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Viral Strain (viral + strain)
Selected AbstractsQuasispecies analysis of novel HIV-1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG,JOURNAL OF MEDICAL VIROLOGY, Issue 9 2007Rebecca L.R. Powell Abstract HIV-1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV-1 infections in Cameroon and is widespread across West and West-Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of pol (HXB2 location 2,612,4,159) and the entire env gene (HXB2 location 6,202,9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West-Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV-1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270,1285, 2007. © Wiley-Liss, Inc. [source] Impact of human coronavirus infections in otherwise healthy children who attended an emergency department,JOURNAL OF MEDICAL VIROLOGY, Issue 12 2006Susanna Esposito Abstract This prospective clinical and virological study of 2,060 otherwise healthy children aged <15 years of age (1,112 males; mean age,±,SD, 3.46,±,3.30 years) who attended the Emergency Department of Milan University's Institute of Pediatrics because of an acute disease excluding trauma during the winter season 2003,2004 was designed to compare the prevalence and clinical importance of human coronaviruses (HCoVs) in children. Real-time polymerase chain reaction (PCR) in nasopharyngeal aspirates revealed HCoV infection in 79 cases (3.8%): 33 HCoV-229E (1.6%), 13 HCoV-NL63 (0.6%), 11 HCoV-OC43 (0.5%), none HCoV-HKU1 genotype A, and 22 (1.1%) co-detections of a HCoV and another respiratory virus. The HCoVs were identified mainly in children with upper respiratory tract infection; there was no significant difference in clinical presentation between single HCoV infections and HCoV co-infections. Diagnostic methods were used in a limited number of patients, and the therapy prescribed and clinical outcomes were similar regardless of the viral strain. There were a few cases of other members of the households of HCoV-positive children falling ill during the 5,7 days following enrollment. These findings suggest that HCoV-229E and HCoV-OC43 have a limited clinical and socioeconomic impact on otherwise healthy children and their household contacts, and the HCoV-NL63 identified recently does not seem to be any different. The quantitative and qualitative role of HCoV-HKU1 genotype A is apparently very marginal. J. Med. Virol. 78:1609,1615, 2006. © 2006 Wiley-Liss, Inc. [source] Comparative analysis of NK/T-cell lymphoma and peripheral T-cell lymphoma in Korea: Clinicopathological correlations and analysis of EBV strain type and 30-bp deletion variant LMP1PATHOLOGY INTERNATIONAL, Issue 11 2003Ji Eun Kim Natural killer/T-cell lymphoma (NKTL) and peripheral T-cell lymphomas (PTCL) are prevalent in the Asian population and exhibit a high association with the Epstein,Barr virus (EBV). Moreover, differentiation of these two groups is often difficult and problematic. We investigated 35 cases of NKTL (22 nasal cases and 13 extranasal cases) and 30 cases of PTCL in terms of their clinical features, immunohistology, EBV positivity, EBV strain-type polymorphism and latent membrane protein 1 (LMP1) deletion variant distribution. Eighteen cases (82%) of nasal NKTL and seven (54%) of extranasal NKTL showed EBV positivity by EBV in situ hybridization. Fifteen cases (50%) of PTCL revealed EBV positivity. EBV strain type A was predominant in NKTL (18:5), and EBV strain types A and B were distributed evenly in PTCL (6:6). EBV-positive patients had significantly shorter survival than EBV-negative patients (P < 0.05), and EBV positivity correlated with advanced clinical stage (P < 0.05). Patients harboring type A EBV showed slightly poorer prognoses than those having type B, though it was not obviously statistically different (P = 0.07). The LMP1 deletion variant was prevalent in both NKTL (three wild-type LMP1, 15 deletion variants) and PTCL (three wild-type LMP1, eight deletion variants, two coexistent forms) patients, but did not have prognostic impact. Our results indicate that EBV acts as a negative prognostic factor in NKTL and PTCL, and that the intrinsic properties of a specific viral strain might influence the clinical behavior of these diseases. [source] Nail Matrix Arrest Following Hand-Foot-Mouth Disease: A Report of Five ChildrenPEDIATRIC DERMATOLOGY, Issue 1 2000Gina C. Clementz B.S. Nail matrix arrest has been associated with a variety of drug exposures and systemic illnesses, including infections, and may result in a variety of changes, including transverse ridging (Beau's lines) and nail shedding (onychomadesis). The association of HFMD with Beau's lines and onychomadesis has not been reported previously. Five children, ages 22 months,4 years, presented with Beau's lines and/or onychomadesis following physician-diagnosed HFMD by 3,8 weeks. Three of the five patients experienced fever with HFMD, and none had a history of nail trauma, periungual dermatitis, periungual vesicular lesions, or a significant medication intake history. All patients experienced HFMD within 4 weeks of one another, and all resided in the suburbs of the Chicago metropolitan area. In all patients the nail changes were temporary with spontaneous normal regrowth. The mechanism of the nail matrix arrest is unclear, but the timing and geographic clustering of the patients suggests an epidemic caused by the same viral strain. [source] Naturally occurring dominant resistance mutations to hepatitis C virus protease and polymerase inhibitors in treatment-naïve patients,,§HEPATOLOGY, Issue 6 2008Thomas Kuntzen Resistance mutations to hepatitis C virus (HCV) nonstructural protein 3 (NS3) protease inhibitors in <1% of the viral quasispecies may still allow >1000-fold viral load reductions upon treatment, consistent with their reported reduced replicative fitness in vitro. Recently, however, an R155K protease mutation was reported as the dominant quasispecies in a treatment-naïve individual, raising concerns about possible full drug resistance. To investigate the prevalence of dominant resistance mutations against specifically targeted antiviral therapy for HCV (STAT-C) in the population, we analyzed HCV genome sequences from 507 treatment-naïve patients infected with HCV genotype 1 from the United States, Germany, and Switzerland. Phylogenetic sequence analysis and viral load data were used to identify the possible spread of replication-competent, drug-resistant viral strains in the population and to infer the consequences of these mutations upon viral replication in vivo. Mutations described to confer resistance to the protease inhibitors Telaprevir, BILN2061, ITMN-191, SCH6 and Boceprevir; the NS5B polymerase inhibitor AG-021541; and to the NS4A antagonist ACH-806 were observed mostly as sporadic, unrelated cases, at frequencies between 0.3% and 2.8% in the population, including two patients with possible multidrug resistance. Collectively, however, 8.6% of the patients infected with genotype 1a and 1.4% of those infected with genotype 1b carried at least one dominant resistance mutation. Viral loads were high in the majority of these patients, suggesting that drug-resistant viral strains might achieve replication levels comparable to nonresistant viruses in vivo. Conclusion: Naturally occurring dominant STAT-C resistance mutations are common in treatment-naïve patients infected with HCV genotype 1. Their influence on treatment outcome should further be characterized to evaluate possible benefits of drug resistance testing for individual tailoring of drug combinations when treatment options are limited due to previous nonresponse to peginterferon and ribavirin. (HEPATOLOGY 2008;48:1769,1778.) [source] Synthesis and antiviral activity of new benzothiadiazine dioxide derivativesJOURNAL OF HETEROCYCLIC CHEMISTRY, Issue 5 2004Annalisa Tait A series of 2,1,3- and 1,2,4-benzothiadiazine derivatives were synthesized by alkylation via Mitsunobu reaction and evaluated for their antiviral activity against ADV, HHV-6, Cox-B5 and H-CMV. Most of them were active at micromolar level against one or more viral strains. All the molecules studied are poorly cytotoxic (maximum non toxic concentrations were >25,M), except one compound that presents a higher cytotoxicity (maximum non toxic concentration was 6 ,M). [source] Cauliflower mosaic virus: still in the newsMOLECULAR PLANT PATHOLOGY, Issue 6 2002Muriel Haas SUMMARY Taxonomic relationship:Cauliflower mosaic virus (CaMV) is the type member of the Caulimovirus genus in the Caulimoviridae family, which comprises five other genera. CaMV replicates its DNA genome by reverse transcription of a pregenomic RNA and thus belongs to the pararetrovirus supergroup, which includes the Hepadnaviridae family infecting vertebrates. Physical properties:, Virions are non-enveloped isometric particles, 53 nm in diameter (Fig. 1). They are constituted by 420 capsid protein subunits organized following T= 7 icosahedral symmetry (Cheng, R.H., Olson, N.H. and Baker, T.S. (1992) Cauliflower mosaic virus: a 420 subunit (T= 7), multilayer structure. Virology, 16, 655,668). The genome consists of a double-stranded circular DNA of approximately 8000 bp that is embedded in the inner surface of the capsid. Figure 1. Electron micrograph of CaMV virions. Courtesy of J. Menissier de Murcia, Ecole Supérieure de Biotechnologie de Strasbourg. Viral proteins: The CaMV genome encodes six proteins, a cell-to-cell movement protein (P1), two aphid transmission factors (P2 and P3), the precursor of the capsid proteins (P4), a polyprotein precursor of proteinase, reverse transcriptase and ribonuclease H (P5) and an inclusion body protein/translation transactivator (P6). Hosts: The host range of CaMV is limited to plants of the Cruciferae family, i.e. Brassicae species and Arabidopsis thaliana, but some viral strains can also infect solanaceous plants. In nature, CaMV is transmitted by aphids in a non-circulative manner. [source] Quantifying Viral Propagation in Vitro: Toward a Method for Characterization of Complex PhenotypesBIOTECHNOLOGY PROGRESS, Issue 6 2001Karen A. Duca For a eukaryotic virus to successfully infect and propagate in cultured cells several events must occur: the virion must identify and bind to its cellular receptor, become internalized, uncoat, synthesize viral proteins, replicate its genome, assemble progeny virions, and exit the host cell. While these events are taking place, intrinsic host defenses activate in order to defeat the virus, e.g., activation of the interferon system, induction of apoptosis, and attempted elicitation of immune responses via chemokine and cytokine production. As a first step in developing an imaging methodology to facilitate direct observation of such complex host/virus dynamics, we have designed an immunofluorescence-based system that extends the traditional plaque assay, permitting simultaneous quantification of the rate of viral spread, as indicated by the presence of a labeled viral protein, and cell death in vitro, as indicated by cell loss. We propose that our propagation and cell death profiles serve as phenotypic read-outs, complementing genetic analysis of viral strains. As our virus/host system we used vesicular stomatitis virus (VSV) propagating in hamster kidney epithelial (BHK-21) and murine astrocytoma (DBT) cell lines. Viral propagation and death profiles were strikingly different in these two cell lines, displaying both very different initial titer and cell age effects. The rate of viral spread and cell death tracked reliably in both cell lines. In BHK-21 cells, the rate of viral propagation, as well as maximal spread, was relatively insensitive to initial titer and was roughly linear over several days. In contrast, viral plaque expansion in DBT cells was contained early in the infections with high titers, while low titer infections spread in a manner similar to the BHK-21 cells. The effect of cell age on infection spread was negligible in BHK-21 cells but not in DBTs. Neither of these effects was clearly observed by plaque assay. [source] | |||||||||||||