anciendaze
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This report at Medical Express is much more solid research than the continuing stream of medical articles suggesting psychobabble may be effective in treating poorly defined conditions. The caution here is that it concerns in vitro studies. What it does show is that some infected cells with many copies of defective viral genomes can persist when apoptosis destroys other cells which have only copies of the reference viral genome.
This, in turn, points to a mechanism for prolonged immune activation following an acute viral infection. It also gives a plausible reason that testing for a particular viral sequence would fail to find these cells: surviving cells do not have the same genome as in the acute phase of viral infection.
One thing which surprised me here was that all the named viruses are single-strand RNA viruses, which are notoriously unstable. This has led researchers to concentrate on the acute disease phase and neglect possible chronic conditions resulting from these. The acute diseases can be lethal, and I believe one brother of mine died of HRSV in his first year of life.
Surviving infected cells avoid apoptosis and become strong stimulators of antiviral immune response. This could be the cause of persistent respiratory problems in patients who survive acute HRSV infection, since there are a lot of different respiratory viral infections possible, but would also offer some degree of immunity to similar viruses which might be lethal.
We are still a long way from application to human medical treatments, but the hypothesis of a chronic state of peculiar antiviral immune response following an acute viral infection with "flu-like symptoms" should not be dismissed as patient imagination.
I will also point out that major pandemics commonly involve more than one infectious agent. The virus for which the outbreak is blamed may only be one of several active in the patient population. Since HRSV was only discovered in infants in 1956 it is unlikely that anyone was looking for it in adults during the Asian flu epidemic of 1957, which was "the worst flu of my life". Because my brother had died of a characteristic infection just before the RSV virus was discovered, I could quite plausibly have been exposed prior to the time the Asian flu (H2N2) reached the U.S.
Incidentally, my father, who had survived the Spanish flu (H1N1) as an infant, was not affected by the Asian flu. Nor were several other family members alive at the time (1918). Those born too late to be exposed were strongly affected. He seems to have had a persistent antiviral response almost 40 years after exposure. Up until now this kind of thing has been hard to explain for viruses as changeable as influenza.
This, in turn, points to a mechanism for prolonged immune activation following an acute viral infection. It also gives a plausible reason that testing for a particular viral sequence would fail to find these cells: surviving cells do not have the same genome as in the acute phase of viral infection.
One thing which surprised me here was that all the named viruses are single-strand RNA viruses, which are notoriously unstable. This has led researchers to concentrate on the acute disease phase and neglect possible chronic conditions resulting from these. The acute diseases can be lethal, and I believe one brother of mine died of HRSV in his first year of life.
Surviving infected cells avoid apoptosis and become strong stimulators of antiviral immune response. This could be the cause of persistent respiratory problems in patients who survive acute HRSV infection, since there are a lot of different respiratory viral infections possible, but would also offer some degree of immunity to similar viruses which might be lethal.
We are still a long way from application to human medical treatments, but the hypothesis of a chronic state of peculiar antiviral immune response following an acute viral infection with "flu-like symptoms" should not be dismissed as patient imagination.
I will also point out that major pandemics commonly involve more than one infectious agent. The virus for which the outbreak is blamed may only be one of several active in the patient population. Since HRSV was only discovered in infants in 1956 it is unlikely that anyone was looking for it in adults during the Asian flu epidemic of 1957, which was "the worst flu of my life". Because my brother had died of a characteristic infection just before the RSV virus was discovered, I could quite plausibly have been exposed prior to the time the Asian flu (H2N2) reached the U.S.
Incidentally, my father, who had survived the Spanish flu (H1N1) as an infant, was not affected by the Asian flu. Nor were several other family members alive at the time (1918). Those born too late to be exposed were strongly affected. He seems to have had a persistent antiviral response almost 40 years after exposure. Up until now this kind of thing has been hard to explain for viruses as changeable as influenza.
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