‘If this thing boomerangs’: Second wave of infections feared

Agencies
May 8, 2020

As Europe and the US loosen their lockdowns against the coronavirus, health experts are expressing growing dread over what they say is an all-but-certain second wave of deaths and infections that could force governments to clamp back down.

"We are risking a backslide that will be intolerable," said Dr Ian Lipkin of Columbia University's Center for Infection and Immunity.

Around the world, German authorities began drawing up plans in case of a resurgence of the virus. Experts in Italy urged intensified efforts to identify new victims and trace their contacts. And France, which has not yet eased its lockdown, has already worked up a "reconfinement plan" in the event of a new wave.

"There will be a second wave, but the problem is to which extent. Is it a small wave or a big wave? It is too early to say," said Olivier Schwartz, head of the virus unit at France's Pasteur Institute.

In the US, with about half of the states easing their shutdowns to get their economies restarted and cellphone data showing that people are becoming restless and increasingly leaving home, public health authorities are worried.

Many states have not put in place the robust testing that experts believe is necessary to detect and contain new outbreaks. And many governors have pressed ahead before their states met one of the key benchmarks in the Trump administration's guidelines for reopening -- a 14-day downward trajectory in new illnesses and infections.

"If we relax these measures without having the proper public health safeguards in place, we can expect many more cases and, unfortunately, more deaths," said Josh Michaud, associate director of global health policy with the Kaiser Family Foundation in Washington.

Cases have continued to rise steadily in places such as Iowa and Missouri since the governors began reopening, while new infections have yo-yoed in Georgia, Tennessee and Texas.

Lipkin said he is most worried about two things: the reopening of bars, where people crowd together and lose their inhibitions, and large gatherings such as sporting events, concerts and plays. Preventing outbreaks will require aggressive contact tracing powered by armies of public health workers hundreds of thousands of people strong, which the US does not yet have, Lipkin said.

Worldwide the virus has infected more than 36 lakh people and killed over a quarter-million, according to a tally by Johns Hopkins University that experts agree understates the dimensions of the disaster because of limited testing, differences in counting the dead and concealment by some governments.

The US has recorded over 70,000 deaths and 12 lakh confirmed infections, while Europe has reported over 140,000 dead.

This week, the researchers behind a widely cited model from the University of Washington nearly doubled their projection of deaths in the US to around 134,000 through early August, in large part because of the easing of state stay-at-home restrictions. Newly confirmed infections per day in the US exceed 20,000 and deaths per day are running well over 1,000.

In hard-hit New York City, which has managed to bring down deaths dramatically even as confirmed infections continue to rise around the rest of the country, Mayor Bill de Blasio warned that some states may be reopening too quickly.

"My message to the rest of the country is learn from how much effort, how much discipline it took to finally bring these numbers down and follow the same path until you are sure that it is being beaten back," he said on CNN, "or else, if this thing boomerangs, you are putting off any kind of restart or recovery a hell of a lot longer."

A century ago, the Spanish flu epidemic's second wave was far deadlier than its first, in part because authorities allowed mass gatherings from Philadelphia to San Francisco.

"It is clear to me that we are in a critical moment of this fight. We risk complacency and accepting the preventable deaths of 2,000 Americans each day," epidemiologist Caitlin Rivers, a professor at Johns Hopkins, told a House subcommittee in Washington.

President Donald Trump, who has pressed hard to ease the restrictions that have throttled the economy and thrown more than three crore Americans out of work, pulled back Wednesday on White House plans revealed a day earlier to wind down the coronavirus task force.

He tweeted that the task force will continue meeting indefinitely with a "focus on SAFETY & OPENING UP OUR COUNTRY AGAIN".

Underscoring those economic concerns, the European Union predicted the worst recession in its quarter-century history. And the US unemployment rate for April, which comes out on Friday, is expected to hit a staggering 16 per cent, a level last seen during the Great Depression of the 1930s.

Governors continue to face demands, even lawsuits, to reopen. In Michigan, where armed demonstrators entered the Capitol last week, the Republican-led Legislature sued Democratic Governor Gretchen Whitmer, asking a judge to declare invalid her stay-at-home order, which runs at least through May 15.

In hard-hit Italy, which has begun easing restrictions, Dr Silvio Brusaferro, president of the Superior Institute of Health, urged "a huge investment" of resources to train medical personnel to monitor possible new cases of the virus, which has killed about 30,000 people nationwide.

He said that contact-tracing apps which are being built by dozens of countries and companies are not enough to manage future waves of infection.

German Chancellor Angela Merkel said after meeting with the country's 16 governors that restaurants and other businesses will be allowed to reopen in the coming weeks but that regional authorities will have to draw up a "restriction concept" for any county that reports 50 new cases for every 100,000 inhabitants within a week.

Lothar Wieler, head of Germany's national disease control centre, said scientists "know with great certainty that there will be a second wave" of infections.

Britain, with over 30,000 dead, the second-highest death toll in the world behind the US, plans to extend its lockdown but has begun recruiting 18,000 people to trace contacts of those infected.

In other developments, the US Centers for Disease Control and Prevention said nearly 5,000 coronavirus illnesses and at least 88 deaths have been reported among inmates in American jails and prisons. An additional 2,800 cases and 15 deaths were reported among guards and other staff members.

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Agencies
January 25,2020

Washington D.C., Jan 25: A new study conducted by a team of researchers reveals why individuals who have a history of early life adversity (ELA) are disproportionately prone to opioid addiction.

The study conducted examined how early adversities interact with factors such as increased access to opioids to directly influence brain development and function, causing a higher potential for opioid addiction.

The study was lead by UCI researchers and was published in Molecular Psychiatry.

Tallie Z. Baram, MD, PhD, the Danette Shepard Chair in Neurological Sciences at the UCI School of Medicine and one of the senior researchers for the study, was on the take that the widely known factor genetics that plays major role in addiction vulnerability, cannot be solely held responsible for the recent rise in opioid abuse.

To further clarify, the researchers simulated ELA in rats by limiting bedding and nesting materials during a short, postnatal period of time.

In female rats, this led to striking opioid addiction-like characteristics including an increased relapse- behaviour, for example.

As observed in addicted humans, the rats were willing to work very hard (pay a very high price) to obtain the drug.

Baram said: "Ultimately, we found that conditions during sensitive developmental periods can lead to vulnerability to the addictive effects of opioid drugs, especially in females, which is consistent with the prevalence of ELA in heroin-addicted women."

These findings can be used to highlight the importance given to sex differences in future ELA-related studies on opioid addiction, and in future prevention or intervention strategies being developed to address the growing opioid crisis.

The study conducted examined how early adversities interact with factors such as increased access to opioids to directly influence brain development and function, causing a higher potential for opioid addiction.

The study was lead by UCI researchers and was published in Molecular Psychiatry.

The study found that unpredictable, fragmented early life environments may lead to abnormal maturation of certain brain circuits, which profoundly impacts brain function and persists into adolescence and adulthood.

Tallie Z. Baram, MD, PhD, the Danette Shepard Chair in Neurological Sciences at the UCI School of Medicine and one of the senior researchers for the study, was on the take that the widely known factor genetics that plays major role in addiction vulnerability, cannot be solely held responsible for the recent rise in opioid abuse.

To further clarify, the researchers implanted ELA in rats by limiting bedding and nesting materials during a short, postnatal period of time.

In female rats, this led to striking opioid addiction-like characteristics including an increased relapse- behaviour, for example.

As observed in addicted humans, the rats were willing to work very hard (pay a very high price) to obtain the drug.

Baram said: "Ultimately, we found that conditions during sensitive developmental periods can lead to vulnerability to the addictive effects of opioid drugs, especially in females, which is consistent with the prevalence of ELA in heroin-addicted women."

These findings can be used to highlight the importance given to sex differences in future ELA-related studies on opioid addiction, and in future prevention or intervention strategies being developed to address the growing opioid crisis.

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Agencies
May 19,2020

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.

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Agencies
July 5,2020

The deadly coronavirus that entered India while there was still nip in the air has beaten rising mercury, humid conditions, unique Indian genome and has entered monsoon season with more potency as fresh cases are only breaking all records in the country.

India recorded a single-day spike of record 24,850 new coronavirus cases on Sunday, taking its total tally to 6.73 lakh corona-positive cases.

Top Indian microbiologists were hopeful in March that after the 21-day lockdown, as summer approaches, the rise in temperature would play an important role in preventing the drastic spread of COVID-19 virus in India.

Several virologists hinted that by June this year, the impact of COVID-19 would be less than what it appeared in March-April.

The claims have fallen flat as the virus is mutating fast, becoming more potent than ever.

According to experts, the novel coronavirus is a new virus whose seasonality and response to hot humid weather was never fully understood.

"The theory was based on the fact that high temperatures can kill the virus as in sterilisation techniques used in healthcare. But these are controlled environment conditions. There are many other factors besides temperature, humidity which influence the transmission rate among humans," Dr Anu Gupta, Head, Microbiologist and Infection Control, Fortis Escorts Heart Institute, told IANS.

There is no built-up immunity to COVID-19 in humans.

"Also, asymptomatic people might be passing it to many others unknowingly. New viruses tend not to follow the seasonal trend in their first year," Gupta emphasized.

Globally, as several countries are now experiencing hot weather, the World Health Organization (WHO) reported a record hike in the number of coronavirus cases, with the total rising by 2,12,326 in 24 hours in the highest single-day increase since COVID-19 broke out.

So far over 11 million people worldwide have tested positive for the disease which has led to over 5,25,000 deaths, according to data from Johns Hopkins University. The US remained the worst-hit country with over 28 lakh cases, followed by Brazil with 15.8 lakh.

According to Sandeep Nayar, Senior Consultant and HOD, Respiratory Medicine, Allergy & Sleep Disorders, BLK Super Speciality Hospital in New Delhi, whether temperature plays a role in COVID-19 infection is highly debated.

One school of thought said in the tropical regions of South Asia, the virus might not thrive longer.

"On the other hand, another school of thought has found that novel Coronavirus can survive in a hot and humid environment and tropical climate does not make a difference to the virus. According to them, this is what distinguishes the novel coronavirus from other common viruses, which usually wane in hot weather," stressed Nayar.

Not much has been studied in the past and no definite treatment or vaccine is available to date.

"Every day, new properties and manifestation of the disease come up. As of now, the only way to prevent this monster is by taking appropriate precautions. Hand hygiene, social distancing, cough etiquette and face masks definitely reduce spread of COVID-19 infection," Nayar told IANS.

Not just top Indian health experts, even Indian-American scientists had this theory in mind that sunshine and summer may ebb the spread of the coronavirus.

Ravi Godse, Director of Discharge Planning, UPMC Shadyside Pennsylvania in the US told IANS in April: "In the summer, the humidity can go up as well, meaning more water drops in the air. If the air is saturated with water and somebody sneezes virus droplets into such air, it is likely that the droplets will fall to the ground quicker, making them less infectious. So the short answer is yes, summer/sunshine could be bettera.

According to Dr Puneet Khanna, Head of Respiratory Medicine and Pulmonology, Manipal Hospital, Delhi, COVID-19 death rates are not too different in tropical countries but since the disease affected them late it was yet to show its peak in these areas.

"The virus can survive well in hot and humid countries and this is proven now," he stressed.

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