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Category Archives: Health

Chart: China New COVID-19 Daily Cases Surpass Peak Hit in April 2022

Source : Nikkei Asia and The Economist

Chart: Fragile Fertility

Source : Statista

There Might Be a Perfect Indoor Humidity to Curb COVID Spread

Dennis Thompson wrote . . . . . . . . .

It’s sort of like the Goldilocks principle — a room that’s either too dry or too humid can influence transmission of COVID-19 and cause more illness or death, Massachusetts Institute of Technology researchers say.

Maintaining an indoor relative humidity between 40% and 60% is associated with lower rates of COVID-19 infections and deaths, they reported Nov. 16 in the Journal of the Royal Society Interface.

Indoor conditions outside that range are associated with worse COVID outcomes, according to the report.

“There’s potentially a protective effect of this intermediate indoor relative humidity,” said lead author Connor Verheyen, a doctoral student in the Harvard-MIT Program in Health Sciences and Technology, in Cambridge, Mass.

The research team noted that most people are comfortable between 30% and 50% relative humidity. An airplane cabin is kept around 20%.

Until now, researchers have considered that COVID-19 could be influenced by the seasons, but they tended to examine the virus’ patterns in the context of outdoor weather conditions.

The MIT team decided that other researchers might be looking in the wrong direction, given that people in most places spend more than 90% of their time indoors. Indoor conditions also are where most viral transmission occurs.

For the study, the investigators combined COVID data with meteorological measurements taken from 121 countries.

They gathered COVID case counts and deaths from between January and August 2020, before vaccines were available, and then compared each day of data with an average estimated indoor humidity on that day.

For example, they reasoned that if outdoor temperatures fell below the typical human comfort range of 66 to 77 degrees Fahrenheit, folks would crank on the heat — and thus cause indoor humidity to fall.

As a result, they found that indoor relative humidity tended to drop below 40% during colder periods, and that COVID cases and deaths also spiked at those times.

The team also found a gradual rise of indoor humidity during tropical countries’ summer season reflected in a gradual increase in COVID deaths as humidity went past 60%.

COVID-19 cases and deaths tended to increase when a region’s average estimated indoor humidity was lower than 40% or higher than 60%, regardless of the time of year.

Nearly all regions had fewer COVID infections and deaths when average indoor humidity hovered in the “sweet spot” between 40% and 60%, the study authors said.

“We were very skeptical initially, especially as the COVID-19 data can be noisy and inconsistent,” said co-researcher Lydia Bourouiba, director of the MIT Fluid Dynamics of Disease Transmission Laboratory. “We thus were very thorough trying to poke holes in our own analysis,” she noted in an MIT news release.

Bourouiba said the team used a range of approaches to test the findings, including taking into account factors such as government intervention.

“Despite all our best efforts, we found that even when considering countries with very strong versus very weak COVID-19 mitigation policies, or wildly different outdoor conditions, indoor — rather than outdoor — relative humidity maintains an underlying strong and robust link with COVID-19 outcomes,” Bourouiba said.

The researchers aren’t sure why indoor humidity might have such an influence over COVID’s virulence, but follow-up studies have suggested that germs might survive longer in respiratory droplets in either very dry or very humid conditions.

Source: HealthDay

Chart: The U.S. Accounts for Nearly Half of Global Diabetes Drug Sales

Source : Statista

Damage to Health Mounts With Each New COVID Infection

Dennis Thompson wrote . . . . . . . . .

Every time a person gets infected with COVID-19, their risk of dying or suffering serious long-term health problems increases dramatically, a new study has found.

People with repeated COVID-19 infections are twice as likely to die and three times as likely to be hospitalized compared to those only infected once, according to the report published online in the journal Nature Medicine.

Repeat COVID-19 patients are also three times more likely to develop lung and heart problems, and 60% more likely to develop a brain condition, the researchers found.

“Without ambiguity, our research showed that getting an infection a second, third or fourth time contributes to additional health risks in the acute phase, meaning the first 30 days after infection, and in the months beyond, meaning the long COVID phase,” said senior researcher Dr. Ziyad Al-Aly. He is a clinical epidemiologist at Washington University School of Medicine in St. Louis.

The researchers also found that the risk rises with each additional infection.

“This means that even if you’ve had two COVID-19 infections, it’s better to avoid a third,” Al-Aly said in a university news release. “And if you’ve had three infections, it’s best to avoid the fourth.”

For the study, the investigators analyzed medical records of about 5.8 million patients treated by the U.S. Department of Veterans Affairs, the nation’s largest integrated health care system.

The researchers compared nearly 41,000 people who had two or more documented COVID-19 infections with more than 443,000 people who had been infected once and 5.3 million others who were COVID-free between March 2020 and April 2022.

Most of the people who had been reinfected had gone through two or three bouts with COVID-19. A small number had four infections, and no one had five or more.

Statistical modeling assessed the health risks of repeat COVID-19 infections within the first month after contracting the virus, and then up to six months after.

The results pierce the “air of invincibility among people who have had COVID-19 or their vaccinations and boosters, and especially among people who have had an infection and also received vaccines,” Al-Aly said.

People who have had COVID-19 once should take every possible precaution to protect their health and prevent reinfection, he advised.

“Going into the winter season, people should be aware of the risks and practice vigilance to reduce their risk of infection or reinfection with SARS-CoV-2,” Al-Aly said.

He urged people to wear a mask, get all of their eligible boosters and stay home when they’re ill.

“Also, get a flu shot to prevent illness,” Al-Aly added. “We really need to do our best to reduce the chance we will have a twin-demic of both COVID-19 and the flu this winter season.”

Source: HealthDay

Chart: U.S. Flu Season Back Ealier Than Usual

Flu hospitalizations reach their highest point since 2010 according to the CDC.

Pandemic-popularized precautions such as social distancing, regular handwashing, and wearing face masks, led to a remarkable period which, according to lab data compiled by the WHO, saw influenza infections almost disappear for 18 months.

Source : Chartr

Why We Still Don’t Have a Vaccine for the Common Cold

Bill Gourgey wrote . . . . . . . . .

Feeling yucky? Runny nose, scratchy throat? Maybe a cough, with light chills and aches, possibly a low-grade fever? We’ve all been there. Statistically, everyone comes down with these symptoms multiple times a year. These past few years, it would be tempting to blame some variant of the COVID-19 coronavirus, or SARS-CoV-2, for such symptoms. However, there’s also a strong possibility that it’s a distant cousin on the human virus family tree, one that is responsible for more sick days and visits to the doctor each year than any other pathogen—rhinovirus. Common cold symptoms can be caused by many viruses, but the odds you’re fighting a rhinovirus are high: the virus accounts for as much as half of all common colds.

Traditionally, there has been a certain seasonality to respiratory viruses in the US. Influenza tends to peak in fall and again in early spring, while common colds, such as respiratory syncytial viruses (RSVs), non-COVID coronaviruses, adenoviruses, and rhinoviruses pick up in mid-winter. But COVID-19 seems to have disrupted the normal pattern. “We typically see RSV at the peak of winter season,” says Richard Martinello, a respiratory virus specialist at Yale School of Medicine in Connecticut. “But our hospital’s already full. We’re trying to figure out where to put patients and how to care for them.” It’s not just RSV. “We’re actually seeing occasional kids with pretty severe rhinovirus infections,” Martinello adds, “and adults with severe rhinovirus infections in the hospital this year.”

Every year, we’re encouraged to get our annual flu shot—and it seems COVID vaccinations are headed down a similar path. Yet, we don’t get one for the common cold. With more than a billion cases each year in the US alone—far more than any other virus, including COVID-19 and the flu combined—it’s hard to overstate the uplift a universal common cold vaccine would have. The hunt for such a vaccine began more than half a century ago, as Popular Science reported in November 1955.

Dating back to the 19th century, a slew of vaccines have been developed for many of humanity’s most pervasive pathogens, from the very first vaccine in 1798 for smallpox to cholera and typhoid in 1896 to the COVID-19 vaccines in 2020—but no common cold vaccine.

In the 1950s, however, flush with the success of Jonas Salk’s polio vaccine, virologists were convinced it would be just a handful of years before the common cold would be eradicated by vaccine. In the 1955 Popular Science article, prolific virologist Robert Huebner estimated that a vaccine for the common cold might be available to the general public in as little as a year. While Huebner—who is credited with discovering oncogenes (genes with the propensity to cause cancer)—was successful in developing an adenovirus vaccine specifically for pharyngoconjunctival fever, he never fulfilled his quest for a common cold vaccine.

Although Popular Science’s story focused on Huebner’s 1953 discovery of adenovirus as a root cause for the common cold, it wasn’t until Winston Price’s 1956 discovery that virologists realized rhinovirus was the chief common-cold culprit. Since Price’s discovery, three species of rhinovirus have been discovered (A, B, and C), including more than 150 distinct strains. Plus, a majority of the known rhinovirus genomes have been sequenced in an effort to find commonalities that might serve as the basis for a universal vaccine.

“Considering there are more than 100 types of A and B rhinoviruses,” notes Yury Bochkov, a respiratory virus specialist at the University of Wisconsin School of Medicine and Public Health, “you would have to put all 100 types in one vial of vaccine in order to enable protection” against just A and B rhinoviruses. Add in all the C rhinovirus types (more than 50), then cram in RSV’s virus types (more than 40), and that same vaccine would have to be packed with more than 200 strains. Even then, it would only offer protection against about two-thirds of all common colds. “That was considered the major obstacle in development of those vaccines,” Bochkov says.

When it comes to manufacturing universal vaccines, scientists hunt for the lowest common denominator—a common trait that the vaccine can target—shared by all variants of a virus. Unfortunately, viruses aren’t that cooperative. Breaking them down to find common traits is not so easy. To trigger antibody production, human immune systems must be able to recognize those common viral traits as belonging to an intruder. That means the traits must be exposed, or on the surface of the virus. Traits locked inside the virus particle, or in its capsid structure, are not detectable until after the virus has begun to replicate, which is too late to avoid infection.

Antibodies, which are made of protein-based immunoglobulins such as IgM and IgG, are Y-shaped cells that continuously circulate through our blood, and latch onto invading pathogens, which are recognizable by certain sequences in their surface proteins. Antibodies are capable of disabling the invaders until the white blood cell, or leukocyte, troops can arrive to kill them. The goal of a universal vaccine is to not only find an antibody-triggering trait common across those many distinct types of the same virus, but also find a trait that is slow to mutate—or one that doesn’t mutate at all. In the cases of universal coronavirus and influenza vaccines currently under development, researchers have focused on more than just the surface protein, targeting other viral parts, such as the surface protein’s stalk, that are still detectable by our immune systems, but less likely to mutate from one variant to the next.

Viruses travel light, in other words they don’t carry around the machinery to replicate on their own. Instead, they use their surface proteins to bind to our bodies’ cells, then trick them into replicating virus particles. Coronaviruses, for instance, are known for their distinctive spike surface proteins, which became the focus of COVID-19 vaccines. Similarly, rhinoviruses have their own distinguishing surface protein shaped like a cloverleaf, which plays an essential role in the virus’s ability to hijack cells and replicate. Unfortunately, surface proteins tend to mutate quickly, enabling viruses to shapeshift and evade detection by our immune systems. That’s a chief reason why flu vaccines, and now COVID-19 vaccines, must be updated at least annually.

Fortunately for RSV, scientists have identified such commonalities. RSV is considered among the most dangerous of common cold viruses, especially for infants and children who are susceptible to respiratory tract infections. After a failed human trial in the 1960s that led to the death of two infants, it took another half century before scientists identified an immutable common trait—RSV’s surface fusion protein, or F protein, that binds to cells. Now, four different vaccines are already in the final third phase of human trials. “And they’re working,” Martinello notes, “they’re working amazingly well. It’s a very exciting time for RSV right now.”

But for a common cold vaccine to make a dent in annual infections, protection against rhinovirus must be developed, too. While progress has been made on RSV, the quest for a universal rhinovirus vaccine has received less attention. That may be changing.

Since the 1960s, there have been several human clinical trials of rhinovirus vaccine candidates, although none have been universal. Still, some results have been promising—one trial reduced symptomatic colds from 47 percent to 3.5 percent. However, the vaccines have only been effective on a few of the more than 150 strains. In the 2010s, researchers developed synthetic peptide immunogens capable of triggering immune responses in rabbits exposed to 48 different strains; peptides are the building blocks of proteins, which give cells their shape, and peptide immunogens attract antibodies, encouraging their production. In a 2019 study, researchers identified a way in mice to deprive rhinoviruses (and other viruses) of a specific enzyme they need to replicate.

In 2016, a 50-valent rhinovirus vaccine, or 50 strains in one shot, was successfully trialed in rhesus macaques, and a vaccine with 25 strains in mice. But even if such vaccines make it into human trials, that leaves more than 100 unaccounted-for rhinovirus strains.

“What if you could split [all the different strains] into several groups?” Bochkov says. “Then I think you would have higher chances of finding something that would be conserved within a group.” It’s like breaking fractions into similar groups and finding the least common denominator for each—or, in this case, separating out groups of strains with common traits and developing individual vaccines for each, which are all later combined into one super-packed vaccine. That’s precisely the direction research team’s like Bochkov’s are heading with rhinovirus species C. Once separate vaccines are developed for individual groups, they might be bundled into a single shot, which is called a polyvalent vaccine. This approach of targeting multiple strains in one shot has already been proven a successful way to control viral diseases. The annual flu vaccine, for instance, is a polyvalent vaccine designed to target three or four of the flu strains most likely to circulate in a given year. Similarly, the new bivalent COVID booster shots create an immune response to both the original strain of SARS-CoV-2, as well as recent Omicron strains.

Better tools for genome sequencing are also on the rise, including AI software that can be used to analyze surface proteins and predict possible mutations, like Google’s AlphaFold. This combined with mRNA platform technologies that expedite vaccine development makes Martinello and Bochkov optimistic that more respiratory virus vaccines will be developed in the coming years. “Maybe we’ll see a flu, COVID, RSV vaccine all combined in one,” Bochkov says, adding that “vaccination would be the way to go in fighting the common cold.”

Even as progress has been made on a universal flu vaccine and a universal coronavirus vaccine, the quest for a universal common cold vaccine has received less attention. That’s in part because public health efforts need to focus and allocate vaccine-development on the deadliest and most infectious pathogens first. As contagious as common cold viruses are—they spread through droplets that are airborne or left on surfaces—COVID-19 is at least 10 times deadlier than the flu, and the flu is deadlier than the common cold. Still, the common cold can lead to serious complications for people who are immunocompromised or have lung conditions, like asthma and chronic obstructive pulmonary disease.

While the search for a universal common cold vaccine began several decades ago, it is not likely to be fulfilled anytime soon, despite recent advances like the RSV vaccine trials. So, keep those tissues handy and wash your hands frequently. Wearing face masks as a prevention tactic isn’t exclusive to fighting COVID—they also work against the spread of other respiratory illnesses, including the common cold. “We have to be cognizant of what the risks are and thoughtful about how we protect ourselves from getting sick,” Martinello notes. “If you are sick, stay home, keep your kids home, because you know when you’re out and about that’s how that’s how things further spread.”

And when common cold vaccines do arrive, even if they’re virus-specific at first, don’t hesitate to get your jab.

Source : Popular Science

The “Swiss Cheese Model” for Pandemic Defense

The “Swiss cheese model” of accident causation (more accurately called Emmental or Emmentaler cheese model [104]) originated with James T. Reason and Rob Lee in the 1990s (and was potentially influenced by other researchers).

As applied to COVID-19, this model recognizes the additive success of using multiple preventive interventions to reduce the risk of SARS-CoV-2 infection. No single slice of cheese (public health strategy) is perfect or sufficient at preventing the spread of SARS-CoV-2. Each slice has holes (inherent weaknesses or limitations) with variable number, size, and location over circumstances or time, which may allow viral transmission. SARS-CoV-2 infection occurs when multiple holes happen to align at the same time permitting a trajectory of successful transmission. When several interventions are used together and consistently and properly, the weaknesses in any one of them should be offset by the strengths of another.

The preventive interventions can be broken into personal and shared, although some interventions may be both. The order of the slices and holes in the illustration are not reflective of the degree of effectiveness of the interventions, given that the scenarios of transmission are variable and complex.

The black rats eating the slices of cheese represent factors undermining prevention efforts while the extra cheese represents a source of factors and opportunities favoring prevention efforts.

Source : BMC Infectious Disease

China Vows to Continue with ‘Dynamic-clearing’ COVID Strategy

China will persevere with its “dynamic-clearing” approach to COVID-19 cases as soon as they emerge, health officials said on Saturday, adding that measures must be implemented more precisely and meet the needs of vulnerable people.

The country’s strict COVID containment approach is still able to control the virus, despite the high transmissibility of COVID variants and asymptomatic carriers, an official from the China National Health Commission told a news conference.

China’s zero-COVID policy includes lockdowns, quarantining and rigorous testing, aimed at stopping the spread of the coronavirus.

Asked if there would be a change of policy in the near term, disease control official Hu Xiang said China’s measures are “completely correct, as well as the most economical and effective.”

“We should adhere to the principle of putting people and lives first, and the broader strategy of preventing imports from outside and internal rebounds,” she said.

The briefing followed a week in which markets surged on hope China would relax restrictions, buoyed further on Friday when a former disease control official told a banking conference that China would make “substantial” changes to COVID policy in the coming months.

Some areas had been guilty of unscientific “one-size-fits-all” lockdowns, the officials said, singling out the southwestern cities of Nanchong and Bijie, and Zhengzhou city officials in central Henan province for deliberately turning thousands of citizens’ health codes red.

“We attach great importance to these problems and are rectifying them,” said Tuo Jia, another disease control official.

Epidemic-hit areas must meet the needs of the elderly, sick, disabled, young and pregnant, Tuo said.

Officials said they would begin a push to increase vaccinations among the elderly, noting that while 86.35% of citizens aged 60 and over are fully vaccinated, fewer people 80 and older have had vaccinations and boosters.

China reported 3,837 new COVID-19 infections for Friday, of which 657 were symptomatic and 3,180 were asymptomatic, a slight decrease from the six-month-high of 4,045 new COVID-19 infections reported a day earlier.

Officials in Guangzhou said on Saturday the southern megacity is facing its most severe and complicated outbreak in three years of the virus, with 111 new locally transmitted symptomatic and 635 asymptomatic cases reported for a day earlier.

Source : Reuters

Bad Sleep Might Raise Your Odds for Glaucoma

Cara Murez wrote . . . . . . . . .

Poor sleep may be linked to glaucoma, a leading cause of blindness, new research suggests.

The study drew on a database of more than 400,000 people to explore links between sleep and vision loss.

Glaucoma is marked by progressive loss of light-sensitive cells in the eye and optic nerve damage. Left untreated, it can cause irreversible blindness. As many as 112 million people worldwide could be affected by 2040.

For the new study, the researchers considered a variety of sleep behaviors. These included too much sleep as well as too little, insomnia and daytime sleepiness, being a “night owl” or a “morning lark,” as well as snoring.

The investigators used data from more than 409,000 participants in the UK Biobank (average age: 57). The study defined normal sleep duration as seven to nine hours. The researchers used medical records and death data to track the health and lifespan of all participants until a first diagnosis of glaucoma, death, emigration or end of monitoring in 2021.

During an average 10.5-year monitoring period, the researchers identified 8,690 cases of glaucoma.

Frequent daytime sleepiness was associated with a 20% higher risk for the disease. The risk rose 12% with insomnia and 8% with short or long sleep duration. Snoring was associated with a 4% higher risk.

Compared to folks who had a healthy sleep pattern, people who snored or had daytime sleepiness were 10% more likely to have glaucoma. Insomniacs and those with a pattern of too much or too little sleep were 13% more likely to have the condition.

Compared to those not diagnosed with the disease, participants with glaucoma tended to be older and male, have high blood pressure or diabetes, and a history of smoking at some point.

The findings were published oneline in BMJ Open.

The study authors said it’s possible that glaucoma itself might influence sleep patterns rather than the other way around. The team included Huan Song from the West China Biomedical Big Data Center at West China Hospital at Sichuan University in China.

The investigators also pointed to plausible biological explanations for the link. The internal pressure of the eye, a key factor in the development of glaucoma, rises when a person is lying down and when sleep hormones are out of kilter, as occurs in insomnia, the researchers explained in a journal news release.

Depression and anxiety, which may accompany insomnia, may also increase internal eye pressure, possibly because of dysregulated cortisol production, the authors noted.

Repetitive or prolonged episodes of low oxygen due to sleep apnea (the sudden stopping of breathing during sleep) may also damage the optic nerve, they suggested.

As an observational study, this research doesn’t prove cause and effect.

But the findings underscore the need for sleep therapy in people who are at high risk of glaucoma. Eye checks in patients with chronic sleep disorders could look for early signs of the disease, and targeted screening might be cost-effective in high-risk groups, Song’s team said.

“As sleep behaviors are modifiable, these findings underscore the necessity of sleep intervention for individuals at high risk of glaucoma and potential ophthalmologic screening among individuals with chronic sleep problems to help prevent glaucoma,” the researchers concluded.

Source: HealthDay