Five years ago, COVID was all we could think about. Today, we’d rather forget about lockdowns, testing queues and social distancing. But the virus that sparked the pandemic, SARS-CoV-2, is still circulating.

Most people who get COVID today will experience only a mild illness. But some people are still at risk of severe illness and are more likely to be hospitalised with COVID. This includes older people, those who are immunocompromised by conditions such as cancer, and people with other health conditions such as diabetes.

Outcomes also tend to be more severe in those who experience social inequities such as homelessness. In the United Kingdom, people living in the 20% most deprived areas have double chance of being hospitalised from infectious diseases than those in the least deprived areas.

How many cases and hospitalisations?

In Australia, 58,000 COVID cases have been reported so far in 2025. However, testing rates have declined and not all positive cases are reported to the government, so case numbers in the community are likely much higher.

Latest data from FluCan, a network of 14 hospitals, found 781 people were hospitalised for COVID complications in the first three months of the year. This “sentinel surveillance” data gives a snapshot from a handful of hospitals, so the actual number of hospitalisations across Australia is expected to be much higher.

While deaths are lower than previous years, 289 people died from COVID-related respiratory infections in the first two months of the year.

What can we expect as we head into winter?

We often see an increase in respiratory infections in winter.

However, COVID peaks aren’t just necessarily seasonal. Over the past few years, peaks have tended to appear around every six months.

What are the most common COVID symptoms?

Typical early symptoms of COVID included fever, cough, sore throat, runny nose and shortness of breath. These have remained the most common COVID symptoms across the multiple variant waves.

Early in the pandemic, we realised COVID caused a unique symptom called anosmia – the changed sense of taste or smell. Anosmia lasts about a week and in some cases can last longer. Anosmia was more frequently reported from infections due to the ancestral, Gamma, and Delta variants but not for the Omicron variant, which emerged in 2021.

However, loss of smell still seems to be associated with some newer variants. A recent French study found anosmia was more frequently reported in people with JN.1.

But the researchers didn’t find any differences for other COVID symptoms between older and newer variants.

Should you bother doing a test?

Yes. Testing is particularly important if you experience COVID-like symptoms or were recently exposed to someone with COVID and are at high-risk of severe COVID. You might require timely treatment.

If you are at risk of severe COVID, you can see a doctor or visit a clinic with point-of-care testing services to access confirmatory PCR (polymerase chain reaction) testing.

Rapid antigen tests (RATs) approved by Australia’s regulator are also still available for personal use.

But a negative RAT doesn’t mean that you don’t have COVID – especially if you are symptomatic.

If you do test positive, while you don’t have to isolate, it’s best to stay at home.

If you do leave the house while experiencing COVID symptoms, minimise the spread to others by wearing a well-fitted mask, avoiding public places such as hospitals and avoiding contact with those at higher risk of severe COVID.

How long does COVID last these days?

In most people with mild to moderate COVID, it can last 7–10 days.

Symptomatic people can spread the infection to others from about 48 hours before you develop symptoms to about ten days after developing symptoms. Few people are infectious beyond that.

But symptoms can persist in more severe cases for longer.

A UK study which tracked the persistence of symptoms in 5,000 health-care workers found symptoms were less likely to last for more than 12 weeks in subsequent infections.

General fatigue, for example, was reported in 17.3% of people after the first infection compared with 12.8% after the second infection and 10.8% following the third infection.

Unvaccinated people also had more persistent symptoms.

Vaccinated people who catch COVID tend to present with milder disease and recover faster. This may be because vaccination prevents over-activation of the innate immune response.

Vaccination remains the best way to prevent COVID

Vaccination against COVID continues to be one of the most effective ways to prevent COVID and protect against it. Data from Europe’s most recent winter, which is yet to be peer reviewed, reports COVID vaccines were 66% effective at preventing symptomatic, confirmed COVID cases.

Most people in Australia have had at least one dose of the COVID vaccine. But if you haven’t, people over 18 years of age are recommended to have a COVID vaccine.

Boosters are available for adults over 18 years of age. If you don’t have any underlying immune issues, you’re eligible to receive a funded dose every 12 months.

Boosters are recommended for adults 65–74 years every 12 months and for those over 75 years every six months.

Adults over 18 years who are at higher risk because of weaker immune systems are recommended to get a COVID vaccine every 12 months and are eligible every six months.

Check your status and eligibility using this booster eligibility tool and you can access your vaccine history here.

A new review of more than 4,300 studies found full vaccination before a SARS-CoV-2 infection could reduce the risk of long COVID by 27% relative to no vaccination for the general adult population.

With ongoing circulation of COVID, hybrid immunity from natural infection supplemented with booster vaccination can help prevent large-scale COVID waves.

Meru Sheel, Associate Professor and Epidemiologist, Infectious Diseases, Immunisation and Emergencies (IDIE) Group, Sydney School of Public Health, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

The common cold sore virus, which is often caught in childhood, usually stays in the body for life – quietly dormant in the nerves. Now and then, things like stress, illness or injury can trigger it, bringing on a cold sore in some people. But this same virus – called herpes simplex virus type 1 – may also play an important role in something far more serious: Alzheimer’s disease.

Over 30 years ago, my colleagues and I made a surprising discovery. We found that this cold sore virus can be present in the brains of older people. It was the first clear sign that a virus could be quietly living in the brain, which was long thought to be completely germ-free – protected by the so-called “blood-brain barrier”.

Then we discovered something even more striking. People who have a certain version of a gene (called APOE-e4) that increases their risk of Alzheimer’s, and who have been infected with this virus, have a risk that is many times greater.

To investigate further, we studied brain cells that we infected with the virus. They produced the same abnormal proteins (amyloid and tau) found in the brains of people with Alzheimer’s.

We believe that the virus stays mainly dormant in the body for years – possibly decades. But later in life, as the immune system gets weaker, it can enter the brain and reactivate there. When it does, it will damage brain cells and trigger inflammation. Over time, repeated flare-ups could gradually cause the kind of damage that leads to Alzheimer’s in some people.

We later found the virus’s DNA inside the sticky clumps of these proteins, which are found in the brains of Alzheimer’s patients. Even more encouragingly, antiviral treatments reduced this damage in the lab, suggesting that drugs might one day help to slow or even prevent the disease.

Large population studies by others found that severe infections, specifically with the cold sore virus, was a strong predictor of Alzheimer’s, and that specific antiviral treatment reduced the risk.

Our research didn’t stop there. We wondered if other viruses that lie dormant in the body might have similar effects – such as the one responsible for chickenpox and shingles.

Shingles vaccine offers another clue

When we studied health records from hundreds of thousands of people in the UK, we saw something interesting. People who had shingles had only a slightly higher risk of developing dementia. Yet those who had the shingles vaccine were less likely to develop dementia at all.

A new Stanford University-led study gave similar results.

This supported our long-held proposal that preventing common infections could lower the risk of Alzheimer’s. Consistently, studies by others showed that infections were indeed a risk and that some other vaccines were protective against Alzheimer’s.

We then explored how risk factors for Alzheimer’s such as infections and head injuries could trigger the hidden virus in the brain.

Using an advanced 3D model of the brain with a dormant herpes infection, we found that when we introduced other infections or simulated a brain injury, the cold sore virus reactivated and caused damage similar to that seen in Alzheimer’s. But when we used a treatment to reduce inflammation, the virus stayed inactive, and the damage didn’t happen.

All of this suggests that the virus that causes cold sores could be an important contributor to Alzheimer’s, especially in people with certain genetic risk factors. It also opens the door to possible new ways of preventing the disease, such as vaccines or antiviral treatments that stop the virus from waking up and harming the brain.

What began as a link between cold sores and memory loss has grown into a much bigger story – one that may help us understand, and eventually reduce, the risk of one of the most feared diseases of our time.

Ruth Itzhaki, Professor Emeritus of Molecular Neurobiology at the University of Manchester and a Visiting Professorial Fellow, University of Oxford

This article is republished from The Conversation under a Creative Commons license. Read the original article.

We’ve all heard it before: eat your five-a-day, and try to get some exercise. It’s advice that’s simple in theory, yet in practice, not everyone is able to follow it. So what’s standing in the way?

Our research examined this question in depth. Using data from UK adults over the age of 50, we explored how socioeconomic status affects the likelihood of meeting the World Health Organization’s recommendations for physical activity and diet. These guidelines include at least 150 minutes of moderate-intensity (or 75 minutes of vigorous-intensity) physical activity per week and a daily intake of at least five portions of fruit and vegetables.

What we found points to a clear and concerning disparity. Wealthier older adults are nearly twice as likely to meet both exercise and dietary recommendations compared to their less affluent peers. And perhaps even more striking, those who don’t meet these health guidelines are significantly more likely to suffer from depression.

We analysed survey responses from more than 3,000 adults aged 50 to 90, using data from the English Longitudinal Study of Ageing. While nearly 70% of participants reported doing some form of physical activity, the data revealed a sharp wealth divide.

Adults in the highest wealth quintile (the top 20%) were almost twice as likely to be physically active as those in the lowest quintile. A similar pattern emerged for diet. Over 70% of those in the wealthiest group reported meeting the five-a-day guideline, compared to just over 40% in the lowest income bracket.

This matters, because not meeting government guidelines for physical activity and diet can have serious long-term health consequences. Regular exercise is known to increase HDL (or “good”) cholesterol, improve cardiovascular health, and reduce the risk of chronic conditions like type 2 diabetes, heart disease, and some cancers.

It also benefits brain health by lowering inflammation and even promoting the growth of new brain cells. Similarly, diets rich in fibre, vitamins, and antioxidants – found in fruits and vegetables – are associated with lower the risks of disease and cognitive decline, including conditions like Alzheimer’s.

Depression disparity

But the impact isn’t just physical. Our research also explored links between lifestyle and mental health. Around 19% of participants met the criteria for clinical depression, with the highest risk found among women, people living alone, smokers and those with lower incomes.

Alarmingly, rates of depression were nearly three times higher among those in the lowest wealth quintile (32.6% were depressed) compared to those in the highest (11.1%).

Lifestyle clearly played a role in depression levels. Among inactive participants, 30% reported symptoms of depression – more than double the rate seen in those who were physically active (13.7%). Likewise, those who didn’t meet the five-a-day guideline had a depression rate of 23.4%, compared to 15.7% among those who did.

These results suggest that staying physically active and eating well not only improves physical health but may also play a protective role in mental wellbeing. Yet not everyone has equal access to the resources, time, or environments that support healthy living. There is also the role of social isolation as a compounding factor.

Social disconnection is strongly linked to both poor physical and mental health, including depression and even increased mortality risk. Physical activity programmes that also offer social interaction – such as walking groups or community exercise classes – may provide even greater benefits.

Healthy ageing for everyone

The evidence shows that health disparities in later life are deeply tied to wealth and socioeconomic status. This means that addressing them requires more than encouraging personal responsibility – it calls for policy action.

Financial barriers to healthy food and physical activity need to be tackled through targeted programmes, subsidies and infrastructure investments. Making healthy options accessible and affordable – especially for those in lower-income groups – will benefit people and reduce strain on healthcare systems.

As populations continue to age, promoting health in later life is a public health priority. But that effort will only succeed if it recognises – and works to reduce – the inequalities that hold people back from living healthy, fulfilling lives.

Simon Evans, Lecturer in Neuroscience, School of Psychology, University of Surrey

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Arthritis – an umbrella term for around 100 conditions that damage the joints – affects 4.1 million Australians. This is expected to rise by 31% to 5.4 million by 2040 and cost the Australian health-care system an estimated $12 billion each year.

The two most common types, osteoarthritis and rheumatoid arthritis, can both cause joint pain, swelling and stiffness. Both are more common in women. Neither can be cured.

But their causes, risk factors and treatments are different – here’s what you need to know.

What is osteoarthritis?

Osteoarthritis is the most common form of arthritis. It affects 2.1 million Australians, mostly older people. About a third of Australians aged 75 and older have the condition.

It can affect any joint but is most common in the knees, hips, fingers, thumbs and big toes.

The main symptom is pain, especially during movement. Other symptoms may include swelling, stiffness and changes to the shape of joints.

The main risk factors are ageing and obesity, as well as previous injuries or surgery. For osteoarthritis in the hands, genetics also play a big role.

Signs of osteoarthritis can appear on knee scans from around age 45 and become more common with age.

However, this type of arthritis not simply the “wear and tear” of ageing. Osteoarthritis is a complex disease that affects the whole joint. This includes the cartilage (“shock-absorbing” connective tissue protecting your bones), bones, ligaments (connective tissue holding bones and body parts in place) and joint lining.

How is it diagnosed?

Diagnosis is based on symptoms (such as pain and restricted movement) and a physical exam.

The disease generally worsens over time and cannot be reversed. But the severity of damage does not always correlate with pain levels.

For this reason, x-rays and MRI scans are usually unhelpful. Some people with early osteoarthritis experience severe pain, but the damage won’t show up on a scan. Others with advanced and visible osteoarthritis may have few symptoms or none at all.

What about rheumatoid arthritis?

Unlike osteoarthritis, rheumatoid arthritis is an autoimmune disease. This means the immune system attacks the joint lining, causing inflammation and damage.

Common symptoms include pain, joint swelling and stiffness, especially in the morning.

Rheumatoid arthritis is less common than osteoarthritis, affecting around 514,000 Australians. It mostly impacts the wrists and small joints in the hands and feet, though larger joints such as the elbows, shoulders, knees and ankles can also be involved.

It can also affect other organs, including the skin, lungs, eyes, heart and blood vessels. Fortunately, disease outside the joint has become less common in recent years, likely due to better and earlier treatment.

Rheumatoid arthritis often develops earlier than osteoarthritis but can occur at any age. Onset is most frequent in those aged 35–64. Smoking increases your risk.

How is it diagnosed?

As with osteoarthritis, your doctor will diagnose rheumatoid arthritis based on your symptoms and a physical exam.

Some other tests can be useful. Blood tests may pick up specific antibodies that indicate rheumatoid arthritis, although you can still have the condition with negative results.

X-rays may also reveal joint damage if the disease is advanced. If there is uncertainty, an ultrasound or MRI can help detect inflammation.

How is osteoarthritis treated?

No treatment can stop osteoarthritis progressing. However many people manage their symptoms well with advice from their doctor and self-care. Exercise, weight management and pain medicines can help.

Exercise has been shown to be safe for osteoarthritis of the knee, hip and hand. Many types of exercise are effective at reducing pain, so you can choose what suits you best.

For knee osteoarthritis, managing weight through diet and/or exercise is strongly recommended. This may be because it reduces pressure on the joint or because losing weight can reduce inflammation. Anti-obesity medicines may also reduce pain.

Topical and oral anti-inflammatories are usually recommended to manage pain. However, opioids (such as tramadol or oxycodone) are not, due to their risks and limited evidence they help.

In some cases antidepressants such as duloxetine may also be considered as a treatment for pain though, again, evidence they help is limited.

What about rheumatoid arthritis?

Treatments for rheumatoid arthritis focus on preventing joint damage and reducing inflammation.

It’s essential to get an early referral to a rheumatologist, so that treatment with medication – called “disease-modifying anti-rheumatic drugs” – can begin quickly.

These medicines suppress the immune system to stop inflammation and prevent damage to the joint.

With no cure, the overall goal is to achieve remission (where the disease is inactive) or get symptoms under control.

Advances in treatment

There is an increasing interest in prevention for both types of arthritis.

A large international clinical trial is currently investigating whether a diet and exercise program can prevent knee osteoarthritis in those with higher risk – in this case, women who are overweight and obese.

For those already affected, new medicines in early-stage clinical trials show promise in reducing pain and improving function.

There is also hope for rheumatoid arthritis with Australian researchers developing a new immunotherapy. This treatment aims to reprogram the immune system, similar to a vaccine, to help people achieve long-term remission without lifelong treatment.

Giovanni E. Ferreira, NHMRC Emerging Leader Research Fellow, Institute of Musculoskeletal Health, University of Sydney and Rachelle Buchbinder, Professor of Clinical Epidemiology and Rheumatologist, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.