What the latest science says about New Zealand’s Covid-19 policy

[Wandering Eyes]

Simon Thornley, Gerhard Sundborn

4 July 2020

With a smattering of new cases emerging from returnees in hotels prompting both sides of the house to double down on our tight quarantine the key question is coming into focus: where does our nation go from here?

Sir Peter Gluckman, Rob Fyfe and Helen Clark have recommended starting to reopen our borders. On the other hand, both Dr Ashley Bloomfield and PM Jacinda Ardern have talked about being prepared for further lockdown-like restrictions, with tight border control. Victoria, a state with similar characteristics to New Zealand, has had a recent spike of cases and has decided to enforce local lockdowns, which is a worrying prospect. Which road is best? To open up or to hunker down? Can science help us with this decision?

The latest information on the virus can help us decide which of the Covid-19 roads is best. Its relevance is underlined by the fact it also helps explain why some of the predictions about the fatalities from the virus in New Zealand were 500 to 3,600 times greater than what is happening.

The assumption until now has been that we were all sitting ducks and that we were — and remain — completely at the mercy of the virus. And that assumption underlies the current anxiety about reopening without an effective vaccine to protect us.

The latest science reveals the battle our bodies have had with this virus —and it indicates we are not as defenseless as we might think. Our blood has two major weapons in the fight against viruses:  B and T cells, which together are called lymphocytes or pus cells. B cells are like missile factories, making antibodies that lock onto free virus in the body. Most tests to see if anyone has been exposed to the virus look for these antibody B cells.

T cells are more like hitmen who destroy host cells already infected with the virus. T cells are less commonly considered in testing for previous exposure. A feature of Covid-19 is that levels of both these cells (lymphocytes) are unusually low in severe cases most likely because they have been working overtime to fight infection.

A recent study out of the Karolinska Institute in Sweden confirms this idea. A team of researchers tested the blood of 203 people, some of whom had had Covid-19 (by genetic test), looking for evidence that the immune system of these subjects had seen the virus. Among healthy blood donors, who had never tested positive for Covid-19, the researchers found that 4/31 (13%) had antibodies but 9/31 (29%) had positive T cell responses to the virus. That indicates that many more people had been exposed to the virus (and not fallen ill) than indicated by B cell tests alone.

In family members of people with Covid-19, 17/28 (60%) had positive antibodies (B cells), but almost all (26/28; 93%) had positive T cell tests. Almost all genetic test positive cases of Covid-19 had both immune markers. Some may debate the importance of the T cell tests and whether they confer immunity. The researchers are guarded, but indicate that such responses are similar to the immune response of vaccines for other viruses.

What relevance does this knowledge have to us here in New Zealand, considering who to let in and out of the border? As indicated above, it explains why modelling of Covid-19 was so staggeringly inaccurate. Many more of us than we ever knew have microscopic missiles and hitmen in our system on our side. This helps explain why the predicted flood of cases to our intensive care wards and hospitals never eventuated. And this helps us be more realistic about the risk posed by the virus.

What else can we learn from this study? A critical question now is how immune is our population? We have previously summarised the rates of Covid-19 antibodies measured in populations around the world ranges from 0.5 to 26%. The Swedish researchers have shown that the proportion of people in the general population who are likely to be protected from Covid-19 is actually about three times the proportion who have Covid-19 antibodies. This would mean that likely protection from the virus is far more widespread than the antibody surveys indicate. In New Zealand, we are still waiting for any results from antibody tests. The media has reported that tests have been carried out but no data is being made available. Surely the results of this study, even if preliminary, are of critical importance?

So, how does this help us address the border question? If we really want to know what our risk is posed by the virus, we need to take a keen interest in our population’s immune status, as the Swedes have done. The findings of the Covid-19 virus in France and Spain well before the ‘official epidemic’ hit means that many of us have likely encountered the virus before without even knowing it.

Now, in many countries, deaths with the virus are waning, even if in some countries, cases are increasing. The lack of large second waves as Europe is progressively opening up gives us some confidence that immunity to the virus is much more widespread than we initially thought. The debate about our supposed exalted status having ‘eliminated’ the virus is becoming less relevant as evidence accumulates that many of us have already seen the virus, become immune and moved on.

Some commentators have highlighted the paradox of being a Covid-free cul-de-sac. It is our view that we need to adjust to living with the virus and accept that further cases are likely to occur. If our level of natural protection is much higher than thought we need to urgently reconsider whether the elimination strategy, its implications for further lockdown, and an unknowable period of continued border closure, is really worth the financial pain it will continue to inflict. And let’s not forget Covid-19 is not entirely unique. We already accept the risks of living with a number of coronaviruses that have similar characteristics to Covid-19, including: HKU1, 229E, OC43 and NL63.

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