Mechanisms of Viral Defence, Infection and Recovery
A Virus is an ultramicroscopic infectious agent.
The H1N1 A 2009 (Swine Flu) is a novel strain of the influenza virus.
Viruses cannot reproduce on their own. To reproduce, a virus must bind to a living cell inside some organism, insert its genetic material into that “host” cell, and take over the cell’s reproductive “machinery.” The virus then makes copies of itself – maybe hundreds of thousands. Sooner or later, this kills the infected cell – causing the virus to leave the cell and cause illness. Once out of the host cell new viruses start the process over, attacking other cells until the immune system, and or medication controls their activity and replication. The H1N1 Influenza A virus once inside a cell can produce approximately 100,000 new virions in about 8 hours.
A person with H1N1 (swine flu) appears to be able to spread it to others for one (and possibly two) days before symptoms first occur. This is because a person infected with swine flu virus may have it present in their nose, mouth and throat for one to two days before they get symptoms. Spread of infection can continue for up to 7 days after symptoms first appear. Children, especially younger children, might potentially be contagious for up to 10 days.The virus replicates in the cells lining the nose and are coughed or sneezed out in droplets of mucous. A single sneeze can contain 40,000 droplets, a single one may be all that is required to cause infection.
Viruses Must First Circumvent The Mucosal Immune System.
Mucosal immunity is important for long-term protection and forms a first line of defence against mucosally transmitted pathogens such as influenza. Mucosal defence against pathogens consists of both innate barriers, such as mucous, epithelium, and innate immune mechanisms, and adaptive host immunity. The latter consists predominately, at mucosal surfaces of specialised thymic derived cells called CD4+ T cells, secretory immunoglobulin A (SIgA), secretory immunoglobulin M (SIgM) and antigen-specific (memory primed) cytotoxic T-lymphocytes (CTLs). Although not confirmed SIgM may compensate for IgA deficiency in the gut and lungs.
If the infective assault on mucosal tissues is successful, by intracellular pathogens such as a virus it will result in the induction of cell-mediated immunity. This includes the production of CD4+ T helper-type 1 cells, as well as CD8+ cytotoxic T-lymphocytes. These responses are normally accompanied by the synthesis of secretory immunoglobulin A (SIgA) antibodies, which provide an important first line of defence against invasion into deeper tissues by these pathogens. It is possible to stimulate the B cells and plasma cells to increase production of SIgA and SIgM by using colostrum and Saccharomyces Boulrdii two natural agents of immune support.
The H1N1 Swine Flu virus is a novel strain of influenza. Existing vaccines against seasonal flu provide no protection, and there is currently no vaccine for this strain. A study at the U.S. Centres for Disease Control and Prevention published in May 2009 found that children had no preexisting immunity to the new strain but that adults, particularly those over 60, had some degree of immunity
Experts writing in the July New England Journal of Medicine note that “historically, pandemic viruses have evolved between seasons, and the current strain may become more severe or transmissible in the coming months.” The H1N1 swine flu variant may be prone to reassortment ( Reassortment is the mixing of the genetic material of two similar viruses that are infecting the same cell) and mutation. NEJM Influenza Centre contains further information of value.
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