INFLUENZA RESERVOIRS AND REASSORTMENT
The reservoir for influenza is wild, migratory waterfowl. They carry influenza virus in their gastrointestinal tracts and
serve as a natural reservoir for periodic outbreaks in people. New H1N1 is a quadruple reassorted virus that has gene sequences
derived from Eurasian swine, classic swine, people, and birds. And even though it is H1N1 and our immune system recognizes
its two major antigenic constituents—hemagglutinin and neuraminidase—antibodies to the recently circulating seasonal H1N1
virus offer no or little protection. A substantial variation and mutational rate in the H1 portion has occurred—up to 20 amino
acids are different.
THE ROLE OF PIGS IN THE EPIDEMIOLOGY AND SPREAD OF INFLUENZA
Pigs are a good intermediate host to condition influenza viruses to exist in people. Influenza virus is indigenous to waterfowl,
and waterfowl interact with domesticated fowl and transmit the virus. Bird-adapted influenza has specific conformational epitopes
to bind to host membranes, and the virus particularly likes alpha 2,3-linked sialic acid receptors to bind hemagglutinin.
This preference is bad for birds, but people have few alpha 2,3 sialic acid receptors in their respiratory epithelium. The
human upper airways (nose, trachea, major bronchi) contain alpha 2,6 sialic acid receptors for hemagglutinin, so people are
relatively immune to bird influenza. Unfortunately, pigs express both alpha 2,3 and alpha 2,6 sialic acid receptors in their
respiratory and gastrointestinal tracts, so pigs are an intermediate host in which bird-adapted and human-adapted viruses
can coexist. The intermixing of these viruses often occurs in pigs, and epidemics often arise, which appears to be the case
with the current H1N1 epidemic.
People do have alpha 2, 3 sialic acid-galactose linkages in their lower respiratory apparatus. So if an avian influenza virus
passes through the upper airways, it has ample opportunity to cause severe disease in people.
The good news for people is that new H1N1 has low virulence potential. It does not appear to be any more virulent than the
typical seasonal influenza that we have been exposed to for the last several decades. It can injure a subset of the population
and cause death, but it lacks many of the virulence factors mentioned above. The bad news is that H1N1 is highly transmissible
and is approaching transmission rates similar to that of wild-type seasonal influenza, and people have no preexisting immunity,
so all are susceptible.
What keeps virologists up at night is the possibility of a viral reassortment leading to an H5N1-H1N1 hybrid that is highly
virulent and highly transmissible. If a virus with a 70% mortality rate infects 30% of the world's population in a year, a
population die-off would occur.
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