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zoals gepost in ander topic
You may not know this, but all H1N1 flu's are descendants of the 1918 pandemic strain. The reason why the flu shot may or may not work, however, from year to year, is due to mutations. Therefore, there's no vaccine available for this current hybrid flu strain, and naturally, this is feeding the fear that millions of people will die before a vaccine can be made.
However, let me remind you of one very important fact here.
Just a couple of months ago, scientists concluded that the 1918 flu pandemic that killed between 50-100 million people worldwide in a matter of 18 months -- which all these worst case scenarios are built upon -- was NOT due to the flu itself!4
Instead, they discovered the real culprit was strep infections.People with influenza often get what is known as a "superinfection" with a bacterial agent. In 1918 it appears to have been Streptococcus pneumoniae. Since strep is much easier to treat than the flu using modern medicine, a new pandemic would likely be much less dire than it was in the early 20th century, the researchers concludedhttp://articles.mercola.c(...)04/29/Swine-Flu.aspxIncreased susceptibility for superinfection with Streptococcus pneumoniae during influenza virus infection is not caused by TLR7-mediated lymphopeniaOtto-von-Guericke University, Institute of Molecular and Clinical Immunology, Magdeburg, Germany.
Influenza A virus (IAV) causes respiratory tract infections leading to recurring epidemics with high rates of morbidity and mortality. In the past century IAV induced several world-wide pandemics, the most aggressive occurring in 1918 with a death toll of 20-50 million cases. However, infection with IAV alone is rarely fatal. Instead, death associated with IAV is usually mediated by superinfection with bacteria, mainly Streptococcus pneumoniae. The reasons for this increased susceptibility to bacterial superinfection have not been fully elucidated. We previously demonstrated that triggering of TLR7 causes immune incompetence in mice by induction of lymphopenia. IAV is recognized by TLR7 and infections can lead to lymphopenia. Since lymphocytes are critical to protect from S. pneumoniae it has long been speculated that IAV-induced lymphopenia might mediate increased susceptibility to superinfection. Here we show that sub-lethal pre-infections of mice with IAV-PR8/A/34 strongly increased their mortality in non-lethal SP infections, surprisingly despite the absence of detectable lymphopenia. In contrast to SP-infection alone co-infected animals were unable to control the exponential growth of SP. However, lymphopenia forced by TLR7-triggering or antibody-mediated neutropenia did not increase SP-susceptibility or compromise the ability to control SP growth. Thus, the immune-incompetence caused by transient lympho- or leukopenia is not sufficient to inhibit potent antibacterial responses of the host and mechanisms distinct from leukodepletion must account for increased bacterial superinfection during viral defence
http://www.mrwonkish.nl Eurocrisis, Documentaires, Economie