humaines aussi bien négatives que positives. On observe une immunoprécipitation de l'antigène membranaire avec H11b et H16h, le poids moléculaire étant respectivement de 20 et de 110–130 kDa. Une analyse ≪Western blot≫ montre que H3e, H11b et H16h sont fixés aux protéines de 20, 20 et 110–130 kDa respectivement. Ces résultats suggèrent que les protéines de surface de 20 et de 110–130 kDa peuvent jouer un rôle au stade précoce de l'infection par HTLV-I.</p></div>","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 383-392"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80006-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20828458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Research in virologyPub Date : 1998-11-01Epub Date: 1999-10-26DOI: 10.1016/S0923-2516(99)80007-7
M. Neves, J. Périès, A. Saïb
{"title":"Study of human foamy virus proviral integration in chronically infected murine cells","authors":"M. Neves, J. Périès, A. Saïb","doi":"10.1016/S0923-2516(99)80007-7","DOIUrl":"10.1016/S0923-2516(99)80007-7","url":null,"abstract":"<div><p>This report describes integration sites of human foamy virus (HFV) in chronically infected BALB/c murine cells that we isolated by inverse PCR and characterized. We show that integration of HFV proviral genome mainly occurs in highly repetitive and/or transcriptionally active regions and leads to the formation of a 4-bp cellular direct repeat sequence at each provirus extremity. As non-random deletions were previously described in the HFV bel1 transactivator gene as well as in the long terminal repeats (LTRs), these regions were verified in integrated HFV. The analysis reveals that, in the studied chronic state, the defective interfering virus (AHFV) is the main integrated proviral form and is always associated with a small LTR. Our results show that HFV can use a classic retroviral integration process to enter the host cell genome and stress the importance of AHFV and the short LTRs in the establishment of the chronic state of infection.</p></div><div><p>Le rétrovirus HFV (human foamy virus) est le prototype de la famille des <em>Spumavirinae</em>. Nous avons étudié par la technique PCR inverse les sites d'intégration de ce virus dans un système de cellules murines D152 BALB/c chroniquement infectées. Nos résultats montrent qu'HFV s'intègre preférentiellement dans les régions d'ADN cellulaire transcriptionnellement actives ou hautement répétées et induit la formation d'une répétition de 4 bp à ses extrémités. La présence de deletions spécifiques dans la région codante du transactivateur viral Bell et dans les LTR ayant été préalablement décrites, nous les avons recherchées parmi les formes intégrées d'HFV. Cette analyse révèle que dans notre système, le virus défectif ΔHFV est la forme majoritairement intégrée et qu'il est toujours associé avec la forme LTR la plus courte. Ces résultats suggèrent que le virus HFV peut s'intégrer dans le génome cellulaire selon le mécanisme décrit pour les autres rétrovirus. La présence de formes ΔHFV et LTR courte pourrait jouer un rôle dans l'établissement ou le maintien de la persistance virale.</p></div>","PeriodicalId":77352,"journal":{"name":"Research in virology","volume":"149 6","pages":"Pages 393-401"},"PeriodicalIF":0.0,"publicationDate":"1998-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0923-2516(99)80007-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20828459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}