WHEN the Covid pandemic grounded planes, closed borders, and plunged whole swathes of the planet into months-long lockdowns and even longer periods of social distancing, there were plenty of warnings about unintended consequences.

Excess deaths would increase; they have. NHS backlogs for non-Covid care would spiral; they have.

Children would experience developmental problems as a result of socialisation; research has found that infants born during the pandemic score lower, on average, for motor function and communication skills.

READ MORE: Australia flu surge could be very bad news for the NHS 

Less talked about was the potential for the global pandemic response to disrupt other viruses in ways that we are only now beginning to realise.

Some of this was expected; but some of it has been peculiar, and surprising.

Australia's record-breaking influenza season is one of the headline examples.

After all but vanishing for two years, cases began surging two months earlier than normal, in April, and by the time infections peaked in mid-June they were running around three and a half times the five-year average for mid-August (when influenza usually peaks in the southern hemisphere).

The total number of cases reported up to the end of July, at 212,573 compares with 251,147 in the whole of 2017 - until now Australia's worst ever flu year.

Global responses to the pandemic resulted in significantly reduced social interactions and movement of people, disrupting the patterns of other seasonal viruses and in some cases the uptake of routine healthcare, such as childhood vaccinationsAustralia has experienced a rapid and very large surge in flu cases much earlier than normal (red), and well above the five-year average (yellow)

A sudden rebound in flu was anticipated given that Australia fully reopened its borders in February and two years of waning immunity inevitably gifted the virus ample opportunity to spread.

It remains to be seen whether the Australian experience is a bellwether for the UK's winter, but public health chiefs are spooked enough to be preparing for a potential onslaught from late September.

The only bright spot is that the impact of flu on hospitals and mortality has been lower than it might have been.

In 2017, there were 745 flu-related deaths Australia compared to 246 so far this year, suggesting that the form of the virus circulating back in 2017 was around three times more lethal.

The median age for the patients who have died is 81, although most infections were actually reported in children and teenagers.

Global responses to the pandemic resulted in significantly reduced social interactions and movement of people, disrupting the patterns of other seasonal viruses and in some cases the uptake of routine healthcare, such as childhood vaccinationsDespite the record-breaking surge in flu cases this summer, flu-related hospital admissions and deaths have not matched the levels seen in 2017

At its peak, around 400 Australians were in hospital with flu in 2017 compared to around 200 at the height of this year's flu season.

Less optimistically for frontline doctors already battling severe bed shortages on the NHS, however, is the fact that an average Australian flu season would tend to see only around 50-100 hospitalised due to the virus at any one time.

Back in the UK, scientists have also been getting to grips with some of the more anomalous viral consequences of the pandemic.

On Wednesday, the UK Health Security Agency announced an emergency rollout of polio boosters to children aged one to nine in London amid concerns that a strain of vaccine-derived poliovirus (VDPV) is transmitting - so far asymptomatically - in the capital.

It is not entirely unusual for surveillance to detect traces of VDPV in sewage - typically around one to three samples a year will test positive - but in most cases there is no evidence of spread.

READ MORE: 'Urgent' polio boosters for children aged one to nine amid concerns over virus spread in London

In the current outbreak, there is enough genetic similarity between several of the London samples (and samples found in Jerusalem and New York, where a 20-year-old man has been left paralysed) to indicate that the virus has mutated away from its innocuous vaccine form into a "neurovirulent" type which is transmissible and has the potential to cause paralysis, or even death.

If it seems confusing that a vaccine can (in very rare cases) morph into a potentially deadly virus, you need to understand that the vaccine concerned is the oral polio vaccine which contains a weakened, live strain of the virus and is given as droplets onto the tongue in countries such as Afghanistan and Pakistan where polio is still endemic.

This induces immunity in the gut, where poliovirus replicates, but also means that a vaccinated individual can excrete virus in their faeces which can then spread through contact with contaminated surfaces in much the same way as the winter-vomiting bug norovirus.

Overseas visitors to the UK can import it in this way, usually without causing any problems.

Global responses to the pandemic resulted in significantly reduced social interactions and movement of people, disrupting the patterns of other seasonal viruses and in some cases the uptake of routine healthcare, such as childhood vaccinationsEurope has been categorised as 'polio-free' since 2003

Exactly why the VDPV has become infectious this time is unclear, but one concern voiced by UKHSA scientists is that a dip in uptake for routine childhood immunisations in London during the pandemic "may be one of the factors".

To be fully protected, children should have had a three-jag primary course plus a booster, ideally before starting school, but it some of the London boroughs where the VDPV strain has been detected most coverage is just 54 per cent.

The race is now on to build up a wall of immunity to contain it in the capital.

READ MORE: The inside story of Scotland's child hepatitis outbreak 

Meanwhile, a mysterious, global outbreak of paediatric hepatitis has been linked - indirectly - to Covid.

Painstaking analysis, much of it by scientists in Scotland, has identified adeno-associated virus 2 (AAV2) as the likeliest culprit.

The sudden cluster of hepatitis cases coincided with an abnormal surge in adenovirus as Covid restrictions eased. AAV2 is a bystander virus; on its own it can lie dormant in cells for years, but once in contact with adenovirus becomes 'activated'.

Glasgow virologists found it in every one of the hepatitis youngsters they tested - but not at all in any of the healthy control children used for comparison.

linked -Global responses to the pandemic resulted in significantly reduced social interactions and movement of people, disrupting the patterns of other seasonal viruses and in some cases the uptake of routine healthcare, such as childhood vaccinationsThe surge in paediatric hepatitis cases closely overlapped with a surge in adenovirus in early 2022 which could 'trigger'AAV2

Scientists believe that the unique circumstances of the pandemic have not so much caused the outbreak, as uncovered a phenomenon that was already occurring undetected.

Unexplained paediatric hepatitis is not new - it's just that pre-pandemic cases occurred sporadically in a way that wouldn't raise alarm bells or prompt public health investigations.

But the sudden spike in adenovirus cases in a short period of time, just as a population (young children) with little or no immunity began socialising more, led to a clustering effect.

All of a sudden case rates per 100,000 were far above average compared to previous years and, for the first time, resources were targeted into unravelling the cause of this "mystery" hepatitis.

It is the first time AAV2 has been pinpointed as a potential cause of disease - although work is ongoing to confirm the hypothesis and understand better the mechanisms.

READ MORE: Major Scottish study casts doubt on claims that Covid infections caused diabetes spike in children 

Even a 20% spike in type 1 diabetes diagnoses among children under 14 during the pandemic - which largely pre-dated Covid infections in this age group - has been linked by scientists to reduced exposure to other viruses believed to have a protective effect against the onset of the disease.

The hypothesis ties in with evidence that new cases of type 1 diabetes peak annually, in February and September, in line with theories that seasonal viruses can trigger the disease by damaging the cells which produce insulin.

Studies of gut microbes suggest a "ying and yang interplay" where some viruses appear to defend against type 1 diabetes while others increase the risk.

As far as understanding the pandemic's non-Covid viral legacy goes, we may be just getting started.