Scope of respite care for the old people population

<div><p>The molecular pathogenesis of avian influenza infection varies greatly with individual bird species and virus strain. The molecular pathogenesis of the highly pathogenic avian influenza virus (HPAIV) or the low pathogenic avian influenza virus (LPAIV) infection in avian species remains poorly understood. Thus, global immune response of chickens infected with HPAI H5N1 (A/duck/India/02CA10/2011) and LPAI H9N2 (A/duck/India/249800/2010) viruses was studied using microarray to identify crucial host genetic components responsive to these infection. HPAI H5N1 virus induced excessive expression of type I IFNs (IFNA and IFNG), cytokines (IL1B, IL18, IL22, IL13, and IL12B), chemokines (CCL4, CCL19, CCL10, and CX3CL1) and IFN stimulated genes (OASL, MX1, RSAD2, IFITM5, IFIT5, GBP 1, and EIF2AK) in lung tissues. This dysregulation of host innate immune genes may be the critical determinant of the severity and the outcome of the influenza infection in chickens. In contrast, the expression levels of most of these genes was not induced in the lungs of LPAI H9N2 virus infected chickens. This study indicated the relationship between host immune genes and their roles in pathogenesis of HPAIV infection in chickens.</p></div

The host genes were involved in avian influenza virus replication in chicken lung tissues are shown along with fold change expression value.

<p>The host genes were involved in avian influenza virus replication in chicken lung tissues are shown along with fold change expression value.</p

IFN-stimulated genes were expressed in response to HPAIV H5N1 infection in chicken lung tissues.

<p>The IFN-stimulated genes, pro-inflammatory cytokines and chemokines were all upregulated in HPAIV H5N1 infected lung tissues of chicken.</p

Differentially expressed genes in response to infection with HPAIV H5N1 and LPAIV H9N2 virus.

<p>Differentially expressed genes in response to infection with HPAIV H5N1 and LPAIV H9N2 virus.</p

Significantly enriched Gene Ontology terms in response to HPAIV H5N1 infection.

<p>Significantly enriched Gene Ontology terms in response to HPAIV H5N1 infection.</p

KEGG pathways enriched in response to HPAIV H5N1 infection.

<p>Up regulated and down regulated genes differentially enriched in various pathways are shown.</p

Significantly enriched Gene Ontology terms in response to LPAIV H9N2 infection.

<p>Significantly enriched Gene Ontology terms in response to LPAIV H9N2 infection.</p