NATHAN BARTLETT says Australia has recorded 10.4 million cases of COVID-19 during the pandemic, the majority of them this year. This is undoubtedly an underestimate, as not everyone tests for covid or reports positive results.
The latest blood donation study looked at the percentage of people who had antibodies against SARS-CoV-2, the virus that causes COVID-19. It turned out that at least two-thirds of Australians are infected.
That leaves about a third of the population still to have covid.
I am such a “novid” – despite multiple confirmed exposures to COVID-19 during the pandemic, I have yet to have symptoms and test positive.
So what do we know about novids?
Some people who claim they’ve never had COVID-19 may be surprised to learn they have virus-targeted antibodies in their blood that could only have been generated by infection.
The reliance on home rapid antigen tests (RATs), which are less sensitive than PCR tests, will contribute to many people’s failure to definitively determine whether they have COVID-19.
Under ideal testing conditions, the best tests detect SARS-CoV-2 infection in more than 95 percent of cases. However, in the real world, the detection rate is lower.
If you have mild symptoms that don’t last long, you’re less likely to need repeated testing and you may miss your window to get a positive result. Thus, some COVID-19 cases will escape detection by RATs.
At this point, it is important to distinguish between being infected with SARS-CoV-2 and experiencing the disease (COVID-19) caused by this infection. You can be infected without experiencing any COVID-19 symptoms – this is called an asymptomatic infection.
It is unclear what proportion of Omicron subvariant cases are asymptomatic. At the beginning of the pandemic, one in six infected people was asymptomatic and with Omicron this can now rise to 50 percent or more.
Thus, many novices will be infected with SARS-CoV-2, have generated antibodies against the virus, but will not have experienced or noticed any COVID-19 symptoms at that time, will not have been tested and will not have been kept informed of their infection status (and or they were unknowingly transmitting the virus).
What role does the immune system play?
Everyone’s immune system is different. How your immune system responds to a particular infection is influenced by many factors, including your genes, gender, age, diet, sleep patterns, stress levels, history of other infections and illnesses, medications, vaccination status, and level of exposure to viruses.
So are some people less likely to get COVID-19 because of the strength of their immune systems?
The status of our immune system at any given time will affect our susceptibility to disease. So it’s not surprising that the people most susceptible to severe COVID-19 are those with less effective immunity because they have chronic illnesses, have a suppressed immune system or are elderly.
The other important variable is the virus. SARS-CoV-2 continues to evolve with new Omicron subvariants continuing to emerge. This will affect how the virus interacts with us and the relative impact of various factors that influence our immune protection and susceptibility.
SARS-CoV-2 has proven to be particularly adept at evolving to generate viral variants that can evade our established immune protection. In addition, our immune protection is not stable and will begin to decline after a few months if not stimulated by vaccination or infection.
Do my genes protect me?
Let’s look at something relatively stable: your genes.
Scientists looking for associations between specific genes and diseases can conduct genome-wide association studies. The effect of individual genetic variations on disease risk is usually very small, so identifying them requires large numbers of people and consideration of other variables that make us all different.
In one such study, researchers compared the genomes of nearly 50,000 people with COVID-19 to the genomes of two million people with no known infection.
They identified regions in the genome (loci) associated with contracting COVID-19 and other genetic regions associated with disease severity. So this is evidence that, like many other diseases, certain genes modify the risk of COVID-19.
While association is not causation, genomic studies like this point us in a direction to better understand the biology of COVID-19 to answer questions such as who is at risk of severe disease or long-term COVID and to advance the development of new therapies. support to prevent these outcomes.
Another study identified a small number of critically ill COVID-19 patients with rare gene variants. These may be directly related to deficient antiviral immunity.
So for a very small number of people it seems that their genes make them more susceptible to covid. But for the vast majority of people, the picture is much more complicated.
SARS-CoV-2 is not the only respiratory coronavirus that regularly infects humans. Four others – 229E, HKU-1, OC43 and NL63 – bear some resemblance to SARS-CoV-2.
Most adults would be infected by these viruses several times throughout their lives. This raises the possibility that immunity generated from lifetime and/or recent exposure to these other coronaviruses may generate immunity that provides some protection against SARS-CoV-2 infection and symptomatic COVID-19.
More research is needed to better understand this, but the existing evidence is compelling and certainly plausible.
The bottom line is that there are many reasons why people who socialize and inevitably interact with people with COVID-19 think they’ve never had covid themselves. For most novices, it’s a combination of vaccination, leveraging a healthy immune system, wise decisions and luck that has kept them covid-free so far.
Of course, the luck eventually runs out, so enjoy your novid status while you still can.
Nathan Bartlett, Associate Professor, School of Biomedical Sciences and Pharmacy, University of Newcastle. This article was republished from The Conversation.
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