Category: 8. Health

Highlights:

• Human papillomaviruses, or HPVs, cause cutaneous and mucosal infections that may lead to cancer.
• To date, no antiviral treatment options exist for HPVs.
• Researchers have identified a promising new compound that inhibits cutaneous HPV.
• In lab studies, the compound inhibited viral replication genes in cutaneous HPVs without damaging host cells.

Washington, D.C.-Human papillomaviruses, or HPVs, can cause dangerous infections in the skin and mucous membranes and may lead to cancer. Vaccines that prevent mucosal HPV infections aren’t effective against cutaneous infections, which can cause serious diseases, particularly in immunocompromised people.

This week in Journal of Virology, researchers describe a small molecule compound, called NSC51349, that in lab tests has shown promise as an antiviral treatment against cutaneous HPVs. The compound blocks viral replication by targeting a critical protein, and the researchers found that it reduced viral load without harming host cells.

“The inhibitor may represent a new class of HPV-specific antiviral drugs with significant potential,” said molecular virologist and study leader Alla Piirsoo, Ph.D., at the University of Tartu, in Estonia. “Unlike [HPV] vaccines, which rely on the functioning immune system our strategy could benefit people with compromised immunity who currently have very limited therapeutic options.”

Researchers have identified hundreds of different types of HPVs. Though most infections remain harmless and asymptomatic, infections from high-risk HPVs can lead to cervical cancer and head and neck cancers. Others can cause skin lesions including macule and warts, and when combined with other carcinogens can lead to non-melanoma skin cancer. Existing vaccines that target high-risk types of mucosal HPVs are widely available, but these vaccines are ineffective against cutaneous HPV types.

A treatment for cutaneous HPV could help a broad patient population, said Piirsoo. “Such a drug could be especially beneficial for immunocompromised individuals, such as organ transplant recipients, patients undergoing immunosuppressive cancer therapy, HIV-positive individuals and people with rare genetic disorders.”

Piirsoo’s lab studies HPV replication and how it interacts with host cells, with a focus on identifying ways to inhibit viral activity that confer the least harm to the host. For the new work, the researchers used high-throughput screening to test more than 1,500 chemicals for their efficacy against HPV type 5, a cutaneous type of HPV that primarily affects epithelial skin cells and has been associated with increased risk of skin cancer.

They narrowed in on NSC51349, which in further tests inhibited viral replication of HPV 5 in U2OS cells, osteosarcoma cells often used in cancer research. Further analyses showed that the compound also disabled transcription from the viral genome. Models suggested that the compound worked primarily through mechanisms present in cutaneous HPV types, but not in mucosal ones. The team identified a second small molecule that inhibited both mucosal and cutaneous HPV types, but the compound proved toxic to host cells.

Subsequent tests showed that NSC51349 also inhibited 2 additional cutaneous types, HPV8 and HPV38. “The compound may have broad-spectrum activity against multiple cutaneous HPV types without harming host cells,” Piirsoo said.

Bolstered by these promising but early results, the researchers are now working to find the optimal concentration of the compound that inhibits viral replication without harming the host. They’re also planning animal testing, and “if the compound works in the animal model, it would be strong evidence that it could be developed into an effective antiviral treatment for HPVs,” Piirsoo said.

The odds of breast cancer in women aged under 55 years are reduced by treatment with unopposed estrogen hormone therapy (E-HT) vs no hormone therapy, according to a recent study published in The Lancet Oncology.¹

Differing risks based on hormone type

In comparison, the data found increased breast cancer risk in women treated with estrogen plus progestin hormone therapy (EP-HT) vs no hormone therapy. This highlighted different influences on breast cancer risk from 2 common types of hormone therapy, indicating potential guidelines for clinical recommendations about hormone therapy use in young women.¹

“Our study provides greater understanding of the risks associated with different types of hormone therapy, which we hope will help patients and their doctors develop more informed treatment plans,” said Katie O’Brien, PhD, lead author from the National Institute of Health’s National Institute of Environmental Health Sciences (NIEHS).¹

Hormone therapy use in premenopausal women

The trial was conducted to assess the link between exogenous hormones and breast cancer in young women.² According to investigators, this population may undergo hormone therapy as management of premenopausal symptoms or following gynecological surgery.

Women with hysterectomy are the only population recommended to receive E-HT because of the link with uterine cancer risk.¹ However, oophorectomy may lead to E-HT or EP-HT use, alongside menopause symptom onset.

Global data and risk assessment

Data was obtained from 10 to 13 prospective cohorts in North America, Asia, Europe, and Australia. Participants underwent follow-up to identify breast cancer incidence while aged under 55 years.²

Hazard ratios (HRs), were determined through cohort-stratified, multivariable-adjusted Cox proportional hazards regression. Additionally, investigators evaluated risk differences based on cumulative risk until age 55 years.²

Hormone therapy usage and outcomes

There were 459,476 women aged 16 to 54 years included in the analysis. Young-onset breast cancer was reported in 2% of these patients across a median of 7.8 years. Hormone therapy was reported in 15%, with EP-HT reported in 6% and E-HT in 5%. These were the 2 most common types of hormone therapy used in the study cohort.²

In non-users, a cumulative risk of 4.1% was reported for breast cancer. Incident young-onset breast cancer risk was not significantly impacted by hormone therapy overall with an HR of 0.96. However, E-HT use was linked to a decreased risk, with an HR of 0.86.²

For EP-HT use, the risk was increased vs no hormone therapy, with an HR of 1.10. When EP-HT was used for over 2 years, the HR increased to 1.18, highlighting positive associations with long-term use. Similarly, and HR of 1.15 was reported for EP-HT use in women without hysterectomy or bilateral oophorectomy.²

Subtype-specific risks and clinical implications

Similar links were reported for all breast cancer subtypes. However, EP-HT use had more significant associations with estrogen receptor-negative and triple-negative disease than other subtypes, with HRs of 1.55 and 1.50, respectively.²

Overall, the results indicated reduced odds of young-onset breast cancer from E-HT but increased odds from EP-HT. Investigators concluded this data can be used to develop clinical guidelines for hormone use in younger women.

“Women and their health care providers should weigh the benefits of symptom relief against the potential risks associated with hormone therapy, especially EP-HT. For women with an intact uterus and ovaries, the increased risk of breast cancer with EP-HT should prompt careful deliberation,” said Dale Sandler, PhD, senior author and NIEHS scientist.

References

1. Breast cancer risk in younger women may be influenced by hormone therapy. National Institutes of Health. June 30, 2025. Accessed July 8, 2025. https://www.eurekalert.org/news-releases/1088954?
2. O’Brien KM, House MG, Goldberg M, et al. Hormone therapy use and young-onset breast cancer: a pooled analysis of prospective cohorts included in the Premenopausal Breast Cancer Collaborative Group. The Lancet Oncology. 2025;26(7):911-923. doi:10.1016/S1470-2045(25)00211-6

Washington, D.C., July 8, 2025 (PAHO)—The Pan American Health Organization (PAHO) has launched a new interactive dashboard to enhance monitoring and analysis of respiratory virus circulation trends across the Americas, with the goal of strengthening surveillance and facilitating timely analysis of regional trends.

This interactive dashboard presents virological data (from FluNet) and epidemiological data (from FluID) available through the regional data hub (AMart), providing an intuitive, multilingual platform for exploring key indicators.

The dashboard features three main sections:

• Virologic Surveillance presents percent positivity and laboratory sample data for all countries and subregions, enabling detailed tracking of virus circulation patterns.
• Syndromic Surveillance: displays data on reported cases of severe acute respiratory infection (SARI) and influenza-like illness (ILI), along with intensive care unit (ICU) admissions and SARI-related deaths, offering insights into the clinical presentation of circulating respiratory viruses.
• Country Profiles: allows users to select any country in the Americas and view all related virologic and syndromic surveillance data on a single, integrated page.

All dashboard visualizations are interactive, customizable by time period, and available in Spanish, English, French, and Portuguese. The tool is updated weekly and is intended for public health professionals, health authorities, and other stakeholders involved in respiratory virus surveillance.

In addition, the dashboard includes a feature that provides access to an updated regional summary of the virological situation. As of epidemiological week 25 of 2025 (June 15–21), the data show that the circulation of influenza and respiratory syncytial virus (RSV) aligns with historical seasonal patterns, with high activity in the Southern Hemisphere and low activity in the Northern Hemisphere. For SARS-CoV-2, no defined seasonality is observed; however, circulation remains low in most subregions, except for the Caribbean, where higher activity has been detected.

Country profiles offer a more detailed breakdown of the national situation.

For more detailed and up-to-date information on respiratory viruses in the Americas, visit PAHO’s new interactive dashboard.

Sumrin Kalia, a Pakistani woman living abroad, married at 18 and had four children by the time she was 25. She experienced no sign, no overt symptoms of menopause until she did, suddenly and early, at the age of 37.

“I began experiencing excessive bleeding. I went to a doctor, who told me I might be perimenopausal,” Kalia, who is now in her mid-40s, told DW.

The World Health Organization puts the global average age for menopause at between 45 and 55 years.

“No one explained it to me. It was very sudden. I started bleeding heavily and more frequently than usual,” Kalia said.

Kalia had been using an intrauterine device (IUD) for birth control. She had it removed, and her periods stopped altogether without explanation.

Her experience was shared by other South Asian women who spoke to DW. They had their own stories to tell of how they had experienced perimenopause symptoms sooner than their global peers.

Menopause on a faster clock: The big picture

A US-based study found South Asian American women reported an average menopause age of 48 or 49 years. For the general US population, the average age at which menopause begins is 52 years.

In South Asia itself, the average is lower than in the US. In India and Pakistan, women enter menopause at around 46 to 47, and they encounter perimenopausal symptoms before that, as is common for menopause.

Meanwhile, Pakistan’s average number of children per woman has dropped sharply from 3.61 in 2023 to 3.19 in 2024, reflecting shifting fertility patterns. By comparison, India’s rate declined more modestly from 2.14 to 2.12.

Whether or how the two sets of data are connected is unclear, but there are indications that a number of factors may be coming together to affect the aging process of South Asian women.

Genetics, biology, and vitamin D deficiency

Hormonal health expert Palwasha Khan, a consultant physician based in Pakistan, explained that menopause timing is partly genetic.

“There’s no exact rule, but studies show women tend to start and end their periods around the same age as their mothers,” Khan told DW. “The earlier you start menstruating, the earlier menopause is likely to occur.”

Khan also highlighted a lesser-known factor: a rapid depletion of vitamin D levels among South Asian women, which can worsen chronic health issues linked to aging.

Furthermore, Khan said that many women experience ovarian failure in their late 30s or 40s, often compounded by “undiagnosed medical issues” and a lack of quality health care earlier in life.

A cultural pressure cooker: Fertility over health

In South Asia, and particularly in Pakistan, societal expectations push women to have children soon after marriage, often at the cost of their long-term health.

“Women’s health as a distinct concern is largely ignored,” Khan said. Awareness around hormonal health is minimal, and treatments like hormone replacement therapy (HRT) are rare. “You’d have to pick 10,000 women to find two who’ve gone on [HRT].”

This intense focus on fertility often sidelines conversations about menopause and women’s well-being.

Another story: The emotional cost of menopause

Sabina Qazi, a Pakistani woman in her mid-40s, based in Karachi, told DW about the emotional and cognitive challenges she faced as a cost of menopause.

“My husband and children would talk to me, but the words would just fall off in between… I had the constant need to prove that I wasn’t stupid,” she Qazi, describing the cognitive difficulties she experienced after undergoing a radical hysterectomy, a procedure in which her uterus, fallopian tubes, and both ovaries were removed due to cancer risk.

Qazi said her biggest frustration with the medical process — a form of surgical menopause — was how little thought was given to the long-term consequences. Although the surgery was preventive, she felt the emotional weight of the decision was never fully acknowledged.

In fact, the procedure was framed as inevitable, a foregone conclusion: She would reach menopause regardless, in a few years time, so, why not get it over with now?

Qazi later began hormone replacement therapy (HRT) to manage her menopause symptoms. She said one of the most persistent challenges was dealing with brain fog.

While her menopause followed a medically required hysterectomy, the overlap between surgical menopause and broader health risks reflects a pattern that medical consultant Khan has observed: Ovarian failure occurring in the late 30s or 40s among South Asian women, often alongside a range of chronic health conditions that appear interconnected.

The emotional toll of the surgery lingered long after Qazi’s physical recovery. She received little support from her community, and peers in her close circle downplayed her experience, suggesting she needn’t be concerned since she had already had three children.

The cultural implication, said Qazi, was that her reproductive organs had fulfilled their purpose, and her losing her uterus and ovaries was significant.

‘Brown women are burned out’

Khan said various factors appeared to be coming together to accelerate aging in South Asian women: chronic illnesses, stress and other mental health issues, and social pressures. And each individual factor seems to be reinforcing the other.

“Brown women are too burned out,” said Khan. “The weight of society. The weight of mothers-in-law. Brown women end up taking on too much stress, and this makes them age faster.”

Many women face relentless social expectations and little support, which intensifies both physical and emotional health challenges.

One woman of South Asian descent, living in Saudi Arabia, shared: “I feel angry all the time.”

Edited by: Zulfikar Abbany

Researchers in Chicago believe they’ve found a virus that could be a trigger for Parkinson’s disease.

Parkinson’s impacts millions of people in the United States, according to Northwestern Medicine, and while some cases are linked to genetics, most cases are not.

“We wanted to investigate potential environmental factors – such as viruses – that might contribute to Parkinson’s disease,” said Igor Koralnik, MD, the lead author of the study and chief of neuroinfectious diseases and global neurology at Northwestern Medicine. 

ViroFind used to detect HPgV

Researchers at Northwestern Medicine found the Human Pegivirus (HPgV) using ViroFind in the brains of individuals who had Parkinson’s disease.

HPgV belongs to a family of blood-borne illnesses like hepatitis C, but it is not known to cause any diseases.

Dig deeper:

Researchers used samples from over 1,000 participants in the Parkinson’s Progression Markers Initiative, a foundation launched by The Michael J. Fox Foundation and other scientists.

Ten brains from post-mortem patients with Parkinson’s disease and 14 without were observed.

Five out of the 10 post-mortem brains with Parkinson’s had HPgV while the other 14 control brains had none.

The virus was also present in the spinal fluid of Parkinson’s patients but not in the control group.

What they’re saying:

“HPgV is a common, symptomless infection previously not known to frequently infect the brain,” Koralnik said. “We were surprised to find it in the brains of Parkinson’s patients at such high frequency and not in the controls. Even more unexpected was how the immune system responded differently, depending on a person’s genetics. This suggests it could be an environmental factor that interacts with the body in ways we didn’t realize before. For a virus that was thought to be harmless, these findings suggest it may have important effects, in the context of Parkinson’s disease. It may influence how Parkinson’s develops, especially in people with certain genetic backgrounds.”

LRRK2

Researchers also found a potential link between the LRRK2 gene mutation and how patients with Parkinson’s responded to the virus.

“People who had the virus showed different signals from the immune system than those who didn’t, and this pattern was the same, no matter the genetics. But as we followed each person over time, we saw a more complicated picture,” Koralnik continued.

What’s next:

Researchers said going forward, they plan to look more closely at how genes like LRRK2 impact the body’s response to other viral infections to figure out if this is a special effect of HPgV or a broader response to viruses. 

There are also plans to dig deeper into how common the HPgV virus is in Parkinson’s patients and whether it plays a role in the disease. 

Given the number of times this has happened already, it should come as little surprise that we’re now faced with yet another new subvariant of SARS-CoV-2, the virus responsible for COVID.

This new subvariant is known as XFG (nicknamed “Stratus”) and the World Health Organization (WHO) designated it a “variant under monitoring” in late June. XFG is a subvariant of Omicron, of which there are now more than 1,000.

A “variant under monitoring” signifies a variant or subvariant which needs prioritised attention and monitoring due to characteristics that may pose an additional threat compared to other circulating variants.

XFG was one of seven variants under monitoring as of June 25. The most recent addition before XFG was NB.1.8.1 (nicknamed “Nimbus”), which the WHO declared a variant under monitoring on May 23.

Both nimbus and stratus are types of clouds.

Nimbus is currently the dominant subvariant worldwide – but Stratus is edging closer. So what do you need to know about Stratus, or XFG?

A recombinant variant

XFG is a recombinant of LF.7 and LP.8.1.2 which means these two subvariants have shared genetic material to come up with the new subvariant. Recombinants are designated with an X at the start of their name.

While recombination and other spontaneous changes happen often with SARS-CoV-2, it becomes a problem when it creates a subvariant that is changed in such a way that its properties cause more problems for us.

Most commonly this means the virus looks different enough that protection from past infection (and vaccination) doesn’t work so well, called immune evasion. This basically means the population becomes more susceptible and can lead to an increase in cases, and even a whole new wave of COVID infections across the world.

XFG has four key mutations in the spike protein, a protein on the surface of SARS-CoV-2 which allows it to attach to our cells. Some are believed to enhance evasion by certain antibodies.

Early laboratory studies have suggested a nearly two-fold reduction in how well antibodies block the virus compared to LP.8.1.1.

Where is XFG spreading?

The earliest XFG sample was collected on January 27.

As of June 22, there were 1,648 XFG sequences submitted to GISAID from 38 countries (GISAID is the global database used to track the prevalence of different variants around the world). This represents 22.7% of the globally available sequences at the time.

This was a significant rise from 7.4% four weeks prior and only just below the proportion of NB.1.8.1 at 24.9%. Given the now declining proportion of viral sequences of NB.1.8.1 overall, and the rapid rise of XFG, it would seem reasonable to expect XFG to become dominant very soon.

According to Australian data expert Mike Honey, the countries showing the highest rates of detection of XFG as of mid-June include India at more than 50%, followed by Spain at 42%, and the United Kingdom and United States, where the subvariant makes up more than 30% of cases.

In Australia as of June 29, NB.1.8.1 was the dominant subvariant, accounting for 48.6% of sequences. In the most recent report from Australia’s national genomic surveillance platform, there were 24 XFG sequences with 12 collected in the last 28 days meaning it currently comprises approximately 5% of sequences.

The big questions

When we talk about a new subvariant, people often ask questions including if it’s more severe or causes new or different symptoms compared to previous variants. But we’re still learning about XFG and we can’t answer these questions with certainty yet.

Some sources have reported XFG may be more likely to course “hoarseness” or a scratchy or raspy voice. But we need more information to know if this association is truly significant.

Notably, there’s no evidence to suggest XFG causes more severe illness compared to other variants in circulation or that it is necessarily any more transmissible.

Will vaccines still work against XFG?

Relatively frequent changes to the virus means we have continued to update the COVID vaccines. The most recent update, which targets the JN.1 subvariant, became available in Australia from late 2024. XFG is a descendant of the JN.1 subvariant.

Fortunately, based on the evidence available so far, currently approved COVID vaccines are expected to remain effective against XFG, particularly against symptomatic and severe disease.

Because of SARS-CoV-2’s continued evolution, the effect of this on our immune response, as well as the fact protection from COVID vaccines declines over time, COVID vaccines are offered regularly, and recommended for those at the highest risk.

One of the major challenges we face at present in Australia is low COVID vaccine uptake. While rates have increased somewhat recently, they remain relatively low, with only 32.3% of people aged 75 years and over having received a vaccine in the past six months. Vaccination rates in younger age groups are significantly lower.

Although the situation with XFG must continue to be monitored, at present the WHO has assessed the global risk posed by this subvariant as low. The advice for combating COVID remains unchanged, including vaccination as recommended and the early administration of antivirals for those who are eligible.

Measures to reduce the risk of transmission, particularly wearing masks in crowded indoor settings and focusing on air quality and ventilation, are worth remembering to protect against COVID and other viral infections.