Biomolecular pathogenicity H1N1 virus

Swine influenza (swine flu) that desebabkan by pathogenic H1N1 virus has properties similar to bird flu (avian influenza). The nature of pathogenicity caused by H1N1 and H5N1 viruses are very complex that includes inflammation (inflammation) due to cytokines, apoptosis (cell death), and oxidative damage due to increased ROS (Reactive Oxygen Stress). Pathogenicity is a biomolecular process through signal transduction pathways within host cells. Tranduksi path signals that influence the pathogenicity of H1N1 virus in the form of NF-kB (Nuclear Factor Kappa B) and MAPK (Mitogen Activated Protein Kinases).

NF-kB is a transcription factor slah one type contained in the form of homodimer or heterodimer (Pande & Ramos, 2003). Transcription factors are located in the cell cytoplasm in the form of a bond with a specific protein IKB (Inhibitory Kappa B) in an inactive form. This transcription factor has a role in cell transformation, tumor growth, apoptosis, differentiation of immune cells, and also regulate viral gene transcription. NF-kB can be activated by several factors, namely TNF-α (Tumor Necrois Factor α), IL-1 (Interleukin 1), lipopolysaccharide, Nitric Oxyde, and ROS. These factors will activate the receptors that are sensitive to stress, then will activate the signal transduction pathway of NF-kB through a variety of protein kinases.

 Based on the picture above, the mechanism of activation of NF-kB (Rel protein and P50) is started when the pengaktivan factor attached to the receptor. After the signal at the receptor, a protein IKK (Inhibitory Kinases Beta Kappa) will phosphorylate proteins IkBα. Next IkBα will experience ubiquitasi and degradation by the proteasome. While NF-kB (Rel protein and P50) will be towards the nucleus of the cell (nucleus) and bind to coactivator and RNA polymerase, and then be attached to DNA for gene transcription (Brasier, 2006; Gilmore, 2006; Perkins, 2007).

The result of the gene transcription of inflammatory mediator production in the form arakrin-autocrine which activates inflammatory cells and occurs Cytokin Storm (Hurricane Cytokines). Cytokin Storm causes severe inflammation in the lung patients. In addition, cytokines also cause an increase in ROS that is followed by apoptosis or cell death.