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Scientists have just described a genetic quirk they observed amid cases in the Delta wave that ended New Zealand's elimination dream – but it's still unclear what this localised trait ever meant.
Stemming from a single incursion into our community last August – perhaps an infected person who flew from Sydney to Auckland's Crowne Plaza on August 7 - the outbreak changed everything for New Zealand's Covid-19 response.
By the time the outbreak was discovered on August 17, the country was already looking at a hidden iceberg of perhaps 800 to 1000 undetected community cases that had built up over a week of undetected spread.
These included dozens who were part of a Birkdale network, which centred around a household that was connected to a tradesman's business in Devonport.
There was also the super-spreader event at the Assembly of God church service in Māngere, attended by 500 mainly Pacific people, from where someone carrying the virus hopped on a plane to Wellington.
On August 18, the whole country woke to Level 4 restrictions, never to return again to Level 1.
The genome of the cases that seeded the church subcluster had a mutation, which allowed ESR scientists to track it in great detail.
Within two weeks, with daily case numbers seemingly peaking at just over 80 and a Wellington chain all but stamped out, scientists became hopeful the lockdown might be working.
The church subcluster itself had grown to around 330 cases but the rate was slowing – and when new daily cases fell below 20, a return to elimination appeared within reach.
Only, there was a picture of undetected transmission that we couldn't see – and it was already too late to have stopped Delta from taking root by spreading to larger, intergenerational households in Auckland.
When the city moved to Level 3 on September 22, some experts were left uneasy at the possibility Delta was being let out of its cage – but it was unlikely the virus could have been snuffed out completely anyway.
In a new study, published ahead of peer review, scientists have reconstructed the outbreak using data from more than 3800 genomes collected between mid-August and December 1.
This showed them that, not only did Delta manage to spread widely and quietly, but also that clusters appeared to die out – only to resurface again.
"We saw genomically-linked clusters seemingly go extinct, but then reappear weeks or even a month later," said study lead author Dr Jemma Geoghegan, a virologist at ESR and Otago University.
"This really highlighted the rate of undetected community transmission that was going on even quite early in the outbreak. Reported cases didn't necessarily reflect the level of infection."
ESR's bioinformatics and genomics lead Dr Joep de Ligt said the new analysis offered a fresh perspective on what the country was truly up against with Delta.
"During the immediate response we were identifying links to clusters and understanding undetected transmissions, now we take a step back to reflect on where Delta slipped through the lockdown net.
"Taking a look back allows us to see where our contact tracing and lockdown efforts did not work as intended and help us understand what improvements could be made."
Having a near complete picture of those early days of the outbreak, he said, provided a unique way to study these dynamics in far greater detail than other countries might have been able to.
Another intriguing aspect of the Delta saga was the emergence of genomes that began bearing a "deletion" of one of the proteins in the virus.
Otago University and ESR virologist Dr Jemma Geoghegan. Photo / Supplied
Before long, genomes with this trait appeared to dominate the samples they were sequencing, suggesting the virus had undergone a genetic shift once it arrived in New Zealand.
"Interestingly, similar deletions in this same gene have occurred numerous times in different regions and in outbreaks around the world," Geoghegan said, adding the same trend had occurred independently in New South Wales' Delta outbreak.
This genetic change seemed to impair the gene it involved, but, beyond that, its function was unclear.
"We don't think this gene is totally required for the virus, so the role of it isn't completely clear – but it seems like a common occurrence that the virus loses this protein made by this gene," Geoghegan said.
"We saw a very near-replacement with genomes possessing this deletion, which might suggest that it gives it some kind of advantage.
"But when we looked at the transmission rate between genomes that had the deletion and others that didn't, we didn't find any significant change.
"So, perhaps the replacement was more luck than advantage."
It might have also been a case of what's called the founder effect – where a selection of genetic patterns dominated most cases we could see, but didn't necessarily mean the virus had become more transmissible.
In any case, the picture was soon muddied when New Zealand effectively pivoted from elimination to suppression in early October.
Up until that point, genomic surveillance was used as a precision tool to help officials carefully untangle chains of transmission, and provide genetic proof to cases they'd been unable to link epidemiologically.
Geoghegan said this "track and trace" role quickly moved to one of population-level surveillance, with the proportion of cases sequenced falling from nearly 90 per cent to a third by the end of 2021.
Amid widespread Omicron, sequencing now targeted specific areas like hospitalisations, borders and representative community sampling.
As recently as last month, this surveillance was still picking up Delta cases – showing that chains of the deadlier variant were still lurking out there amid rampant Omicron.
"It's likely still there in the background," she said.
"Given its increased severity, I think it's still important to sequence enough cases that we can still detect it if it's hanging around."
