Swine Flu "Crowding Out" Seasonal Flu?

[Puppycow]

Can one strain of flu "crowd out" others?
I had thought that the presence of one strain would have no effect on the prevalence of others, but apparently this might not be true.

Swine Flu Means Killer Winter Influenza May Not Come

Dec. 17 (Bloomberg) -- Seasonal flu, which annually kills 30,000 Americans 65 and over, may not appear in the U.S. for the first time in more than 40 years, crowded out by the swine flu pandemic and mass vaccination campaigns.

Seasonal strains are almost nonexistent in reports from countries where swine flu, or H1N1, has taken hold. In the U.S. and Europe, 99 percent of influenza cases tested last week were H1N1, according to government reports. Seasonal versions of virus that usually arrive in December and peak in February may not emerge at all, said Marc Lipsitch, a flu tracker at the Harvard School of Public Health, in Boston.

 

[Mongrel]

People are more aware of the precautions they need to take and have a higher likelihood of stay at home when they're infected.

I'd like to know what the seasonal strain is though, does H1N1 offer any form of immunity to it?

 

[Puppycow]

People are more aware of the precautions they need to take and have a higher likelihood of stay at home when they're infected.

But that wouldn't explain why 99% of cases are the new strain of H1N1, would it? It might result in a lower overall rate of flu, but would not change the ratio of new H1N1 to seasonal flu.

 

[kellyb]

This is to be expected:
http://biomicro.sdstate.edu/WangX/Micr425/Pathogenesis/Influenza_A.pdf

The appearance of a new HA in each pandemic virus typically
marks the dominance of the new virus and the disappearance
of the previous one.

I'd like to know what the seasonal strain is though, does H1N1 offer any form of immunity to it?

There are a few seasonal strains, but the one that caused the greatest number of illnesses was was an "old" H1N1, too. ...

(going back to the 2002 Hilleman PDF)

The pandemic of 1918–1919
was caused by an H1N1 virus, the origin of which is now
being explored (see Section 7.2). According to Scholtissek
et al. [26], the 1947 pandemic H2N2 virus was derived by
reassortment of H1N1 with an unidentified virus (probably
avian) in which new H2, N2, PB1 (see [27]) and PA genes
were acquired. The 1968 pandemic H3N2 virus was derived
through reassortment exchange of the H3 component for the
H2 of the parent H2N2 virus. The reappearance and worldwide
spread of virus subtype H1N1, which was the cause for
the “Russian pandemic” virus of 1977, 20 years following
its disappearance after 1957, is considered to be both aberrant
and remarkable [28,29]. Genetic analyses showed the
1977 Russian isolate [28,29] to be of near genetic identity
with the H1N1 viruses that were circulating in 1950. This
indicates that the virus had been preserved at some undefined
location, probably in frozen storage [28]. The “Russian
pandemic”, as might be expected, was benign and the
disease was restricted mostly to persons who were born after
the late 1950s. This H1N1 subtype, once extinguished
but reintroduced in 1977, now co-circulates with the 1968
H3N2 virus, at the expense of the world population.

 

[Skeptic Ginger]

There are various reasons for one strain of flu to 'drive out' another and some unknown factors as well.

First, speculation we'll only see the 2009H1N1 this winter is just that, absolute pure speculation. It's common for multiple strains to circulate at the same time.

But a single strain that is highly infectious does indeed eventually overtake other circulating strains. There is reason to think that at least temporarily one infulenza infection confers general influenza immunity, even if brief.

Or, it could simply be that when the host cells are occupied with an infection, they are not open to additional invasion.

Except we know that isn't true. Influenza commonly 'shifts' genetically because 2 strains infecting the same cell exchange gene segments which split into 9 sections inside the cell before re-assembling into a single genome before dispersal into the host and the environment.

What is likely happening is the more prolific replicator (the one with little host resistance) is just that, a more prolific replicator. More virus particles to spread simply outnumber the less prolific strain.