"We do not have immunity against it," warn scientists as India’s first bird flu case in cats raises human health concerns

In a worrying first for India, cases of avian influenza (H5N1) have been detected in domestic cats, with Chhindwara district in Madhya Pradesh emerging as the epicentre. Scientists are now raising concerns about the virus mutating in mammals and its potential risk to humans.

How Did the Virus Spread to Cats?

According to a TOI report, scientists from ICAR-NIHSAD and the Union government’s animal husbandry department documented these cases in January. Chhindwara, which borders Nagpur, had already seen big cats succumbing to bird flu in December last year.

H5N1 is primarily an avian virus, but experts warn that mutations can allow it to infect and replicate in mammals. “This adaptability raises concerns because influenza viruses have the potential to trigger pandemics, as seen in past outbreaks like Covid-19,” a scientist told TOI.

What Symptoms Did the Infected Cats Show?

The affected cats showed high fever, loss of appetite, and extreme lethargy before dying within one to three days of showing symptoms. The scientific team identified the virus as belonging to the 2.3.2.1a lineage, a strain responsible for poultry outbreaks in India.

The study further revealed 27 mutations in the virus detected in cats, leading experts to call for enhanced surveillance across poultry, wild birds, and other mammals, including pets and humans.

Is There a Risk to Humans?

While human infections remain rare, virologist Jacob John warned that the possibility of human-to-human transmission cannot be ruled out. “H5N1 is new for humans. We do not have immunity against it. If human-to-human transmission becomes efficient, as an extension of the present pattern of mammalian transmission, it is going to be a concern,” he told TOI.

Website: International Conference on Infectious Diseases

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Clinical Overview of Oropouche Virus Disease

Epidemiology

Oropouche virus belongs to the Simbu serogroup of the viral genus Orthobunyavirus in the Peribunyaviridae family. The virus was first detected in 1955 in a febrile forest worker in a village in Trinidad and Tobago called Vega de Oropouche, near the Oropouche River. Oropouche virus is endemic to the Amazon basin.

Prior to 2000, outbreaks of Oropouche virus were reported in Brazil, Panama, and Peru. Evidence of animals being infected was also noted in Colombia and Trinidad during this time. In the last 25 years, cases of Oropouche have been identified in many countries, including Argentina, Bolivia, Brazil, Colombia, Ecuador, French Guiana, Panama, and Peru. One child was found to be infected in Haiti in 2014.

In late 2023, Oropouche virus was identified as causing large outbreaks in endemic areas and new areas in South America. In June 2024, Cuba reported its first confirmed Oropouche case. For the latest information, see Countries and Territories with Recent or Previous Oropouche Virus Transmission. Currently, there is no evidence of local transmission in the United States.

Clinical features

The majority of people infected with Oropouche virus become symptomatic. The incubation period for Oropouche virus disease is 3–10 days. Typically, disease starts with the abrupt onset of fever (38-40°C) with headache (often severe), chills, myalgia, and arthralgia.

Other signs and symptoms include photophobia, dizziness, retroorbital or eye pain, nausea and vomiting, or maculopapular rash that starts on the trunk and goes to the extremities. Less common symptoms can include conjunctival injection, diarrhea, severe abdominal pain, and hemorrhagic symptoms (e.g., epistaxis, gingival bleeding, melena, menorrhagia, and petechiae).

Symptoms typically last less than a week (2–7 days). However, in up to 60% of patients, symptoms can reoccur a few days or even weeks later. Similar symptoms are reported on relapse.

The symptoms of Oropouche virus disease can be similar to symptoms of dengue, chikungunya, or Zika viruses, or malaria.

Abnormal laboratory findings

Abnormal laboratory findings have been documented in some patients with Oropouche virus disease including lymphopenia and leukopenia, elevated CRP (C-reactive protein), and mildly elevated liver enzymes. Thrombocytopenia also has been reported in a few cases.

Neuroinvasive disease

Oropouche virus can cause neuroinvasive disease (e.g., meningitis and encephalitis). It is estimated that up to 4% of patients will develop neurologic symptoms after their initial febrile illness. Symptoms reported for patients with neuroinvasive disease include intense occipital pain, dizziness, confusion, lethargy, photophobia, nausea, vomiting, nuchal rigidity, and nystagmus. Laboratory abnormalities noted in cerebrospinal fluid (CSF) for patients with neuroinvasive disease include pleocytosis and elevated protein.

Guillain-Barré syndrome

A published report describes three patients who developed Guillain-Barré syndrome (GBS) following infection with Oropouche virus. All three patients had an acute febrile illness and specimens that were RT-PCR positive for Oropouche virus and subsequently developed GBS 10–11 days after initial symptom onset. The patients were hospitalized for 3 to 4 weeks and were discharged without apparent sequelae. While these are the first reports of GBS following Oropouche infection, GBS is associated with other viral infections, including those caused by arboviruses.

CDC is working with international partners to learn more about the possible association between GBS and Oropouche infection.

Prognosis

Persistence of weakness and malaise has been noted in some patients for up to one month following symptom onset. Patients might require hospitalization for more severe signs and symptoms. Patients typically recover without long-term sequalae, including in severe cases. There have been very few deaths reported among people infected with Oropouche virus.

Vertical transmission

On July 17, 2024, the Pan American Health Organization (PAHO) issued an epidemiological alert about cases in Brazil of vertical transmission of Oropouche virus associated with adverse pregnancy outcomes, including fetal deaths and congenital abnormalities. CDC is working with PAHO and other international partners to learn more about the risks of Oropouche during pregnancy. CDC has drafted Interim Clinical Considerations for Pregnant Women with Confirmed or Probable Oropouche Virus Disease.

Counseling pregnant patients

Healthcare providers should be aware of the risk of vertical transmission and possible adverse impacts on the fetus, including fetal death or congenital abnormalities.

Inform pregnant patients of the possible risks to the fetus when considering travel to areas with reported Oropouche virus transmission. Counsel these patients to consider the destination, reason for traveling, and their ability to prevent insect bites.

Pregnant women are currently recommended to reconsider non-essential travel to areas with a Level 2 Travel Health Notice for Oropouche. If a pregnant woman decides to travel, counsel them to strictly prevent insect bites during travel.

Diagnosis

Preliminary diagnosis of Oropouche virus disease is based on the patient's clinical symptoms, location where infection likely occurred (including places and dates of travel), and activities leading to risk of possible exposure. Although there is no specific treatment for Oropouche virus disease, testing patients with suspected disease is recommended to:Determine the best course of clinical management (e.g., avoiding nonsteroidal anti-inflammatory drugs, avoiding unnecessary treatments and procedures, monitoring the patient for severe symptoms or complications).
Counsel the patient on prevention (e.g., avoiding mosquito bites, blood donation, possible sexual transmission).
Provide important information about where viruses are circulating and risk of infection for other patients.

Evidence of the virus can be detected in serum samples during the first week of infection. The virus is readily cultured during the first few days of the infection and is usually not detected beyond day 5. However, viral RNA can be detected for several more days after the virus is no longer present. Toward the end of the first week of illness, IgM antibodies form, followed by IgG antibodies.

In patients with neuroinvasive disease, viral RNA can be detected but is often not present in CSF. Therefore, serologic testing is the preferred method to look for evidence of infection in the CSF. Viral RNA has been detected in saliva and urine of a patient 5 days into the illness. However, testing of these sample types is not currently validated or available in the United States.

Currently, CDC can perform real-time reverse transcription-polymerase chain reaction (RT-PCR) to detect viral RNA in serum and CSF during the acute phase of the illness. CDC also can perform plaque reduction neutralization tests (PRNTs) to detect virus-specific neutralizing antibodies in serum and CSF. To confirm a recent infection using serologic testing, both acute and convalescent samples are needed to document a 4-fold or greater change in antibody titers.

Treatment

There are no medicines to treat Oropouche virus disease. Supportive care is recommended for clinical management of patients. Treatment for symptoms can include rest, fluids, and use of analgesics and antipyretics. Patients who develop more severe symptoms should be hospitalized for close observation and supportive treatment.

All patients with clinically suspected dengue should receive appropriate management without waiting for diagnostic test results. Patients should be advised to avoid aspirin containing drugs or other nonsteroidal anti-inflammatory drugs to reduce the risk of bleeding.

Prevention

The best way people can protect themselves from Oropouche is to prevent bites from biting midges and mosquitoes. There are no vaccines to prevent Oropouche virus disease.
Infection prevention and control

Laboratory, healthcare, and other workers exposed to blood, other body fluids, or cultures of infected individuals may be at risk for Oropouche virus exposure. Healthcare personnel should follow Standard Precautions for all patient care and laboratory personnel should follow standard laboratory procedures.
Possible sexual transmission

A recent scientific report describes the first time Oropouche virus was found in semen of a patient who had Oropouche, which raises concern about the possible risk of sexual transmission. Viruses (e.g., Zika virus, Ebola virus) in semen have been associated with sexual transmission of other infectious diseases. No cases of sexual transmission of Oropouche virus have been reported. CDC has interim recommendations for travelers to areas with a Level 1 or 2 Travel Health Notice for Oropouche to prevent possible transmission during sex.

Blood donation

CDC has not yet determined if Oropouche virus poses a risk to the blood supply. At this time, no cases of blood transfusion transmission of Oropouche virus have been identified. Evidence of the virus can be detected in serum during the first week of infection, but virus and antibody dynamics are currently not well understood. Until more is known about Oropouche virus, FDA suggests people diagnosed with Oropouche virus disease should consult with their blood donation center and consider not donating blood for at least 4 weeks. People diagnosed with Oropouche virus disease shortly after giving blood should tell their blood center.

Website: International Conference on Infectious Diseases

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All About First Aid Kits:

What?
A first aid kit is a box or container containing essential medical equipment such as antiseptic products, bandages, ointments and more. Depending on their contents they can come in various sizes, and the items they contain may vary depending on the setting.

Why?
First aid kits are important because they allow us to respond to emergencies immediately. They allow you to quickly tend to injuries such as cuts, scrapes, insect bites, burns and fractures to prevent the condition from worsening by providing instantaneous care and relief. In some situations, first aid kits can even help save lives.

How?
To respond in an emergency, we must know what is in a first aid kit and how to use it. Here is a brief overview of the essential contents of a kit, what they are, and how to use them:

Hand Sanitizer:Used to avoid the transmission of bacteria and viruses.
Apply before and after putting on gloves

Latex Free Gloves:Protect the first aider from infection and cross-contamination

Sterile Alcohol Pads:Protect the body from potentially harmful germs
Disinfect minor injuries like cuts

Antibiotic Ointment:Applied on top of the skin to kill bacteria
To prevent skin infections and make the healing process faster
Clean the area before applying

Sting Relief:Provides relief from the pain, itching and discomfort that result from bug bites and stings

Adhesive Bandages & Gauze:Absorb blood, compress, help prevent infection, and limit movement in the wound area
Gauze is thin and made of cotton, and it requires an adhesive to keep it in place

Q-tips:Used to apply ointment or clean areas to prepare for treatment

Tweezers:To pull out splinters or insect stingers
To pick up unclean materials such as bloody bandages

Pain Reliever:Over-the-counter medicines to relieve pain
Acetaminophen (Tylenol) is not anti-inflammatory and can temporarily reduce fever or relieve aches and pains
Ibuprofen (Advil & Motrin) are anti-inflammatory, last longer, and can reduce fever, pain, and swelling
Make sure to read and follow dosage recommendations; do not use until you understand the instructions

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Microbe opens the door to carbon-dioxide driven manufacturing

RIKEN scientists looking for clues to the origins of life on Earth have discovered a new microbe that may shed light on how organisms first developed on Earth, the search for life elsewhere in the universe and how to improve microbial factories.

Their research, conducted in the rugged, deep-water-fed springs of northern California, uncovered a microorganism that converts carbon dioxide into other chemicals. This process not only generates energy, but employs a previously unknown metabolic pathway, suggesting novel methods of carbon fixation that may mimic the earliest forms of energy metabolism on our planet.

“It’s really unusual,” says Shino Suzuki, the study’s lead author and a microbiologist who heads the Geobiology and Astrobiology Laboratory at the RIKEN Cluster for Pioneering Research in Wako, Japan.

The unusual conditions in which the microorganisms live could be a candidate for the sort of environment in which life on Earth originated, so this new kind of carbon fixation “could represent one of the earliest energy conversion processes of primitive life”, says Suzuki. It turns out, it might also be able to be harnessed to boost the microbial manufacturing of chemicals and biofuels.

Life origin clues

The microbe, a type of single-celled life form known as an archaeon, comes from an otherworldly ecosystem called The Cedars. Situated about 150 kilometers north of San Francisco’s iconic Golden Gate Bridge, this geological treasure is characterized by bizarre mineral formations caused by certain underground rocks reacting with water. This process creates waters that are rich in calcium, hydrogen and methane gas, but lacking in other ingredients typically necessary for life. Life thrives there nonetheless.

About 15 years ago, Suzuki and her collaborators started characterizing microbes in this hostile environment, using advanced genetic sequencing techniques to identify bacteria and archaea within these uncharted realms. They encountered a variety of exotic microbes, each with distinct genomic features and metabolic functions.

Some fed on hydrogen, while others consumed dissolved minerals in the alkaline waters. Yet perhaps none was more bizarre—and fascinating—than Met12.

Met12 is an abundant archaeon that lives in the deep groundwaters of The Cedars. Genetic analyses revealed that it is closely related to a group of anaerobic microbes known for their ability to produce methane as a byproduct of their metabolism. And yet, Met12 lacks the genes needed to make methane.

Instead, the microbe relies on an alternative metabolic pathway in which carbon dioxide is converted to an organic molecule called acetate, without any methane released in the process. Notably, it is assisted in this operation through a unique gene called MmcX.

This gene, as Suzuki and her team showed, helps boost the electron-importing capacity of Met12, enabling more robust energy metabolism. This adaptation is critical for the microbe to flourish in terrain such as The Cedars that, at first glance, would appear to be utterly inhospitable to such life.

According to Suzuki, the discovery showcases a form of life adapting to extreme environments in unexpected ways, a finding that could reflect how primitive or even extraterrestrial life arose under the kinds of harsh conditions thought to exist on early Earth or other planets. “This could give some insights into the origin of life,” Suzuki says.

When Suzuki, along with collaborators from the United States, Denmark and elsewhere in Japan, first discovered Met12, they didn’t believe their own findings. “I doubted myself,” Suzuki says. “I thought I had made a mistake.”

With only gene sequences available, they had to use a method process to reconstruct the circularized genome of the microbe. Culturing Met12 in the laboratory proved challenging, so they couldn’t verify its existence through traditional microbiological methods. Turning to synthetic biology, the researchers had to use creative verification methods to convince themselves that the organism was real.

They inserted the MmcX gene into a rod-shaped bacterium, genetically engineered not to feature electron transfer activity. This tweak helped to rescue the microbe’s electron-uptake abilities, even to the point that it surpassed normal levels. With further experimentation, the researchers inferred how Met12 is capable of exploiting these electrons to facilitate energy metabolism, with carbon dioxide as the primary fuel source.

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Machine Learning Unlocks Immune System Secrets

A novel artificial intelligence system can access information stored in the immune system about past infections, diseases, and vaccinations and could be harnessed as a clinical tool for medical diagnosis.

The machine learning for immunological diagnosis (Mal-ID) framework, described in the journal Science, could one day lead to a single blood test to diagnose multiple diseases.


The system combines DNA sequencing and machine learning to create a new type of data-driven medical diagnostic that reads the immune system’s record of exposure to disease. Specifically, it captures the vast quantity of information contained in the genetic sequences of B and T immune cell receptors and could act as biomarkers for past immune system activity.

“Our study shows it’s possible to unlock the hidden information in immune receptor sequences in a robust way for many different types of diseases and immune states,” lead researcher Maxim Zaslavsky, PhD, who runs a team at Stanford University, told Inside Precision Medicine.

“We believe this approach may one day be able to help doctors diagnose and treat autoimmune diseases, just like next-generation genomic sequencing transformed cancer care by matching patients to targeted therapies based on their tumor’s genetic profile.”

Clinical diagnosis usually involves physical examinations, a patient’s medical history, laboratory tests, and imaging studies and can result in laborious investigations that may not result in definitive answers, particularly for autoimmune diseases. It also makes little use of the immune system’s own record of exposure to antigens on pathogens and even the body’s own tissues that are reflected in the B and T cell receptors of the immune system.

B and T cell receptor populations change after exposure to pathogens, after vaccination, and in response to autoantigens in autoimmune conditions, which reflects clonal expansion and selection of B cells and T cells during immune responses.

Genes encoding these cells are generated by a random recombination of segments in the genome of individual cells during their development and could potentially represent a diverse set of sequence biomarkers associated with immune system activity.

Zaslavsky and co-workers created the Mal-ID method for identifying B cell receptor heavy chain and T cell receptor beta chain features characteristic of infectious and immunological disorders or generated by therapeutic or prophylactic interventions such as vaccination.

Mal-ID combines traditional immunological analyses such as the detection of shared sequences between people who have the same condition, with more complex features derived from AI models of protein sequences, called protein language models.

While AI systems can be difficult to interpret, the team developed ways to understand how the model made its diagnostic predictions.

Mal-ID accurately identified the immune status of blood samples from 542 people with COVID-19, HIV, lupus, Type 1 diabetes, recent flu vaccination, and healthy individuals, with a multiclass area under the receiver operating characteristic curve (AUROC) of 0.986 on data not used for training.

Combining features from both B cell and T cell receptor data performed best but even with only B cell receptor sequences it achieved an AUROC of 0.959 using an expanded cohort that added 51 individuals for whom only these data were available.

Zaslavsky said: “What we have today is a proof of concept and requires further validation, but this approach of directly measuring the immune cells that may be driving the diseases could give us deeper insight into the underlying mechanisms of disease, especially for diseases that might take years to diagnose and where patients have to endure an agonizing and expensive trial-and-error process to find the right treatment.”

Website: International Conference on Infectious Diseases

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Orchid's nutrient theft from fungi sheds light on photosynthesis-parasitism continuum

Most orchids live in a symbiotic relationship with fungi in their roots: The plants provide sugar they produce through photosynthesis and in return receive water and minerals from the fungi. However, some orchids have stopped producing their own food and completely feed on fungi.

Kobe University botanist Suetsugu Kenji says, "I've always been intrigued by how orchids turn parasitic. Why would a plant give up its reliance on photosynthesis and instead 'steal' from fungi?"

The orchid Oreorchis patens offers a prime opportunity to study this question, as it is a partial parasite, meaning that it can produce its own food but also takes up to half of its budget from fungi. The key question in the field was whether the orchids do so to top up what they can't get enough of through photosynthesis, or whether they actually derive an additional benefit from their parasitism.

Suetsugu explains, "I noticed that Oreorchis patens sometimes grows unusual coral-shaped rootstalks, a trait reminiscent of orchids fully relying on fungi. I thought that this would allow me to compare plants with these organs to those with normal roots, quantify how many extra nutrients they might be gaining, and determine whether that extra translates into enhanced growth or reproductive success."

In a paper now published in The Plant Journal, the Kobe University team shows that when the orchid happens to grow close to rotten wood, it shifts its fungal symbionts to those that decompose the wood and significantly increases the amount of nutrients it takes from them—without ceasing to employ photosynthesis. As a result, the plants are bigger and produce more flowers.

"In short, these orchids aren't merely substituting for diminished photosynthesis, they're boosting their overall nutrient budget. This clear, adaptive link between fungal parasitism and improved plant vigor is, to me, the most thrilling aspect of our discovery, as it provides a concrete ecological explanation for why a photosynthetic plant might choose this path," says Suetsugu.

But then, why do only less than 10% of these orchids exhibit this behavior? The answer might be found in the fact that the researchers could only see parasitic individuals near fallen and rotting tree trunks. Becoming a parasite means that the orchids need to switch from their usual symbionts to different fungi that can handle the increased nutritional load. But appropriate fungi only occur when there is fallen wood and only in certain stages of the decomposition process. In other words, the orchids become parasitic only when they can, not whenever they need to, and this opportunity does not present itself often.

Many questions are still left open, such as what triggers the orchids to develop the coral-like rootstalks and whether environmental factors influence the amount of nutrients the plants take from the fungi.

Suetsugu explains his wider outlook: "This work is part of a broader effort to unravel the continuum from photosynthesis to complete parasitism. Ultimately, I hope such discoveries will deepen our understanding of the diverse strategies orchids employ to balance different lifestyles, thereby aiding in the preservation of the incredible diversity of these plants in our forests."

Website: International Conference on Infectious Diseases

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Increase in respiratory infections in China

Human metapneumovirus regularly circulates in the EU/EEA during colder months. Currently, the surveillance of acute respiratory infections in the EU/EEA shows increased activity of respiratory viruses, particularly influenza, with no unusual or unexpected pattern for this time of year.

Human metapneumovirus can affect all age groups and normally causes mild-to-moderate respiratory illness but sometimes the infection can be severe in young children, older adults, and immunocompromised individuals. In the EU/EEA, hMPV is most active during late winter and spring, often circulating alongside other respiratory viruses. There is no vaccine or specific antiviral treatment available for hMPV.

Based on the current information, the European Centre for Disease Prevention and Control (ECDC) considers that the current epidemiological situation in China reflects a seasonal rise in respiratory infections caused by common respiratory pathogens and does not pose any specific concern for the EU/EEA.

ECDC continues to monitor the situation in collaboration with the Chinese CDC and WHO/EURO to gather additional information.

On 18 December 2024, ECDC issued an epidemiological update on acute respiratory infections in the EU/EEA. ECDC recommends that Member States prepare for increased respiratory virus cases during the coming winter weeks and consider infection prevention and control practices to reduce transmission in healthcare settings, including long-term care facilities.

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HIV protein switch may help virus squeeze into host cell nucleus

Supercomputer simulations have revealed how changes in the shape of the HIV-1 capsid protein may help the virus squeeze its inner core into the host cell's nuclear membrane. The findings, by a University of Pittsburgh team using the Bridges-2 system at the Pittsburgh Supercomputing Center, suggest how the capsid may deform to fit through the nuclear pores, revealing a potential target for future AIDS therapies.

The method, to be reported in the Proceedings of the National Academy of Sciences, may also be useful for studying flexibility in other important proteins.

The year 2024 was a mixed bag in the fight against AIDS. Modern antiviral therapies have turned HIV into a chronic, but survivable, disease. Death rates are at a 20-year low. On the other hand, doctors are unlikely to meet their goal of eliminating AIDS as a health threat worldwide by 2030. In some populations, HIV infection is actually increasing. And we still don't have a vaccine. That's why scientists studying AIDS continue to search for weak spots in the virus's infection cycle.

HIV inserts its genes into the host cell's nucleus in an unusual way. It doesn't import its RNA genetic material piecemeal. Instead, it stuffs its whole wedge-shaped capsid—basically the whole virus minus its outer membrane—through the nuclear pore in one piece.

The HIV-1 capsid protein makes up most of the protein mesh that forms the capsid. It does this by making connections between separate capsid proteins at different scales. First, either six or five copies of the protein link together via their N-terminal domains to form six-sided hexamers or five-sided pentamers. Then, the opposite end of the protein, the C-terminal domain (CTD), links with CTDs of neighboring hexamers or pentamers to connect them and form a mesh that surrounds the genetic material. The wedge of the capsid is kind of like a soccer ball, which also needs hexagons and pentagons to make a curved shape.

The CTD connections between two proteins—called dimers—in neighboring hexamers or pentamers can adopt different shapes that change the angles between those shapes. Before assembling into the capsid, about 85% of the CTDs connect in the D1 shape; the rest, the D2 shape.

Scientists suspected that the pointy end of the capsid's wedge might help it squeeze through the nuclear pore. What they didn't know was whether the ability of the CTD to shift angles between the hexamers and pentamers might play an additional role in making the capsid more flexible, and better able to deform to push through. One problem was that the D1 to D2 conversion is so fast, and the D2 shape is so outnumbered by D1. Because of this, D2 doesn't show up well in imaging and is hard to simulate. D2 was basically invisible to both methods.

"The capsid has these different subunits on it … and they connect to each other and form [a sort of] mesh," said Darian T. Yang, a postdoctoral scientist at the University of Copenhagen and first author of the PNAS paper. "Those connection points are this protein/protein dimer … But we also know from [nuclear magnetic resonance experiments] … that that dimer has multiple conformations. And we can understand what the major state looks like, the major dimer conformation.

"It's about 85% in this state. But then there's this minor conformation, 10 to 15% of it's in this other state. And it's this very transiently occupied state, right? So we can't really get a good structure of it."

Yang, then a graduate student at the University of Pittsburgh, wanted to know what D2 looks like, and whether the capsid protein's ability to change shape might give the capsid extra flexibility to squeeze through. Working with both Professor of Chemistry Lillian T. Chong and UPMC Rosalind Franklin Chair of Structural Biology Angela M. Gronenborn at Pitt, he carried out an exhaustive series of simulations of the capsid protein with PSC's Bridges-2 supercomputer. He got computing time on Bridges-2 via an allocation from ACCESS, the NSF's high-performance computing network, in which PSC is a leading member.

The simulations would require powerful graphics processing units (GPUs), and plenty of them. Yang's simulations would require many repetitions to work out the different ways in which the proteins can behave. Bridges-2, with 34 GPU nodes containing a total of 280 late-model GPUs, fit the bill nicely. For comparison, a high-end graphic design laptop typically has two GPUs.

The team compared its simulation results with laboratory experiments using an imaging technology called nuclear magnetic resonance, or NMR, which can track the shape of the protein via a fluorine atom that scientists attached to the natural protein. By going back and forth between real-life results and the behavior of the virtual proteins in the computer, they could be more confident the simulations were capturing reality.

"It was really nice when Bridges-2 came out," Yang said. "It was a big shift in the amount of speed that we could get with our simulations. The advantage of having access to [multiple] GPU computing is [that] our particular software package (WESTPA)—it's this method called weighted ensemble path sampling—[is that it's] very efficiently parallelizable across multiple GPUs."

The simulations, which were the first of their kind, produced switching rates and populations of the D1 and D2 shapes that matched the behavior of the capsid in the lab experiments. The results are encouraging because they suggest that simulations can pair with experiments to find new targets for HIV drugs or vaccines. The method should also be useful for scientists studying other biologically and medically important systems.

Website: International Conference on Infectious Diseases

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Superbugs Are Losing to Science, Light, and a Little Spice

Curcumin: A Surprising Ally Against Superbugs

In 2017, a woman admitted to a Nevada hospital with pneumonia died from multiple organ failure and sepsis. The cause? A strain of bacteria resistant to 26 different antibiotics. These antibiotic-resistant bacteria, known as superbugs, pose a serious and growing global health threat.

In the fight against these dangerous pathogens, researchers at Texas A&M have discovered a potential new tool—curcumin, the natural compound that gives turmeric its bright yellow color.

Their study found that when bacteria consume curcumin and are then exposed to light, harmful reactions occur within the microbes, ultimately killing them. This approach reduces the number of antibiotic-resistant strains and restores the effectiveness of conventional antibiotics.

The findings were published in Scientific Reports.
The Antibiotic Crisis and the Rise of Superbugs

Before antibiotics, infectious diseases were the leading cause of death and disability around the world. With the advent of these life-saving medications, the human lifespan has increased by 23 years on average. In the last several decades, while the discovery of novel antibiotics has plateaued, antibiotic-resistant bacteria have simultaneously become more common, ushering in the era of superbugs, such as methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococcus, and pneumonia, which are all extremely hard to treat. In fact, infectious diseases are projected to be the main causes of human mortality once again, claiming up to 10 million lives annually.

A New Strategy to Overcome Antibiotic Failure

“When bacteria start becoming resistant to conventional antibiotics, we have what we call an antibiotic catastrophe,” said Dr. Vanderlei Bagnato, professor in the Department of Biomedical Engineering and senior author on the study. “To overcome this challenge, we need alternative ways to either kill the superbugs or find a novel way to modify natural processes within the bacteria so that antibiotics start to act again.”

Bacteria display natural variation within a given population. This heterogeneity introduces variations in cell behaviors, including response to antibiotics, which can directly contribute to treatment resistance if some strains survive antimicrobial medication and continue replicating. Thus, the researchers wanted to curb bacterial heterogeneity to control bacterial resistance.
Harnessing Light to Kill Drug-Resistant Bacteria

Photodynamic inactivation, a technique that has shown promise in combating bacterial resistance, uses light and light-sensitive molecules, called photosensitizers, to produce reactive oxygen species that can kill microorganisms by disrupting their metabolic processes. In their experiments, the team used curcumin, which is also a natural food for bacteria. They tested this technique on strains of Staphylococcus aureus that are resistant to amoxicillin, erythromycin, and gentamicin.
A Game-Changer for Antibiotic Effectiveness

The researchers exposed the bacteria to many cycles of light exposure and then compared the minimum concentration of antibiotics needed to kill the bacteria after light exposure versus those that did not get light exposure.

“When we have a mixed population of bacteria where some are resistant, we can use photodynamic inactivation to narrow the bacterial distribution, leaving behind strains that are more or less similar in their response to antibiotics,” said Bagnato. “It’s much easier now to predict the precise antibiotic dose needed to remove the infection.”
Expanding the Potential of Curcumin Therapy

The team noted that photodynamic inactivation using curcumin has tremendous potential as an adjuvant or additional therapy with antibiotics for diseases, like pneumonia, caused by antibiotic-resistant bacteria.

“Photodynamic inactivation offers a cost-effective treatment option, which is crucial for reducing medical expenses not only in developing countries but also in the United States,” said Dr. Vladislav Yakovlev, professor in the Department of Biomedical Engineering and author on the study. “It also has potential applications in military medicine, where this technology could be used to treat battlefield wounds and prevent the development and spread of antimicrobial resistance, a significant concern in combat situations.”

Website: International Conference on Infectious Diseases

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The mystery of why Covid-19 seems to be becoming milder

Covid-19 is now ubiquitous – but hospitalisations seem to be on a downward trajectory. No one knows why.

When virologists took their first peek at XEC, the Covid-19 variant which started to become dominant in the autumn of 2024, the early signs were ominous.

The latest descendant of the Omicron variant of SARS-CoV-2, XEC had arisen through recombination, a process where two other variants had forged their genetic material together. Tests seemed to indicate that this would easily allow it to evade the immune protection offered by past infections or the latest iterations of the Covid-19 vaccines, based on the older JN.1 and KP.2 variants.

"The spike protein is quite different from previous variants, so it was quite easy to assume that XEC has the potential to evade immunity induced by JN.1 infection," says Kei Sato, a virology professor at the University of Tokyo, who carried out one of the first studies of XEC, published in December 2024.

In the US, infectious disease specialists braced themselves for an immediate surge in hospitalisations in the wake of the Thanksgiving holiday weekend. But it didn't happen. Surveillance testing carried out by measuring Covid in wastewater samples across major cities indicated that XEC was definitely infecting people. However, the numbers of people actually ending up in hospital was considerably less than previous winters. According to CDC data, the rate of hospitalisations at the start of Dec 2023 was 6.1 per 100,000 people. During the equivalent week in December 2024, that had fallen to two per 100,000 people.

What was going on?

"Right now, we're seeing pretty low levels of people who are critically ill, even though there's an astronomical amount of Covid in wastewater," says Peter Chin-Hong, a professor in the Health Division of Infectious Diseases at the University of California, San Francisco. "It just shows that regardless of how scary a variant might look in the lab, the environment in which it lands is much more inhospitable."

Some indications suggest that Covid in 2025 is a milder disease. The once common symptoms of loss of taste and smell are becoming less common. And though some people are being hospitalised and dying, Chin-Hong says the vast majority of people will either be asymptomatic or experience a cold so mild that some might well mistake it for a seasonal allergy, such as a pollen complaint. While immunocompromised individuals are still particularly vulnerable, he believes that the major risk factor for more severe Covid is now simply being over the age of 75.

Despite this, experts have advised that all vulnerable groups should get the latest Covid-19 vaccine, which can provide vital protection against serious illness, hospitalisation and death. And while XEC seems to cause less severe disease, there's no guarantee that more severe variants won't emerge in the future. This means the threat posed by Covid-19 is far from over and the virus should not be underestimated. Experts expect it to continue being a significant and persistent threat to public health. The risk of developing Long Covid has not gone away either. For some people, the condition can last years.

At the Icahn School of Medicine at Mount Sinai in New York, microbiology associate professor Harm Van Backel is a co-leader of the Mount Sinai Pathogen Surveillance Program, which applies the latest genomics technologies to conduct real-time tracking of bacterial, viral and fungal infections within the Mount Sinai health system. Van Backel explains that the data shows that Covid is contributing relatively little to the caseload so far this winter, despite the emergence of XEC. "For the past six months, I'd say it's been relatively quiet," he says. "In comparison with other respiratory viruses, I would say that SARS-CoV-2 is maybe, at least in hospitalised cases, about 10% of the respiratory virus infection burden that we're seeing this season."

Even when patients are admitted to hospital, the treatment protocols have changed markedly in the last two to three years. Chin-Hong recalls that anticoagulants or blood thinning medications would immediately be administered to lower the chances of clotting, but this is now no longer considered necessary. While steroids such as dexamethasone are still used in certain severe cases, he says that these tend to be exceptions, with antivirals being the predominant treatment needed.

"I think Omicron and its subvariants have increasingly focused more on causing milder upper respiratory cold symptoms rather than pneumonia and some of the invasive manifestations we've seen in the past like cardiovascular disease and clotting," says Chin-Hong. "It means that when people come into hospital, they tend to be in and out in a shorter period of time."

So what's happening?

As part of his work tracking various respiratory viruses at the University of Missouri School of Medicine, the molecular virologist Marc Johnson uses all kinds of avenues to examine the levels of Covid currently circulating. Just like Chin-Hong, he can confirm that there is plenty of it around.

"We started doing air sampling at a lot of sites around the university, and it's pretty rare that we could pull out a sample from around the students and not detect Covid," he says. "We're still getting exposed all the time, but most infections are probably just getting blunted."

Covid could still take some twists and turns

So far, Omicron, which emerged in November 2021, remains the latest Covid "supervariant", following the previous Alpha and Delta variants. While dozens of subvariants have subsequently appeared in the last three years, none have pointed to a radically new change in Covid's trajectory.

However, Johnson says that if an immunocompromised individual was to now be infected with an older strain of Covid such as the Delta variant from 2020, it could lead to something radically different. He believes this could have a more drastic impact in terms of illness and hospitalisations as it would look completely foreign to our body.

"They aren't as prevalent as they once were, but we still occasionally detect some of these strains from the first year or two," says Johnson. "We know that there's people who have a Delta infection [a variant first identified in India in December 2020]. If one of those older strains broke out and started spreading more widely, people's immunity would be kind of confused because it would look so different from everything we've seen in the past three years."

It's also plausible that something even stranger might unfold. According to Johnson, there are some early signs that Covid's eventual trajectory could lead it to become a faecal-oral virus, more akin to norovirus, cholera or hepatitis A than the common cold.

On the social media platform X, Johnson describes himself as a "wastewater detective", and he says that some of the most revealing predictions can be made from tracking Covid in the sewers. SARS-CoV-2 has been known to sometimes persist in the gut over the long term, and Johnson and his colleagues have identified various individuals who seem to have persistent gut infections. This has been possible because of Covid viruses with unusual patterns of RNA that have only been spotted in the sewer system – and not in samples from clinical settings such as hospitals. Each of these "cryptic lineages", as they are termed, are being repeatedly excreted by a particular anonymous individual.

Johnson's hunch is that this occasionally happens because a strain of Covid has acquired mutations which allow it to become a persistent gastrointestinal infection. As a result, he believes it is plausible that SARS-CoV-2 could eventually find a way of being spread via stool particles, just like other faecal-oral viruses.

"A lot of the bat coronaviruses, that's how they spread," says Johnson. "Interestingly, the evolutionary ancestors of Covid were not respiratory viruses, they were enteric viruses [those that live in the gut], spread via faecal-oral routes such as contaminated food, water or interpersonal contact. So it's possible that Covid could become an entirely food-borne pathogen, but that's probably not happening any time soon."

Website: International Conference on Infectious Diseases

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H5 Bird Flu: Current Situation

What to know

H5 bird flu is widespread in wild birds worldwide and is causing outbreaks in poultry and U.S. dairy cows with several recent human cases in U.S. dairy and poultry workers.
While the current public health risk is low, CDC is watching the situation carefully and working with states to monitor people with animal exposures.
CDC is using its flu surveillance systems to monitor for H5 bird flu activity in people.

Current situation

National situation summary

Person-to-person spread

None

There is no known person-to-person spread at this time.

Current public health risk

Low

The current public health risk is Low.

Cases in the U.S.

68 cases

Deaths in U.S.

1 cases


When a case tests positive for H5 at a public health laboratory but testing at CDC is not able to confirm H5 infection, per Council of State and Territorial Epidemiologists (CSTE) guidance, a case is reported as probable.

Confirmed and probable cases are typically updated by 5 PM EST on Mondays (for cases confirmed by CDC on Friday, Saturday, or Sunday), Wednesdays (for cases confirmed by CDC on Monday or Tuesday), and Fridays (for cases confirmed by CDC on Wednesday and Thursday). Affected states may report cases more frequently.



Detections in Animals11,966 wild birds detected as of 2/11/2025 | Full Report51 jurisdictions with bird flu in wild birds159,307,978 poultry affected as of 2/14/2025 | Full Report51 jurisdictions with outbreaks in poultry968 dairy herds affected as of 2/12/2025 | Full Report16 states with outbreaks in dairy cows

These data will be updated daily, Monday through Friday, after 4 p.m. to reflect any new data.

Cumulative data on wild birds have been collected since January 20, 2022. Cumulative data on poultry have been collected since February 8, 2022. Cumulative data on humans in the U.S. have been collected since April 28, 2022. Cumulative data on dairy cattle have been collected since March 25, 2024.

Website: International Conference on Infectious Diseases

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How celebrity endorsements can shape public health

Sir Keir Starmer has become the first sitting UK prime minister to publicly take an HIV test to reduce stigma around Aids and encourage more people to get tested.

There are historical parallels. In 1956, when Elvis Presley, at the height of his fame, was photographed receiving the polio vaccine at CBS Studio 50.

Do these high-profile gestures really change attitudes and behaviour, or are they just headline-grabbing stunts?

A closer look at the behavioural science behind celebrity endorsements suggests that, under the right conditions, public demonstrations by famous figures can indeed shift social norms, reduce stigma and influence health outcomes. However, the effects depend a lot on the credibility of the endorser, the authenticity of the act and the presence of sustained, follow-up campaigns.

Elvis Presley’s polio jab is one of the most iconic examples of celebrity-led health campaigns. But many other well-known figures have encouraged the public to adopt protective health measures, from actors promoting annual flu jabs to footballers advocating organ donation drives.

The premise is that a celebrity’s endorsement can normalise certain behaviour by tapping into the principles of “social learning theory”, particularly observational learning. That is, when we see someone we admire or trust do something, we are more likely to follow suit.

In the 1950s, polio was a serious threat, capable of causing paralysis or death. After seeing images of Elvis rolling up his sleeve to receive the jab, many teenagers – previously sceptical or apathetic – became far more willing to accept the polio vaccine. That event is now hailed as a masterclass in leveraging popular culture to address a public health crisis.

A cornerstone of behavioural science is the recognition that who delivers a message can be as important as – or sometimes more important than – what the message contains. The so-called “messenger effect” highlights how we are often more persuaded by people we perceive to be credible, relatable or high status.

In the case of Elvis, he was already idolised by millions. He was the perfect conduit to promote vaccination among teenagers who might otherwise dismiss appeals from older authority figures.

Starmer occupies a different kind of influence. Supporters of the Labour party may see him as a trustworthy figure, while others could be sceptical of a politician’s motives. This underscores a key aspect of the messenger effect: if a large segment of the target audience views the figure as partisan or self-serving, the endorsement can backfire or simply fail to register.

Another powerful effect identified in behavioural science is social norms – our shared understandings of what is typical or appropriate – which strongly influence whether we take certain actions.

Stigma around HIV remains a major barrier to testing and treatment. Even though medical advances have changed the landscape of HIV/Aids care, many people still fear the societal consequences of a positive diagnosis. According to the UK Health Security Agency, around 5,000 people in the UK are unaware they are living with HIV, partly because they hesitate to test in the first place.

By publicly taking an HIV test, Starmer aimed to shift perceptions and normalise testing. In terms of social identity theory, seeing a prominent figure within the national community – especially one involved in shaping policies – undergo testing can communicate that “people like us” view HIV testing as a routine, responsible health measure. This may be particularly powerful for people who identify politically with Starmer or who respect his leadership position.

Despite the potential of celebrity or high-profile endorsements, behavioural science also points to authenticity as a vital ingredient. Audiences are more likely to change their behaviour if they believe the celebrity genuinely cares about the issue rather than simply seeking publicity. If endorsements are perceived as insincere or politically opportunistic, their effect can be muted or even counterproductive.

In Elvis’s case, he was known for engaging with young fans and had a track record of public good works, which helped bolster the sense that his polio vaccination was done for more than just a publicity boost.

For Starmer, sustaining the momentum beyond a single test – through continued advocacy, support of free testing programmes, and visibility in HIV-awareness campaigns – could reinforce the perception of a real commitment rather than a fleeting photo opportunity.

Website: International Conference on Infectious Diseases

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