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Results: 5

1.
FIG. 3.

FIG. 3. From: Macaque Proteome Response to Highly Pathogenic Avian Influenza and 1918 Reassortant Influenza Virus Infections .

Heat map of Z-scores of spectral counts for the 400 increased proteins, organized into eight clusters by using the K-means algorithm. The eight clusters are color coded relative to the condition(s) in which proteins were most highly expressed. The number of proteins within a cluster is located to the left of the cluster bar.

Joseph N. Brown, et al. J Virol. 2010 November;84(22):12058-12068.
2.
FIG. 5.

FIG. 5. From: Macaque Proteome Response to Highly Pathogenic Avian Influenza and 1918 Reassortant Influenza Virus Infections .

Influenza virus infection induces proteins involved in several areas of the immune response. Proteins are color coded relative to the cluster to which they belong (Fig. 3). White proteins are proteins that were either not observed or not differentially expressed during infection. A large number of RNA binding proteins that function in recognizing viral nucleic acids and initiating a response were induced primarily during HPAI infection. Gray boxes indicate a functionally related class of proteins (to distinguish them from a subcellular localization compartment).

Joseph N. Brown, et al. J Virol. 2010 November;84(22):12058-12068.
3.
FIG. 2.

FIG. 2. From: Macaque Proteome Response to Highly Pathogenic Avian Influenza and 1918 Reassortant Influenza Virus Infections .

Distinct patterns of increased protein abundance in different viral infections. (A) Box plots indicate the interquartile ranges of Z-scores of spectral counts and whiskers designate the minimum and maximum values for the 400 proteins that increased during viral infection. (B to H) Relative levels of abundance for the 400 proteins were binned, based on Z-score of the spectral count, and are depicted in frequency histograms. Protein abundance was quantified for day 2 p.i. (B to E) and day 7 p.i. (F to H) in the control, Tx91, 1918/Tx, and HPAI groups, respectively.

Joseph N. Brown, et al. J Virol. 2010 November;84(22):12058-12068.
4.
FIG. 4.

FIG. 4. From: Macaque Proteome Response to Highly Pathogenic Avian Influenza and 1918 Reassortant Influenza Virus Infections .

Linear regression of median Z-scores of spectral counts for proteins within individual clusters relative to pathology score following viral infection. Regression lines are color coded to indicate the representative cluster from Fig. 3 and as shown at the top left corner of each graph. Box plots represent interquartile ranges, and whiskers designate minimum and maximum values. The Pearson product-moment correlation coefficent values (r) are indicated on the upper right corner of each plot. The day 7 groups received the greatest pathology score during all infections. Tx91 scores were between 1 and 2, the 1918/Tx group received scores between 3 and 4, and HPAI caused the greatest damage, with scores between 5 and 6.

Joseph N. Brown, et al. J Virol. 2010 November;84(22):12058-12068.
5.
FIG. 1.

FIG. 1. From: Macaque Proteome Response to Highly Pathogenic Avian Influenza and 1918 Reassortant Influenza Virus Infections .

Overview of cellular and viral peptide observations. Fourteen animals were inoculated with HPAI, 1918/Tx, or Tx91, or mock infected, in groups of two animals per sacrifice day, and the pulmonary proteome response was evaluated on days 2 and 7 p.i. (A) Total peptides and proteins observed and how those peptides and proteins were attributed to either the host or different viruses. A single common peptide was detected in HPAI and 1918/Tx infections. (B) Viral proteins were detected exclusively during HPAI and 1918/Tx infections. Gray indicates the absence of detection. Ctrl, control. (C) Venn diagram comparing macaque peptides identified in the current study (Brown et al.; red) and those from the previous Baas et al. study (yellow), reanalyzed with the macaque protein collection list. While the current study identified 35,202 unique cellular peptides, Baas et al. (1) identified 15,390.

Joseph N. Brown, et al. J Virol. 2010 November;84(22):12058-12068.

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