Results: 4

1.
Figure 2

Figure 2. From: Whole genome characterization of non-tissue culture adapted HRSV strains in severely infected children.

Nucleotide alignment and comparative analysis of the Gene Junction (Gene Start - Intergenic Region -Gene End) in strains from hospitalized patients. Genes identification is denoted before their corresponding GS and GE. Similarly corresponding intergenic region positions have also been denoted. An overlap instead of intergenic region is present between M2-L genes. *Clinical strains having difference in the sequences are shown in the table. Thus rest of the sequences matched RSV-1.

Rajni Kumaria, et al. Virol J. 2011;8:372-372.
2.
Figure 3

Figure 3. From: Whole genome characterization of non-tissue culture adapted HRSV strains in severely infected children.

Phylogenetic relationship of 14 clinical strains of HRSVA from patients and 4 representative strains from the Genbank based on whole genome nucleotide sequence. Hospitalized patient strains have been indicated with prefix RSV. The reference strains are indicated by their Genbank accession number. The evolutionary history was inferred using the Neighbour-Joining method. The bootstrap values below 80% are not shown. The scale bar indicates 1% nucleotide sequence divergence. The HRSVB type (Accession number AY353550) has been used as the root.

Rajni Kumaria, et al. Virol J. 2011;8:372-372.
3.
Figure 4

Figure 4. From: Whole genome characterization of non-tissue culture adapted HRSV strains in severely infected children.

Immunofluorescence examination of cells infected with the HRSV clinical strains. (A) Differential infection levels were observed with clinical isolates as compared to lab strain RSVA2. More HEp 2 cells were seen infected with RSVA2, when compared with clinical isolate RSV-8 and RSV-13 between 2 and 4 days post infection. (B). Clinical isolates (b) RSV-13, (c) RSV-8 and (d) RSV-6 also produced similar structures like (a) RSVA2. HEp2 cells were infected with RSVA2 and clincial isolates were stained with anti-RSV antibodies and visualized by immunofluorescence using secondary antibodies conjugated to FITC. Examination of the stained cells at a focal plane showing mainly the i) interior and ii) surface of infected cells are shown in each case. The presence of large cytoplasmic inclusion bodies highlighted by white arrow and presence of structures that resembled the VF are highlighted by star.

Rajni Kumaria, et al. Virol J. 2011;8:372-372.
4.
Figure 1

Figure 1. From: Whole genome characterization of non-tissue culture adapted HRSV strains in severely infected children.

Schematic representation of HRSVA whole genome amplification of HRSV-1 by Reverse transcriptase (RT)-PCR. A. The viral genes with leader at 5' end and trailer at 3' end are schematically presented in the 15,222 bases HRSVA2 genome. The thin lines given below represents the approximate size of each of the fifteen amplified fragments (F) and the position of the respective fragments on the genome. The lines are to the approximate scale. B. All the PCR amplified fragments were run by electrophoresis on 1% agarose gel in TAE buffer and visualized by gel red. The fragments are numbered from F1-F15 and their positions on gel are indicated by arrows. Negative control (NC) is the PCR reaction with water in place of sample. The DNA ladder (L) has highest band position at 3 Kbp and lowest band at 100 bp. The size of fifteen fragments is as F 1 = 1215 bp, F2 = 1343 bp, F3 = 1417 bp, F4 = 1301 bp, F5 = 1373 bp, F6 = 1328 bp, F7 = 1324 bp, F8 = 1392 bp, F9 = 1435 bp, F10 = 1328 bp, F11 = 1403 bp, F12 = 1360 bp, F13 = 1200 bp, F14 = 1334 bp, F15 = 1168 bp.

Rajni Kumaria, et al. Virol J. 2011;8:372-372.

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