How the flu season turned deadly – are NHS vaccine failures to blame?

This year’s flu epidemic is far from over, but the vaccine race has already been lost.

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Influenza comes around every year. So why is this year’s flu season proving much worse than expected, with millions infected and at least 120 people already dead?

The disease is caused by influenza viruses of which four groups exist (types A,B, C and D). The first three infect people, and the first two may cause serious disease. This year, there have been significant numbers of both A and B type infections. The A type has acquired the name Aussie flu because it first started infecting large numbers of people Down Under in June 2017. The current B-type is commonly referred to as Japanese flu, or Yamagata type, based on its initial identification in the 1990s. The reality is that Aussie flu is unlikely to have originated in Australia and Japanese flu has been in circulation around the world for decades. 

Different flu viruses are distinguished from each other in several ways. Each virus contains eight strands of ribonucleic acid, their genome, which encode the proteins they need to replicate and spread within their hosts. Two of these proteins, the so-called H and N proteins, sit at the surface of the virus and allow invasion of host cells where they replicate. As they sit at the virus surface they are vulnerable to attack by our immune system.

But if our immune system has never previously seen particular variants of the H and N proteins, it can’t respond quickly enough to prevent infection. Once we’ve seen those antigens, however, we produce antibodies that can neutralise that particular virus and prevent reinfection. 

This is how vaccines work, too. We can inject people with harmless dead viruses, which still trigger an immune response that prevents subsequent infections. There are at least 18 different types of H and 11 different N proteins in circulation; when multiple viruses meet they can mix and match their different versions. We classify flu viruses based on their H and N types. H5N1 is the hypervirulent bird flu virus, H1N1 the swine flu of 2009, while today’s Aussie type is H3N2. These broad types further mutate as viruses evolve – antibodies generated against a parental type lose efficiency with time. The World Health Organisation monitors circulating viruses so that it can recommend which types to include in the next vaccines.

The B type viruses are less diverse than the A types. This year, however, vaccine manufacturers were advised to prioritise the so-called Victoria B type, rather than the Yamagata type, so even inoculated people have little protection. What is more, the H3N2 virus that went into vaccine production, involving injection into millions of fertilised chicken eggs, mutated in one way, while the circulating virus mutated another way, so antibodies to the vaccine aren’t as effective as hoped. It takes many months to create enough vaccine to inoculate populations en masse; the race is lost this year. 

The NHS is enduring criticism for deciding against a vaccine containing both common B variants of the virus, and certainly fewer infections would be occurring had the more complex (and more expensive) vaccine been used. But affordability is crucial. Global health authorities were condemned for the expensive overreaction to the 2009 swine flu outbreak, which proved to be unexpectedly mild.

However, that virus was of the H1N1 type, another derivative of which had killed up to 50 million in the great flu pandemic of 1918, hence the panic. The decision to intervene was the correct one.

Two bird flu viruses (H5N1 and H7N9) in current circulation continue to cause great concern. H5N1 kills up to half of those who contract it. To date, these viruses have fortunately proven difficult to transmit between people. Cases have been largely confined to Asian poultry workers exposed to high viral doses in birds. 

Yet vaccines against flu are complex. Drugs have proven difficult to find. Tamiflu, for example, inhibits the viruses’ crucial N protein but it turns out to be of only marginal use. If taken within two days of infection, it can diminish symptoms a little and accelerate recovery by around half a day. Although Tamiflu is not a foolproof cure, its benefits remain significant for some of the millions infected and sales have been dramatic this year.

The flu season is far from over and we should deploy all means available against it . Even the flawed vaccine will offer some protection, and simple public health measures such as hand-washing and the use of disposable tissues are critical.

The real problems begin when the virus provokes inflammation in the lungs, or viral damage allows secondary bacterial infection in our lungs, causing pneumonia. At this point, medical intervention is required. Otherwise, staying at home helps us recover and minimises our risk to others. Simple analgesics such as paracetamol and ibuprofen can ameliorate the aches and pains associated with the virus. This year’s flu season is bad, but it could be much worse. 

Michael Barrett is a professor of biochemical parasitology at the Institute of Infection, Immunity and Inflammation at the University of Glasgow

This article appears in the 26 January 2018 issue of the New Statesman, How women took power