We’ve just survived flu season. And, many of us did just fine this year because we got the flu vaccine.

But, let’s take a step back from that statement. Because there is more to that equation than just getting the flu shot. Way more.

Let’s start with the idea that we rely on the CDC (Centers for Disease Control) guessing on the right virus model to employ each year. Which is a real problem when they guess wrong, like they did two years ago. Because getting a shot to deflect the wrong virus is almost akin to getting no shot at all. In the 2014/2015 flu season, the dominant H3 A strain had mutated after vaccine production began- and that antigenic drift meant the effectiveness ranged from 19 to 23% (both numbers have been reported)- the lowest effectiveness in a decade.

And, if you are like me, walking around with an impaired respiratory system, that’s a pretty bad situation for us.

So, it was great hearing that NIAID (National Institute of Allergy and Infectious Diseases) scientists determined that there are better antigens to examine as to whether we have adequate protection against flu.

For years, the marker of choice has been the cell-surface protein hemagglutinin to discern flu protection levels. Hemoagglutinin inhibition (HAI) has been the marker of choice (since way back in 1972) to discern that we are protected from a potential flu infection. The marker range of 18 to 36 seemed to afford a 50% protection level- except now, that level seems to be only providing some 40% protection against the virus. But, the measure of protection desired for a flu vaccine has been to develop an HAI that exceeds 40.

NIAID has determined that neuraminidase (that ‘ase’ ending tells you this is an enzyme) is a better choice to discern if we will develop a flu infection. This enzyme is what the flu virion uses to burrow its way out of the human cells, so that it can replicate itself in other cells around the body. Which means measuring antibodies to neuraminidase may better indicate if we are protected against the infection.

Drs. Matthew Memoli (lead author), Alison Han, Lindsay Czajkowski, Susan Reed, Rani Athotaa, Tyler Bristol, Sarah Fargis, Kyle Risos, John H. Powers, Richard T. Davey Jr., and Jeffery K. Taubenberger (all of NIAID) and Pamela A. Shaw (U of P) published their findings in mBio.

They contrast their ideas to the conventional concept that NAI (neuraminidase inhibition) correlates better with protective levels. Which means less severe infections, with fewer symptoms, shorter durations of viral shedding. The researchers used 65 healthy volunteers, who were inoculated with a 2009 A (H1N1) pandemic challenge virus. The group was divided into HAI titers exceeding 40 and those below. Those with the higher titers did not develop the disease (of mild or severe levels), but were symptomatic. Those with higher NAI were far less symptomatic.

But, the researchers note that monitoring NAI in conjunction with HAI yield even better information about patient condition.

Yet, it still does not help the CDC guess the right virus model- or that the virus not mutate after we begin vaccine production for the year.

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