36 research outputs found

    Additional file 1: of Molecular epidemiology of hepatitis C infections in Ningxia, China: genotype, phylogeny and mutation analysis

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    Supplementary information 1. Section 1: Introduction to HIV sentinel surveillance system. Section 2: Inclusion criteria of screened population. Supplementary information 2. Section 1: Sequence of NS5B and Core. Section 2: Measurement of agreement. Table S1: Comparing HCV genotyping results between the Core and NS5B regions. Supplementary information 3. Table S2: NS5B and Core region-specific primers. Supplementary information 4: Figure S1. The circular phylogenetic tree based on the Core sequences. (DOCX 545 kb

    Sequence analysis of 2-LTR circle junction from selected patients in Group A and B.

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    <p>The circle junction, 3′U5 and 5′U3 were aligned and numbered against HXB2. PCR products amplified from samples at week 0 and 4 were cloned and sequenced. Sequences for patients from group A are above the line while those from group B are under the line.</p

    The patients' HIV-1 RNA loads, CD4 cell counts, and ART.

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    a<p>Viral load was measured by the Amplicor HIV-1 monitor ultrasensitive Method (Roche), with a detection limit of 40 copies/ml of plasma.</p

    Correlation analysis for the change rates of 2-LTR.

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    <p>Relationships between baseline parameters and the later 2-LTR change rates were shown in the left panel, and the correlations between later change rates were shown in the right panel. Inside each panel, the correlations between the rate of changes in 2-LTR and the baseline or the change rate in plasma viral load, the total CD4<sup>+</sup>, memory (RO<sup>+</sup>) (mCD4) and naïve (RA<sup>+</sup>) CD4<sup>+</sup> (nCD4) T cell count for the 12 patients in Group A were shown. Rate of 2-LTR increase or decrease was indicated as below.</p

    Linear regression analysis on the decay rate of the total HIV DNA.

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    <p>During the first 12 weeks of treatment, each patient in Group A (A) and Group B (B) was analyzed, as well as the averages for the two groups (C). Three patients (p5, p7 and p9) in Group A and two (p17 and p18) in Group B did not have applicable decay rates (<i>t</i><sub>1/2 </sub><i>na</i>) and were therefore not included in the calculation of average shown in panel C.</p

    D5 Fab footprints on the surface of the EV71 particles.

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    <p><b>(A-B)</b> Overall and expanded views of the D5 Fab footprints on the F-particle. The surface of the EV71 F-particle is shown as a stereographic projection, in which the polar angles θ and ɸ represent latitude and longitude, respectively. The D5 Fab footprints are indicated by red contour lines. The border of one VP2 (VP0)/VP3/VP1 protomer is outlined by black line. The locations of the 2-fold, 3-fold and 5-fold icosahedral symmetry axes are indicated as black ovals, triangles, and pentagons, respectively. In the expanded view, the amino acid residues of EV71 are denoted. The VP1, VP2 (VP0) and VP3 surfaces are shown in light blue, light green and pink, respectively. <b>(C-D)</b> Overall and expanded views of the D5 Fab footprints on the E-particle.</p

    Single intranasal immunization with chimpanzee adenovirus-based vaccine induces sustained and protective immunity against MERS-CoV infection

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    The recently identified Middle East Respiratory Syndrome Coronavirus (MERS-CoV) causes severe and fatal acute respiratory illness in humans. However, no approved prophylactic and therapeutic interventions are currently available. The MERS-CoV envelope spike protein serves as a crucial target for neutralizing antibodies and vaccine development, as it plays a critical role in mediating viral entry through interactions with the cellular receptor, dipeptidyl peptidase 4 (DPP4). Here, we constructed a recombinant rare serotype of the chimpanzee adenovirus 68 (AdC68) that expresses full-length MERS-CoV S protein (AdC68-S). Single intranasal immunization with AdC68-S induced robust and sustained neutralizing antibody and T cell responses in BALB/c mice. In a human DPP4 knock-in (hDPP4-KI) mouse model, it completely protected against lethal challenge with a mouse-adapted MERS-CoV (MERS-CoV-MA). Passive transfer of immune sera to naïve hDPP4-KI mice also provided survival advantages from lethal MERS-CoV-MA challenge. Analysis of sera absorption and isolated monoclonal antibodies from immunized mice demonstrated that the potent and broad neutralizing activity was largely attributed to antibodies targeting the receptor binding domain (RBD) of the S protein. These results show that AdC68-S can induce protective immune responses in mice and represent a promising candidate for further development against MERS-CoV infection in both dromedaries and humans.</p

    Cryo-EM maps of different EV71 particles or VLP in complex with D5 Fab or intact IgG.

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    <p><b>(A)</b> F-particle in complex with Fab. One icosahedral asymmetric unit of the capsid is indicated by a black triangle. <b>(B)</b> F-particle in complex with IgG. The color bar labels the corresponding radius from the center of the sphere (unit in Ã…). <b>(C)</b> E-particle in complex with Fab. <b>(D)</b> VLP in complex with IgG. The Fab components of the complexes are rendered in green to blue color. In the IgG bound complexes (F-particle-IgG and VLP-IgG), the density of the Fc region of the antibody could not be resolved owning to its extremely dynamic nature. <b>(E)</b> F-particle-Fab map with fitted models of six adjacent protomers around the 2-fold axis. The Fab densities were removed. VP1, VP2 (VP0) and VP3 structures and densities are shown in blue, green and red, respectively. Same color schema was followed throughout. Positions of the 2-fold, 3-fold and 5-fold icosahedral symmetry axes are indicated as grey oval, triangles, and pentagons, respectively. <b>(F)</b> The segmented density of the VP1 compact region from the F-particle-Fab map with the fitted model. <b>(G)</b> Expanded view of a representative portion of the map and model displayed in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005454#ppat.1005454.g001" target="_blank">Fig 1F</a>.</p
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