Category: Corona Virus

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WHO officials warn sharply of the ongoing dangers of the COVID-19 pandemic – WSWS

January 16, 2024

Throughout the world, COVID-19 infections, hospitalizations and deaths are surging amid the fourth winter of the pandemic, as the highly infectious and immune-resistant JN.1 variant spreads globally. Wherever wastewater sampling is conducted, levels of viral transmission are currently at the highest or second-highest levels of the entire pandemic.

This ongoing wave of mass infection underscores the utter criminality of the World Health Organization (WHO), Biden administration and other national health agencies ending their respective COVID-19 public health emergency (PHE) declarations last May. The result of these unscientific and politically motivated decisions was that virtually all pandemic surveillance was lifted, while masses of people were led to falsely believe that the pandemic was over.

In two extraordinary press briefings last week, WHO officials made clear the ongoing dangers of the pandemic, while hypocritically admonishing the global population for no longer taking precautions, ignoring their own culpability in this process.

On Wednesday, January 10, WHO Director-General Dr. Tedros Adhanom Ghebreyesus noted that in December the world had seen a surge in COVID-19 transmission fueled by holiday gatherings and the evolution of the JN.1 variant. He added:

Almost 10,000 deaths from COVID-19 were reported to the WHO in December and there was a 42 percent increase in hospitalizations and 62 percent increase in ICU admissions compared to November. However, the trends [on mortality] are based on data from less than 50 countries, mostly in Europe and the Americas. Its certain that there are also increases in other countries that are not being reported.

Information on the number of hospitalizations admissions is being provided by only 29 countries, while only 21 countries are providing data on ICU admissions. Again, these data are so scant because the vast majority of countries completely dismantled their pandemic surveillance systems in response to the WHOs ending of the PHE last May.

Speaking two days later at another press conference held by the WHO on their UN Web TV, devoted to the co-circulation of COVID, flu and respiratory pathogens, Dr. Maria Van Kerkhove, the WHOs Technical Lead on COVID-19, remarked, Essentially, given the lifting of the public health and social measures, with the world opened up, these viruses, these bacteria that pass efficiently between people through the air, take advantage.

Van Kerkhove stated that access to vaccines remains a challenge in much of the globe, noting that where vaccines are available, demand and uptake are quite low, raising concerns about the elderly and most vulnerable, including immunocompromised people and pregnant women. She then warned starkly:

What is critical to know right now is that the public health risk from COVID remains high globally. We have a pathogen that is circulating in all countries case-based data that is reported to the WHO is not a reliable indicator and has not been a reliable indicator for a couple of years now. If you look at the epidemiology curve it looks like the virus is gone, but it hasnt.

Van Kerkhove added, According to wastewater estimates we have from a number of countries, the actual circulation of SARS-CoV-2 is anywhere from two to 19 times higher than what is being reported. And what is difficult is that the virus is continuing to evolve. Although she noted that the number of deaths has reduced drastically from two years ago, there continues to be around 10,000 official COVID deaths per month.

However, Van Kerkhove cautioned that this represents less than a quarter of all countries reporting data, and half of official deaths were just from the US, meaning there is a massive undercounting simply from lack of reporting. She stated bluntly, We are missing deaths from countries around the world. Just because those countries arent reporting deaths doesnt mean they arent happening.

Official figures for January are expected to rise given the intense circulation of JN.1 and many large indoor gatherings that have taken place surrounding the holidays.

After acknowledging that the pandemic continues unchecked, Van Kerkhove noted:

On the one hand, while we are seeing a reduced impact, we feel that there is far too much burden in countries from COVID when we can prevent them with adequate tests, with adequate access to and use of antivirals, with appropriate clinical care, medical oxygen, and, of course, vaccination COVID is still a public health threat and is causing far too much burden and we can prevent it.

Van Kerkhove estimated that presently hundreds of thousands are hospitalized around the world for COVID, based on the limited data available.

Van Kerkhove then acknowledged that the post-acute phase of COVID-19 infections known as Long COVID is considerable. She said that 6-10 percent of symptomatic cases can evolve into Long COVID, potentially affecting multiple organs throughout the body, with debilitating conditions that can last for 12 months or longer.

Simple math means that tens or hundreds of millions of people will develop some level of Long COVID in the current global surge alone. It is no hyperbole to characterize Long COVID as a mass disabling event and a pandemic within a pandemic.

Van Kerkhove then warned, We dont know the long-term impacts of repeat infections Our concern is in five years from now, ten years from now, in 20 years from now, what are we going to see in terms of cardiac impairment, of pulmonary impairment, of neurological impairment; we dont know. We dont know everything about this virus. She continued to state that the problem is significant and research in better understanding and treating Long COVID is severely financially under-resourced.

Mehring Books

COVID, Capitalism, and Class War: A Social and Political Chronology of the Pandemic

A compilation of the World Socialist Web Site's coverage of this global crisis, available in epub and print formats.

The dire reports from these two leading WHO officials begs the question: why are they not moving to quickly reinstate the PHE and urge all world governments to reimpose strict anti-COVID mitigation measures to slow the spread of the virus.

Clearly, the WHOs abrupt scrapping of their PHE last May, one week before the Biden administration, came under intense pressure from US imperialism, to which they acquiesced. They were motivated by political pressures and not any meaningful change in the ongoing public health threat that COVID-19 clearly still posed.

In light of recent evidence that the JN.1 lineage of Omicron appears to have a higher predilection for the lower respiratory airways and the concomitant risk of the virus reverting to earlier, more virulent forms, it is imperative that the PHE be reimplemented and comprehensive public health programs be massively funded in every country.

Instead, all world governments have imposed a brutal forever COVID policy of endless waves of infections with a highly dangerous virus that harms more than just the respiratory organs, but every organ system in the body, with accumulating evidence that long-term consequences of pursuing these policies will have significant implications for the health of the global population.

As the second part of the World Socialist Web Sites New Year 2024 statement makes clear, the only viable solution to the present and future public health crises is a global elimination strategy that had proven possible even in the face of the highly infectious Omicron variant, as evidenced by efforts in Shanghai in spring of 2023.

Point 28 of the statement notes:

The longstanding success with Zero-COVID in China proved the viability of an elimination strategy towards COVID-19, even in less developed and densely-populated countries. At the same time, its ultimate demise reaffirmed the unviability of any nationally-based program in the epoch of imperialism. What proved to be unviable was the national framework, not the policy itself. Elimination remains both viable and necessary, but can now be attained only through the building of a mass movement fighting for the following principles:

The fight against the pandemic is a political and revolutionary question which requires a socialist solution.

The organization of public health must be on the basis of social need, not corporate profit.

The profit motive must be entirely removed from all healthcare, pharmaceutical and insurance companies.

Only a globally coordinated strategy can address the COVID-19 pandemic and create the conditions to develop comprehensive strategies to prevent potential epidemic and pandemic pathogens. The remarks made by the WHO leaders affirm the conclusions drawn by the WSWS in the New Year statement:

After four years of the pandemic, it is abundantly clear that such a global strategy will never arise under world capitalism, which subordinates all public health spending to the insatiable profit interests of a money-mad financial oligarchy. The very idea that an illness should be eliminated or eradicated, a central concept in public health, has been abandoned. Only through world socialist revolution will it be possible to end the pandemic, as well as stop the further descent into capitalist barbarism and World War III.

Join the fight to end the COVID-19 pandemic

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WHO officials warn sharply of the ongoing dangers of the COVID-19 pandemic - WSWS

Covid-19 vaccines saved 1.4 million lives across Europe, study finds – The Telegraph

January 16, 2024

Covid-19 vaccinations saved more than 1.4 million lives across Europe, according to the World Health Organization (WHO).

A new study analysing the impact of Covid-19 vaccines in 34 countries across Europe, found that they reduced deaths by 57 per cent between December 2020, when the vaccine rollouts began, and March 2023.

The cumulative death toll, currently at 2.5 million, might be as high as 4 million without the vaccines, says the study, with the first vaccine booster saving 700,000 lives alone.

Most people saved were aged 60 and over, the group most vulnerable to risk of severe illness and death from the respiratory virus. The study also found that Covid-19 vaccinations saved most lives during the Omicron wave, from December 2021 to April 2023 when huge numbers became infected.

Previous WHO estimates had put lives saved by the vaccine at 470,000, but that only covered the first months of the vaccine rollout.

Dr Hans Henri P. Kluge, WHOs Regional Director for Europe, welcomed the new data.

[There are] 1.4 million people in our region, most of them elderly, who are around to enjoy life with their loved ones because they took the vital decision to be vaccinated against Covid-19, he said.

This study documents the result of countries implementing that advice. The evidence is irrefutable.

Across the WHOs Europe region, Israel saw the biggest benefits from the vaccine, with a 75 per cent reduction, followed by Malta and Iceland with a 72 and 71 per cent decrease, respectively.

Countries that executed early roll-out programmes - such as Belgium, Ireland, the Netherlands and the UK - saw a greater number of lives saved overall by vaccination.

A landmark NHS study, published earlier this month, analysing the health data from every person in the UK, found that an additional 7,100 hospital admissions and deaths might have been saved in the summer of 2022 if everybody had received all their vaccinations and boosters.

Countries that vaccinated early and vaccinated at high levels were likely to see much higher deaths averted than countries who were vaccinating a bit later, said Dr Marc-Alain Widdowson, WHO Europes lead on infectious hazard management.

As cold weather intensifies across the Northern Hemisphere, Europe is facing a tridemic of respiratory diseases including flu, Covid-19 and RSV that threatens to push health systems to the brink.

Spain and Italy are among the worst affected countries, with Spain reintroducing mandatory face masks in hospitals and health centres earlier this month the decision was made just six months after the obligatory use of masks was stopped.

Dr Kluge said that society has now gained a base level of immunity, either through vaccination, infection, or both.

Covid-19 hasnt gone away. We have merely learned to live with it, he said.

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Covid-19 vaccines saved 1.4 million lives across Europe, study finds - The Telegraph

Long COVID-19 Patients Are at Higher Risk for Digestive Diseases For Up to One Year: Study – The Weather Channel

January 16, 2024

Representational image

Long COVID patients are at a higher risk for digestive diseases, for up to one year, according to a study.

The study, published in the journal BMC Medicine, showed that people who suffered both severe and mild COVID-19 infections suffered from digestive diseases like gastrointestinal (GI) dysfunction, peptic ulcers, gastroesophageal reflux disease (GERD), gallbladder disease, nonalcoholic liver disease, and pancreatic disease.

Our study provides insights into the association between COVID-19 and the long-term risk of digestive system disorders. COVID-19 patients are at a higher risk of developing digestive diseases, said the researchers in the paper.

The risks exhibited a stepwise escalation with the severity of COVID-19, were noted in cases of reinfection, and persisted even after 1-year follow-up. This highlights the need to understand the varying risks of digestive outcomes in COVID-19 patients over time, particularly those who experienced reinfection, and develop appropriate follow-up strategies, they added.

In the study, the team from Southern Medical University in China and University of California Los Angeles, US, compared rates of digestive diseases among COVID survivors 30 or more days after infection (112,311), a contemporary comparison group (359,671), and a pre-COVID group (370,979) in the UK.

Participants were adults aged 37 to 73, and COVID-19 survivors were infected from January 2020 to October 2022. The contemporary group was made up of people who lived at the same time as recruitment of the COVID-19 group, and the historical group was made up of uninfected participants with data from January 2017 to October 2019.

Relative to the contemporary group, elevated risk in COVID-19 survivors was 38% for GI dysfunction, 23% for peptic ulcers, 41% for GERD, 21% for gallbladder disease, 35% for severe liver disease, 27% for nonalcoholic liver disease, and 36% for pancreatic disease.

The risk of GERD rose stepwise with COVID-19 severity, and the risk of GERD and GI dysfunction persisted 1 year after diagnosis. Reinfected participants had a higher likelihood of having pancreatic disease.

This underscores the significance of ensuring that healthcare systems are equipped to provide appropriate care to this population of mild cases, as well as varying degrees of COVID severity.

In addition, the risks of GI dysfunction and GERD did not decrease after 1-year follow-up, revealing the long-term effect of COVID and the risks of digestive disorders.

The researchers said that the reasons for the increased risks may be faecal-oral viral transmission, interactions between the SARS-CoV-2 spike protein and the expression of angiotensin-converting enzyme 2 (ACE2) receptors in the digestive tract, or virus-associated inflammation.

"This underscores the significance of ensuring that healthcare systems are equipped to provide appropriate care to this population of mild cases, as well as varying degrees of COVID-19 severity," they wrote.

**

The above article has been published from a wire agency with minimal modifications to the headline and text.

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Long COVID-19 Patients Are at Higher Risk for Digestive Diseases For Up to One Year: Study - The Weather Channel

Post-COVID dysautonomias: what we know and (mainly) what we dont know – Nature.com

January 16, 2024

Anand, H. et al. Nervous system-systemic crosstalk in SARS-CoV-2/COVID-19: a unique dyshomeostasis syndrome. Front. Neurosci. 15, 727060 (2021).

Article PubMed PubMed Central Google Scholar

Nagai, M., Kato, M. & Keigo, D. Anxiety and hypertension in the COVID-19 era: how is the central autonomic network linked? Hypertens. Res. 45, 922923 (2022).

Article CAS PubMed PubMed Central Google Scholar

Goldstein, D. S. Stress and the extended autonomic system. Auton. Neurosci. 236, 102889 (2021).

Article PubMed PubMed Central Google Scholar

Goldstein, D. S. Adrenaline and the Inner World: An Introduction to Scientific Integrative Medicine (Johns Hopkins University Press, 2006).

Davis, H. E., McCorkell, L., Vogel, J. M. & Topol, E. J. Long COVID: major findings, mechanisms and recommendations. Nat. Rev. Microbiol. 21, 133146 (2023).

Article CAS PubMed PubMed Central Google Scholar

Langley, J. N. The autonomic nervous system. Brain 26, 126 (1903).

Article Google Scholar

Cannon, W. B. & de la Paz, D. Emotional stimulation of adrenal gland secretion. Am. J. Physiol. 28, 6470 (1911).

Article CAS Google Scholar

Dale, H. H. & Feldberg, W. The chemical transmission of secretory impulses to the sweat glands of the cat. J. Physiol. 82, 121128 (1934).

Article CAS PubMed PubMed Central Google Scholar

von Euler, U. S. A specific sympathomimetic ergone in adrenergic nerve fibres (sympathin) and its relations to adrenaline and noradrenaline. Acta Physiol. Scand. 12, 7396 (1946).

Article Google Scholar

Goldstein, D. S. Principles of Autonomic Medicine v. 4.0 https://research.ninds.nih.gov/staff-directory/david-s-goldstein-md-phd (2020).

Goldstein, D. S. et al. Sympathoadrenal imbalance before neurocardiogenic syncope. Am. J. Cardiol. 91, 5358 (2003).

Article PubMed Google Scholar

Wallin, B. G. & Sundlof, G. Sympathetic outflow to muscles during vasovagal syncope. J. Auton. Nerv. Syst. 6, 287291 (1982).

Article CAS PubMed Google Scholar

Meck, J. V. et al. Mechanisms of postspaceflight orthostatic hypotension: low 1-adrenergic receptor responses before flight and central autonomic dysregulation postflight. Am. J. Physiol. Heart Circ. Physiol. 286, H1486H1495 (2004).

Article CAS PubMed Google Scholar

Davis, H. E. et al. Characterizing long COVID in an international cohort: 7 months of symptoms and their impact. EClinicalMedicine 38, 101019 (2021).

Article PubMed PubMed Central Google Scholar

Erdal, Y. et al. Autonomic dysfunction in patients with COVID-19. Acta Neurol. Belg. 122, 885891 (2022).

Article PubMed PubMed Central Google Scholar

Goldstein, D. S. The possible association between COVID-19 and postural tachycardia syndrome. Heart Rhythm. 18, 508509 (2021).

Article PubMed Google Scholar

Miglis, M. G., Stiles, L. E. & Raj, S. R. POTS may be underestimated in Post-COVID assessments. J. Am. Coll. Cardiol. 80, e103 (2022).

Article PubMed PubMed Central Google Scholar

Raj, S. R. et al. Long-COVID postural tachycardia syndrome: an American Autonomic Society statement. Clin. Auton. Res. 31, 365368 (2021).

Article PubMed PubMed Central Google Scholar

Stahlberg, M. et al. Post-COVID-19 tachycardia syndrome: a distinct phenotype of post-acute COVID-19 syndrome. Am. J. Med. 134, 14511456 (2021).

Article PubMed PubMed Central Google Scholar

Ormiston, C. K., Swiatkiewicz, I. & Taub, P. R. Postural orthostatic tachycardia syndrome as a sequela of COVID-19. Heart Rhythm. 19, 18801889 (2022).

Article PubMed PubMed Central Google Scholar

Mallick, D. et al. COVID-19 induced postural orthostatic tachycardia syndrome (POTS): a review. Cureus 15, e36955 (2023).

PubMed PubMed Central Google Scholar

Miglis, M. G. et al. A case report of postural tachycardia syndrome after COVID-19. Clin. Auton. Res. 30, 449451 (2020).

Article PubMed PubMed Central Google Scholar

Blitshteyn, S. & Whitelaw, S. Postural orthostatic tachycardia syndrome (POTS) and other autonomic disorders after COVID-19 infection: a case series of 20 patients. Immunol. Res. 69, 205211 (2021).

Article CAS PubMed PubMed Central Google Scholar

Gall, N. P., James, S. & Kavi, L. Observational case series of postural tachycardia syndrome (PoTS) in post-COVID-19 patients. Br. J. Cardiol. 29, 3 (2022).

PubMed PubMed Central Google Scholar

Johansson, M. et al. Long-haul post-COVID-19 symptoms presenting as a variant of postural orthostatic tachycardia syndrome. The Swedish experience. J. Am. Coll. Cardiol. Case Rep. 3, 573580 (2021).

Google Scholar

Parker, W. H. et al. COVID-19 and postural tachycardia syndrome: a case series. Eur. Heart J. Case Rep. 5, ytab325 (2021).

Article PubMed PubMed Central Google Scholar

Bosco, J. & Titano, R. Severe post-COVID-19 dysautonomia: a case report. BMC Infect. Dis. 22, 214 (2022).

Article CAS PubMed PubMed Central Google Scholar

Drogalis-Kim, D., Kramer, C. & Duran, S. Ongoing dizziness following acute COVID-19 infection: a single center pediatric case series. Pediatrics 150, e2022056860 (2022).

Article PubMed Google Scholar

Hanson, J., Richley, M., Hsu, J. J., Lin, J. & Afshar, Y. Postural orthostatic tachycardia syndrome and orthostatic hypotension in post-acute sequelae of COVID-19 during pregnancy: a case report. Eur. Heart J. Case Rep. 6, ytac453 (2022).

Article PubMed PubMed Central Google Scholar

Fanciulli, A. et al. Impact of the COVID-19 pandemic on clinical autonomic practice in Europe. A survey of the European Academy of Neurology (EAN) and the European Federation of Autonomic Societies (EFAS).Eur. J. Neurol. https://doi.org/10.1111/ene.15787 (2023).

Seeley, M. C., Gallagher, C., Langdon, A., Ong, E. & Lau, D. H. Postural orthostatic tachycardia syndrome is prevalent in postacute sequela of COVID-19? Clin. Auton. Res. 32, 368 (2022).

Google Scholar

Varma-Doyle, A., Freeman, R., Mandeville, R. & Gibbons, C. Neuromuscular and autonomic features in Long COVID-19: a single-center retrospective review of clinical and objective findings. Clin. Auton. Res. 32, 370 (2022).

Google Scholar

Hastie, C. E. et al. Outcomes among confirmed cases and a matched comparison group in the Long-COVID in Scotland study. Nat. Commun. 13, 5663 (2022).

Article CAS PubMed PubMed Central Google Scholar

Sharma, V., Pattnaik, S., Ahluwalia, H. & Kaur, M. Pre-pandemic autonomic function as a predictor of the COVID clinical course in young adults. Clin. Exp. Pharmacol. Physiol. 87, 594603 (2023).

Article Google Scholar

Sletten, D. M., Suarez, G. A., Low, P. A., Mandrekar, J. & Singer, W. COMPASS 31: a refined and abbreviated composite autonomic symptom score. Mayo Clin. Proc. 87, 11961201 (2012).

Article PubMed PubMed Central Google Scholar

Buoite Stella, A. et al. Autonomic dysfunction in post-COVID patients with and without neurological symptoms: a prospective multidomain observational study. J. Neurol. 269, 587596 (2021).

Article PubMed PubMed Central Google Scholar

Eldokla, A. M. et al. Prevalence and patterns of symptoms of dysautonomia in patients with long-COVID syndrome: a cross-sectional study. Ann. Clin. Transl. Neurol. 9, 778785 (2022).

Article CAS PubMed PubMed Central Google Scholar

Ser, M. H. et al. Autonomic and neuropathic complaints of long-COVID objectified: an investigation from electrophysiological perspective. Neurol. Sci. 43, 61676177 (2022).

Article PubMed PubMed Central Google Scholar

Larsen, N. W. et al. Characterization of autonomic symptom burden in long COVID: a global survey of 2,314 adults. Front. Neurol. 13, 1012668 (2022).

Article PubMed PubMed Central Google Scholar

Rinaldi, L. et al. Incidence of post-COVID-19 autonomic syndrome in working-age patients within 6 months from hospital discharge. Clin. Auton. Res. 32, 367 (2022).

Google Scholar

Bryarly, M., Cabrera, J., Tarpara, K., Barshikar, S. & Vernino, S. Minimal objective autonomic dysfunction in long-COVID. Clin. Auton. Res. 32, 362 (2022).

Google Scholar

Jamal, S. M. et al. Prospective evaluation of autonomic dysfunction in post-acute sequela of COVID-19. J. Am. Coll. Cardiol. 79, 23252330 (2022).

Article PubMed PubMed Central Google Scholar

Oakley, J. C. & Hendrickson, R. C. Central and peripheral hyperadrenergic symptoms significantly contribute to symptom burden in people with post-acute sequela of COVID-19. Clin. Auton. Res. 32, 366 (2022).

Google Scholar

Townsend, L. et al. Fatigue following COVID-19 infection is not associated with autonomic dysfunction. PLoS One 16, e0247280 (2021).

Article CAS PubMed PubMed Central Google Scholar

Chung, T. H. & Azar, A. Autonomic nerve involvement in post-acute sequelae of SARS-CoV-2 syndrome (PASC). J. Clin. Med. 12, 73 (2022).

Article PubMed PubMed Central Google Scholar

Shouman, K. et al. Autonomic dysfunction following COVID-19 infection: an early experience. Clin. Auton. Res. 31, 385394 (2021).

Article PubMed PubMed Central Google Scholar

Low, P. A. Autonomic nervous system function. J. Clin. Neurophysiol. 10, 1427 (1993).

Article CAS PubMed Google Scholar

Acanfora, D. et al. Impaired vagal activity in long-COVID-19 patients. Viruses 14, 1035 (2022).

Article CAS PubMed PubMed Central Google Scholar

Asarcikli, L. D. et al. Heart rate variability and cardiac autonomic functions in post-COVID period. J. Interv. Cardiovasc. Electrophysiol. 63, 715721 (2022).

Article Google Scholar

Marques, K. C. et al. Reduction of cardiac autonomic modulation and increased sympathetic activity by heart rate variability in patients with long COVID. Front. Cardiovasc. Med. 9, 862001 (2022).

Article CAS PubMed PubMed Central Google Scholar

Menezes Junior, A. D. S., Schroder, A. A., Botelho, S. M. & Resende, A. L. Cardiac autonomic function in long COVID-19 using heart rate variability: an observational cross-sectional study. J. Clin. Med. 12, 100 (2022).

Article PubMed PubMed Central Google Scholar

Mohammadian, M. & Golchoobian, R. Potential autonomic nervous system dysfunction in COVID-19 patients detected by heart rate variability is a sign of SARS-CoV-2 neurotropic features. Mol. Biol. Rep. 49, 81318137 (2022).

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Post-COVID dysautonomias: what we know and (mainly) what we dont know - Nature.com

Go Vegetarian to Avoid COVID? Making Dialysis Centers Work Better – Medpage Today

January 16, 2024

TTHealthWatch is a weekly podcast from Texas Tech. In it, Elizabeth Tracey, director of electronic media for Johns Hopkins Medicine in Baltimore, and Rick Lange, MD, president of the Texas Tech University Health Sciences Center in El Paso, look at the top medical stories of the week.

This week's topics include a proteomic approach to cancer screening, vegetarian diet and COVID risk, performance of dialysis centers, and medical errors in hospitalized patients.

Program notes:

0:40 Incentivizing dialysis centers

1:40 Over 1,000 dialysis centers

2:40 How to adjust for neighborhood?

3:41 Comprehensive approach needed

4:00 Vegetarian diet and COVID risk

5:03 Importance of diet and disease

6:00 Immunity and foods

6:12 Diagnostic errors in hospitalized patients

7:12 Problems assessing the patient

8:18 Novel proteomics-based cancer screening

9:18 10 proteins with high accuracy

10:18 Different in men and women

11:18 Most useful biomarkers the low concentration ones

12:05 End

Transcript:

Elizabeth: Does being a vegetarian help you avoid COVID infection?

Rick: How often do we see diagnostic errors in hospitalized patients who die or are transferred to the ICU?

Elizabeth: Looking at proteomics to look for multiple cancers.

Rick: And looking at social risk and how it affects dialysis facility performance.

Elizabeth: That's what we're talking about this week on TTHealthWatch, your weekly look at the medical headlines from Texas Tech University Health Sciences Center in El Paso. I'm Elizabeth Tracey, a Baltimore-based medical journalist.

Rick: And I'm Rick Lange, president of Texas Tech University Health Sciences Center in El Paso, where I'm also dean of the Paul L. Foster School of Medicine.

Elizabeth: Rick, the one that you served up from JAMA about what happens in these dialysis facilities is one that really speaks to my heart having had multiple patients who have had circumstances that have been a little questionable surrounding dialysis. Are you okay with it if we start with that one?

Rick: Yeah. No, I think it's great, Elizabeth. It's an attempt to try to improve performance in dialysis centers by using incentives. How effective is it? We know that individuals that are on Medicaid in low-income situations, certain races, their outcome oftentimes at dialysis centers isn't quite as good. Things that we're trying to push people towards -- that is, doing home dialysis, it's less likely that they're able to participate.

But what CMS has tried to do was to compose a model that would reward facilities that have really good outcomes, take money away from centers that have a poor outcome. They thought by doing this, by the way, that they could actually drive and improve outcomes. By the way, they did that in about 30% of dialysis studies.

What this study did was they looked to see how effective that was. They analyzed almost 126,000 patients at over 1,000 dialysis centers. They noticed that about 50% of them had no social risk -- that is, they weren't African American and they didn't live in a low-income area. Then about 22% had two or more of these risk factors.

If you had two or more of these risk factors, you were much more likely to have money taken away from you than if you had none. In fact, if you had none you were more likely to have an incentive provided. Well, that's just the opposite of what we're trying to do. What we want to do is we want to try to take those centers and actually contribute more money to get a better outcome.

Now, in fairness, they tried to adjust these for individual patient-centered differences, but what they discovered is there are things that happen in the neighborhood that aren't captured by things like this: education status, transportation, crime, and access. If you actually incorporated these things, that also added some predictive value. It may mean that we need to adjust our incentives not only based upon the individual, but also a neighborhood or societal things as well.

Elizabeth: Help me to construct that model. What would it look like to try to adjust for the neighborhood and for social factors that surround the center?

Rick: If you're in a neighborhood that has a high crime rate, doesn't have transportation, doesn't have healthy food, doesn't have a transport center nearby, it's not surprising that you're going to have a worse outcome. We want to take those centers where they're going to and actually provide them additional monies or additional resources, so they can improve the outcome. We don't want to take money away from them. We actually want to incentivize them.

One of the indexes you can use is what's called an area deprivation index (ADI). It looks at an individual neighborhood to say, "Is that neighborhood deprived of things that will provide good outcomes for the patient?" We can use that to help adjust for these things.

Elizabeth: Remember, last week we talked about this comprehensive approach to pre-pregnancy, pregnancy, and post-pregnancy with regard to early childhood outcomes. What this study says to me is that this comprehensive approach to health, which is, of course, one of those "duh" conclusions -- I'm really good at restating the obvious -- is really the important thing here.

Rick: Yes. We're trying to make sure that all individuals have the same quality of care and some individuals, some neighborhoods, just need more attention to get there. This is a societal problem. If we don't address this, it costs us more as a society.

Elizabeth: Since we're talking about cost of health care, let's turn to the BMJ Nutrition, Prevention & Health. This is an examination that came from Brazil, of vegetarian and plant-based diets and their association with COVID-19 infection. It's observational, 702 participants, where sociodemographic characteristics, dietary information, and COVID-19 outcomes were collected between March and July of 2022.

When they took a closer look at these folks, their omnivorous group comprised 424 people and their plant-based group 278. They adjusted for all kinds of confounders -- BMI, physical activity, preexisting medical conditions -- and found that the plant-based and vegetarian group had a 39% reduced incidence of COVID-19 infection compared with the omnivorous group. Gosh, this vegetarian and plant-based thing is something we should probably be looking at more closely from a societal and policy perspective.

Rick: We have talked before about the importance of diet in a number of disease entities in terms of reducing inflammation and reducing high blood pressure. I'm going to put a little bit of a cautionary note to this. First of all, do I think that eating healthy is good? Yes, I do. At best, this is an association. You and I know that these individuals that eat healthy also have other healthy lifestyle behaviors. They are more likely to exercise. They have less weight. They have less comorbidities. I'm wondering whether it's not that the diet, but we just have a group of individuals that are more likely to wear a mask, or more likely to be isolated, or more likely to wash their hands, or more likely to have other healthy lifestyle things that could account for it.

Elizabeth: There is no question that the vegetarians have a lower BMI, a lower prevalence of overweight, obesity, and metabolic syndrome, and that they exercised more. That probably had some impact on how often they got infected with COVID-19. Then they also make the point about the relationship between immunity and foods, which is something that we seem to be seeing a lot more.

Rick: In the end, Elizabeth, whether we decide there is a causality or association, I think we're both in agreement that a healthy diet is in fact a healthy diet.

Elizabeth: You got that right. Let's turn then to JAMA Internal Medicine, this issue of diagnostic errors.

Rick: We've known for well over a decade now that diagnostic errors play an important role in patients receiving care in the hospital. This particular study focused on two groups of individuals: those individuals who die in the hospital, or those who are hospitalized and then are transferred to an intensive care unit. They ask a very simple question: "How often do we see diagnostic errors in these individuals?"

To determine the presence, the underlying cause, and actually the harms of diagnostic errors, they did a retrospective study of 29 different academic medical centers. They had two trained clinicians comb the charts to see whether there were any diagnostic errors or not, and if so, did they result in harm?

After examining the records of about 2,400 patients, they discovered that about a fourth of these, 23%, had experienced a diagnostic error. This error was judged to have contributed to harm in about 20% (17.8%).

When they look at the most common diagnostic errors, they fell in primarily two groups: problems assessing the patient -- either we didn't get the right diagnosis or we didn't establish it quickly enough; or secondly, problems with test ordering and interpretation. We didn't order the right test, we ordered the test and didn't look at it, or we ordered the test and didn't see how it fit in the entire picture at all.

What this study doesn't tell us is, would the outcome of these patients have been any different? Regardless, this is an area that we still need to address.

Elizabeth: Yeah. This has, of course, emerged as a cause clbre in lots of arenas and it's unclear to me exactly how we're going to get our arms around it, because they seem like fairly variable kinds of errors.

Rick: Yep, and you're right. There were six or seven different types. I focused on the two that were most common. We're hopeful that artificial intelligence can help in some ways. Unfortunately, as we talked about a couple of weeks ago, it can actually make the problem worse if the data in and the way you're analyzing it isn't particularly helpful.

Are there other things that we can do? We can educate the physician workforce better, make sure we're not anchoring on a specific diagnosis, and not overburdening the physicians and healthcare providers. A number of different ways to address this.

Elizabeth: Finally, let's turn to BMJ Oncology and this is a look at a novel proteomics-based plasma test for early detection of multiple cancers in the general population. This is obviously an objective. Wouldn't it be great to be able to just draw blood and assess somebody for the presence of very early cancers? It's also helpful in terms of early detection, early treatment, and better outcomes, although that is not a solid-line relationship.

This paper describes this novel proteome-based multicancer screening test. They had 440 participants, healthy and diagnosed with 18 early-stage solid tumors. In this group, they measured more than 3,000 high-abundance and low-abundance proteins in each sample using a number of approaches. They identified a limited set of sex-specific proteins that could detect early-stage cancers and their tissue of origin with high accuracy.

They were able to boil this down to 10 proteins that showed high accuracy for both males and females -- in the males, 98%, and in the females, 98% at stage 1, and a specificity of 99%. Their panels were able to identify 93% of cancers among the males and 84% of the cancers among the females. They were able to identify in more than 80% of cases the tissue of origin of the cancer. A lot of pretty impressive results in people they already knew had cancer, and this proteome-based screening test is promising and they say clearly should be followed up.

Rick: Elizabeth, I would agree. It does need follow-up and validation. They're all patients from the Ukraine. They are all racially or ethnically very similar.

The thing that was fascinating is, they test over 3,000 proteins. They found that 10 specific proteins could identify the presence of cancer, but they were different in men than they were in women. The second thing that was fascinating is they tried to identify was the cancer present, but where was it located, and they had to use over 150 different proteins to do that.

It would be nice to take a blood test and to be able to screen. To be able to do that, it's got to be very sensitive and very specific. Ultimately, as you mentioned, it needs to improve cancer outcome. The thought is if you can detect it early, you can treat it, get rid of it early and improve outcomes. That may be true in some cancers and may not be true in others.

The other thing I would say is that most of the cancers they detected weren't as early as they thought. They weren't stage 1 cancers. Most of them were stage 2 and stage 3. We know as cancers evolve their proteins change, so a lot of work to be done, but I'm glad that people are pursuing this.

Elizabeth: Oh, absolutely. They cite something that I thought was really interesting. They say that nearly 60% of cancer-related deaths are due to cancers for which no screening test exists. I was really unaware of that particular statistic. The other thing I would note about their test, not only the fact that men and women screen very differently, but that their most useful biomarkers for early-stage cancers were those that were present in low concentrations, not the ones that were present in high concentrations, which is also a novel finding.

Rick: It is and what it means is that you've got to have very sensitive ways of looking for protein that's at a very low level. I hope that in 20 or 30 years we're able to crack this nut.

Elizabeth: I'm hoping it's not going to be 20 or 30 years. On that note then, that's a look at this week's medical headlines from Texas Tech. I'm Elizabeth Tracey.

Rick: And I'm Rick Lange. Y'all listen up and make healthy choices.

Link:

Go Vegetarian to Avoid COVID? Making Dialysis Centers Work Better - Medpage Today

Covid Cases in India: India logs 605 new Covid cases, four deaths in past 24 hours – Times of India

January 16, 2024

15:32 (IST), Jan 9

61 new COVID cases reported in Maharashtra

Sixty-one new cases were recorded in the state on Monday, as per an official update on COVID-19 from the Public Health Department of Maharashtra.The department also reported that 70 patients were discharged on the same day. The recovery rate in the state was recorded at 98.17 per cent while the case fatality rate stood at 1.81 per cent.A total of 2728 COVID tests were conducted in the state on Monday, which included 1439 first RT-PCR tests and 1305 RAT tests. The positivity rate for the day was 2.23 per cent. As of today, 250 patients have been infected with the JN.1 variant in the state.Meanwhile, according to sources, there were a total of 682 cases of JN. 1 sub-variant of COVID-19 has been reported from 12 states across the country as of January 6.199 cases were reported in Karnataka, 148 in Kerala, 139 in Maharashtra, 47 in Goa, 36 from Gujarat, 30 each from Andhra Pradesh and Rajasthan, 26 in Tamil Nadu, 21 in New Delhi, 3 in Odisha, 2 in Telangana and one in Haryana.

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Covid Cases in India: India logs 605 new Covid cases, four deaths in past 24 hours - Times of India

Chinese scientists ‘create’ a mutant coronavirus strain that attacks the BRAIN and has a 100% kill rate in mic – Daily Mail

January 16, 2024

By Caitlin Tilley, Health Reporter For Dailymail.Com 17:59 16 Jan 2024, updated 21:34 16 Jan 2024

Chinese scientists have been experimenting with a mutantcoronavirusstrain that is 100 percent lethal in mice despite concerns such research could spark another pandemic.

Scientists in Beijing who are linked to the Chinese military cloned a Covid-like virus found in pangolins,known asGX_P2V, and used it to infect mice.

The mice had been 'humanized', meaning they were engineered to express a protein found in people, with the goal being to assess how the virus might react in humans.

Every rodent that was infected with the pathogen died within eight days, which the researchers described as 'surprisingly' quick.

The team were also surprised to find high levels of viral load in the mice's brains and eyes - suggesting the virus, despite being related to Covid, multiplies and spreads through the body in a unique way.

Writing in a scientific paper that has not yet been published, they warned the finding 'underscores a spillover risk of GX_P2V into humans'.

Professor Francois Balloux,an infectious disease expert based at University College London, wrote on Twitter (X): 'It's a terrible study, scientifically totally pointless.

'I can see nothing of vague interest that could be learned from force-infecting a weird breed of humanized mice with a random virus. Conversely, I could see how such stuff might go wrong...'

Professor Richard Ebright, a chemist at Rutgers University in New Brunswick, New Jersey, told DailyMail.com he wholeheartedly agreed with Professor Balloux's assessment.

He added: 'The preprint does not specify the biosafety level and biosafety precautions used for the research.

'The absence of this information raises the concerning possibility that part or all of this research, like the research in Wuhan in 2016-2019 that likely caused the Covid-19 pandemic, recklessly was performed without the minimal biosafety containment and practices essential for research with a potential pandemic pathogens.'

A research group whose work is feared to have started the Covid pandemic is being funded by the US Government to do similar experiments in other parts of the world.

According to the study, carried out by theBeijingUniversity of Chemical Technology, the virus was discovered in 2017prior to the Covid outbreak.

It was discovered in Malaysia in pangolins - scaly mammals that are known harborers of coronaviruses andwere heavily speculated to be the intermediate host that passed Covid from bats to humans.

The researcherscloned the virus and stored multiple copes in the Beijing lab, where it continued to evolve.

It is unclear when the newly surfaced study was conducted. But the researchers said it was possible the virus had undergone a 'virulence-enhancing mutation' in storage, which made it more deadly.

For the new research, eight mice were infected with the virus, eight were infected with an inactivated virus and eight were used as a control group.

All mice infected with the virus died. They succumbed to the infection between seven and eight days after being infected.

Symptoms included their eyes turning completely white, rapid weight loss and fatigue.

Researchers found 'significant amounts' of the virus in the rodents' brains, lungs, noses, eyes and windpipes.

By day six, the viral load had 'significantly decreased' in the lungs, but the animals' brains had shrunk and there were 'exceptionally high' virus levels in their brains.

The results suggest that the virus infects via the respiratory system and then migrates to the brain - unlike Covid which causes lower lung infections and pneumonia in severe cases. However, there have been examples of Covid being found in brain tissue of severely sick patients.

'Severe brain infection during the later stages of infection may be the key cause of death in these mice,' the researchers said.

They concluded: 'This is the first report showing that a SARS-CoV-2-related pangolin coronavirus can cause 100 percent mortality in hACE2 mice, suggesting a risk for GX_P2V to spill over into humans.'

However, the original strain of Covid also killed 100 percent in mice in some studies, meaning the new results may not be directly applicable to humans.

Dr Gennadi Glinsky, a retired professor of medicine at Stanford, said on social media: 'This madness must be stopped before [it is] too late.'

DailyMail.com exposed in 2022 how similar research virus-manipulation research was being carried out by Boston University.

Researchers were found to have created a new Covid strain that had an 80 percent death rate among mice.

It sparked nationwide debate about whether the experiments were an illegal form of research known as 'gain of function' - which involves purposefully making viruses more deadly or infectious to study their evolution.

The Biden Administration tightened rules around such research in October 2022, but the definition of gain of function remains contested.

Dr Christina Parks, a molecular biologist from the University of Michigan, said the Chinese study was 'classic gain of function, whether they tell you it is or not.'

One of the Chinese researchers was Dr YigangTong, who trained at the Academy of Military Medical Sciences, a Chinese military medical research institute run by thePeople's Liberation Army.

Dr Tong studied there between 1988 and 1991 for a master of science and then again between 1997 and 2000 for a PhD.

He also co-authored a paper in 2023 with 'bat woman' Zheng-Li Shi, who helps run the Wuhan Institute of Virology (WIV).

The WIV has been designated the most likely source of the Covid pandemic by the FBI and US Department of Energy in what has been dubbed the 'lab leak' theory.

Researchers there, with US Government grants, were performing gain of function experiments on coronaviruses in the months leading up to the Covid outbreak.

The virus first emerged miles away from the WIV, where researchers were known to be working on coronaviruses found in bats.

It comes asDr Peter Daszak, head of the New York based non-profit EcoHealth Alliance, whichfunded controversial experiments inWuhanwhich some fear started the pandemic, presented the discovery of a never-before-seen virus with 'almost' as much potential to infect humans as Covid.

Dr Daszak, a friend of Dr Anthony Fauci, the ex-chief medical advisor to the US President, revealed his team have already found one bat coronavirus of considerable interest.

'We found a lot of SARS-related coronaviruses, but one in particular we found was quite common in bats where people were commonly exposed,' he told the WHO event, attended by MailOnline.

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Chinese scientists 'create' a mutant coronavirus strain that attacks the BRAIN and has a 100% kill rate in mic - Daily Mail

Innovative COVID-19 analysis supports prevention protocols in health care settings – Medical Xpress

January 16, 2024

This article has been reviewed according to ScienceX's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:

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In early 2020, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a highly contagious and pathogenic virus, made its alarming debut and quickly spread worldwide, causing the novel coronavirus (COVID-19) pandemic that threatened human health and public safety.

While the world was brought to a standstill, hospitals and health care systems entered uncharted territory and quickly adapted to the evolving health crisis to care for their community and keep potentially sick patients and health care workers from spreading the virus.

The magnitude of response involved the reinforced universal masking of health care workers and patients at the hospital and regular SARS-CoV-2 testing of all health care workers and patients upon admission, regardless of symptoms, and strict isolation protocols for those infected with the virus.

Approximately four years after the pandemic was declared, researchers at University of California San Diego School of Medicine used high-end technology and an innovative approach to evaluate the effectiveness of those prevention measures implemented in the health care setting during the last three waves of the pandemic.

The study, published in the January 16, 2024, online edition of Clinical Infectious Diseases, was a first of its kind to use information from electronic health and contact tracing records to closely analyze the genetic makeup of the virus combined with the comparison of how the diverse strains were physically being spread among patients and health care workers in the hospital.

Researchers found that the implemented infection prevention parameters in the health care setting, including ventilation standards of at least five clean air changes per hour, combined with universal masking, prevented most SARS-CoV-2 transmissions. In patients who tested positive for the virus, personal protective equipment (PPE) shielded and virtually eliminated health careassociated transmission.

"When the pandemic started, it was scary because initially we did not have rapid diagnostic nor treatments available, and we did not fully understand how the virus was transmitted or if our infection prevention protocols were adequate," said Francesca Torriani, MD, senior author of the study, and program director of Infection Prevention and infectious disease specialist at UC San Diego Health.

"Therefore, the potential implications of the virus and the welfare of our workforce and patients was an utmost concern. I witnessed health care workers fearful of contracting the virus at work and potentially infecting their loved ones at home."

Torriani adds that limiting the spread of infection and blocking the virus at the source became the highest priority.

"In response to the progressing pandemic and with the trust and support from executive leadership at UC San Diego Health, we learned many life-saving lessons and strengthened infection prevention control measures to reduce the risk of transmission between patients and health care workers. The swift adoption and modification of infection prevention protocols in health care were felt to be an opportunity for deeper exploration of the effectiveness of our procedures."

The researchers took an innovative approach never used before to evaluate the different variants of the samples to identify if they were temporarily or physically near one another, suggesting health care transmission.

Electronic health record data of patients, whose identities were protected throughout the study, and metadata about staff access and movement to these records, accompanied by a robust contact tracing program, were used to classify, isolate and assess individuals exposed to specific strains of the virus.

"While the virus strains were very distinguishable in the second and third wave of the pandemic, during the explosive and homogenous omicron wave, we found that we could not rely on genetic data alone," said Christopher Longhurst, MD, co-author of the study, executive director of Jacobs Center for Health Innovation, and chief medical officer and chief digital officer at UC San Diego Health.

"We had to dive deeper into the electronic documentation and social network analysis, such as individuals with similar virus strains, and considering their physical interaction in the hospital, to determine what really happened and how the virus was being spread."

Researchers examined the genetic makeup of SARS-CoV-2 during three consecutive waves and compared how closely a person's genetic variant was related to another's.

The study involved the collection of 12,933 virus samples from 35,666 patients and health care professionals from November 1, 2020 to February 27, 2022.

"Even when hundreds of health care workers were becoming infected every week during the peak of the omicron wave, we found that they were no more likely to acquire the virus in the hospital system," said Joel Wertheim, Ph.D., co-senior author of the study and associate professor at UC San Diego School of Medicine. "The outcomes reveal the hidden patterns of viral transmission."

The results from both the genetic and social networking analysis showed that while universal masking was key to prevent transmissions, airborne negative pressure rooms, universal N95 respirator masks or even closing the door of a patient's room were not essential elements to protect against transmission in the health care setting.

In fact, most transmissions occurred outside of the health care setting, physical contact in the community, between households or when universal masking was not followed in the setting of unrecognized SARS-CoV-2 infection. Viral transmission was more likely to occur in shared spaces, such as break-rooms or lobbies.

"Our analysis really highlights that our health care system, with its safety measures including ventilation standards, robust viral testing, and early implementation of universal masking, was able to protect health care workers and patients during the pandemic," said Shira Abeles, MD, co-author of the study, associate professor in the Department of Medicine at UC San Diego School of Medicine and infectious disease specialist at UC San Diego Health.

Longhurst adds the type of technological approach used can be a model for future studies and a tool deployed for epidemics of highly contagious infectious diseases.

"The pandemic has shown us what's at stake. This novel methodology, combining a digital social network derived from electronic health record data with genomic analysis of viral strains, can be used again in the future to model spread of health care associated infections," said Longhurst.

More information: Clinical Infectious Diseases (2024).

Journal information: Clinical Infectious Diseases

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Innovative COVID-19 analysis supports prevention protocols in health care settings - Medical Xpress

SARS-CoV-2 biology and host interactions – Nature.com

January 16, 2024

Gorbalenya, A. E. et al. The species severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nat. Microbiol. 5, 536544 (2020).

Article Google Scholar

Zhou, P. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270273 (2020).

Article CAS PubMed PubMed Central Google Scholar

Zhu, N. et al. A novel coronavirus from patients with pneumonia in China, 2019. N. Engl. J. Med. 382, 727733 (2020).

Article CAS PubMed PubMed Central Google Scholar

Coronavirus (COVID-19) Dashboard. WHO https://covid19.who.int/ (2022).

Telenti, A., Hodcroft, E. B. & Robertson, D. L. The evolution and biology of SARS-CoV-2 variants. Cold Spring Harb. Persp. Med. 12, a041390 (2022).

Article CAS Google Scholar

Harvey, W. T. et al. SARS-CoV-2 variants, spike mutations and immune escape. Nat. Rev. Microbiol. 19, 409424 (2021).

Article CAS PubMed PubMed Central Google Scholar

Grant, R. et al. When to update COVID-19 vaccine composition. Nat. Med. 29, 776780 (2023).

Article CAS PubMed Google Scholar

Jungreis, I., Sealfon, R. & Kellis, M. SARS-CoV-2 gene content and COVID-19 mutation impact by comparing 44 Sarbecovirus genomes. Nat. Commun. 12, 2642 (2021).

Article CAS PubMed PubMed Central Google Scholar

Jungreis, I. et al. Conflicting and ambiguous names of overlapping ORFs in the SARS-CoV-2 genome: a homology-based resolution. Virology 558, 145151 (2021).

Article CAS PubMed Google Scholar

Finkel, Y. et al. The coding capacity of SARS-CoV-2. Nature 589, 125130 (2020).

Article PubMed Google Scholar

Gordon, D. E. et al. A SARS-CoV-2 protein interaction map reveals targets for drug repurposing. Nature 583, 459468 (2020).

Article CAS PubMed PubMed Central Google Scholar

Kim, D. et al. The architecture of SARS-CoV-2 transcriptome. Cell 181, 914921.e10 (2020).

Article CAS PubMed PubMed Central Google Scholar

Huston, N. C. et al. Comprehensive in vivo secondary structure of the SARS-CoV-2 genome reveals novel regulatory motifs and mechanisms. Mol. Cell 81, 584598.e5 (2021).

Article CAS PubMed PubMed Central Google Scholar

Lan, T. C. T. et al. Secondary structural ensembles of the SARS-CoV-2 RNA genome in infected cells. Nat. Commun. 13, 1128 (2022).

Article CAS PubMed PubMed Central Google Scholar

Ziv, O. et al. The short- and long-range RNARNA interactome of SARS-CoV-2. Mol. Cell 80, 10671077.e5 (2020).

Article CAS PubMed PubMed Central Google Scholar

Madhugiri, R., Fricke, M., Marz, M. & Ziebuhr, J. Coronavirus cis-acting RNA elements. Adv. Virus Res. 96, 127163 (2016).

Article CAS PubMed PubMed Central Google Scholar

Tidu, A. et al. The viral protein NSP1 acts as a ribosome gatekeeper for shutting down host translation and fostering SARS-CoV-2 translation. RNA 27, 253264 (2021). This publication demonstrated that SARS-CoV-2 relies on stem loop 1 in the 5 UTR to evade the nsp1-induced translational shutoff of its own genes.

Article CAS PubMed Central Google Scholar

Bujanic, L. et al. The key features of SARS-CoV-2 leader and NSP1 required for viral escape of NSP1-mediated repression. RNA 28, 766779 (2022).

Article CAS PubMed PubMed Central Google Scholar

Iserman, C. et al. Genomic RNA elements drive phase separation of the SARS-CoV-2 nucleocapsid. Mol. Cell 80, 10781091.e6 (2020).

Article CAS PubMed PubMed Central Google Scholar

Bhatt, P. R. et al. Structural basis of ribosomal frameshifting during translation of the SARS-CoV-2 RNA genome. Science 372, 13061313 (2021). In-depth structural and biochemical analysis into the mechanism of the programmed ribosomal frameshift for SARS-CoV-2.

Article CAS PubMed PubMed Central Google Scholar

Sun, L. et al. In vivo structural characterization of the SARS-CoV-2 RNA genome identifies host proteins vulnerable to repurposed drugs. Cell 184, 18651883.e20 (2021).

Article CAS PubMed PubMed Central Google Scholar

Jackson, C. B., Farzan, M., Chen, B. & Choe, H. Mechanisms of SARS-CoV-2 entry into cells. Nat. Rev. Mol. Cell Biol. 23, 320 (2021). Comprehensive review on SARS-CoV-2 entry mechanism.

Article PubMed PubMed Central Google Scholar

Hoffmann, M., Kleine-Weber, H. & Phlmann, S. A multibasic cleavage site in the spike protein of SARS-CoV-2 is essential for infection of human lung cells. Mol. Cell 78, 779784.e5 (2020). This article highlights the presence of a multibasic S1/S2 cleavage site in the SARS-CoV-2 spike protein that can be cut by furin and is a prerequisite for viral entry into lung cells.

Article CAS PubMed PubMed Central Google Scholar

Hansen, J. et al. Studies in humanized mice and convalescent humans yield a SARS-CoV-2 antibody cocktail. Science 369, 10101014 (2020).

Article CAS PubMed PubMed Central Google Scholar

Robbiani, D. F. et al. Convergent antibody responses to SARS-CoV-2 in convalescent individuals. Nature 584, 437442 (2020).

Article CAS PubMed PubMed Central Google Scholar

Pinto, D. et al. Cross-neutralization of SARS-CoV-2 by a human monoclonal SARS-CoV antibody. Nature 583, 290295 (2020).

Article CAS PubMed Google Scholar

Yuan, M. et al. A highly conserved cryptic epitope in the receptor binding domains of SARS-CoV-2 and SARS-CoV. Science 368, 630633 (2020).

Article CAS PubMed PubMed Central Google Scholar

Liu, L. et al. Potent neutralizing antibodies against multiple epitopes on SARS-CoV-2 spike. Nature 584, 450456 (2020). This is one of the first publications to report the receptor-binding domain (RBD) and N-terminal domain (NTD) epitopes as the two main neutralization targets on the SARS-CoV-2 spike protein.

Article CAS PubMed Google Scholar

Chi, X. et al. A neutralizing human antibody binds to the N-terminal domain of the spike protein of SARS-CoV-2. Science 369, 650655 (2020).

Article CAS PubMed PubMed Central Google Scholar

Meng, B. et al. SARS-CoV-2 spike N-terminal domain modulates TMPRSS2-dependent viral entry and fusogenicity. Cell Rep. 40, 111220 (2022). Here, it was shown that the SARS-CoV-2 spike proteins NTD can modulate S1/S2 cleavage and influence TMPRSS2 usage and fusogenicity.

Article CAS PubMed PubMed Central Google Scholar

Hoffmann, M. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 181, 271280.e8 (2020). The first publication to confirm that, similar to SARS-CoV, the processing of the SARS-CoV-2 spike protein is mediated by TMPRSS2.

Article CAS PubMed PubMed Central Google Scholar

Zhao, M. M. et al. Cathepsin L plays a key role in SARS-CoV-2 infection in humans and humanized mice and is a promising target for new drug development. Signal. Transduct. Target. Ther. 6, 134 (2021).

Article CAS PubMed PubMed Central Google Scholar

Ziegler, C. G. K. et al. SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells and is detected in specific cell subsets across tissues. Cell 181, 10161035.e19 (2020).

Article CAS PubMed PubMed Central Google Scholar

Su, M. C. et al. An atypical RNA pseudoknot stimulator and an upstream attenuation signal for 1 ribosomal frameshifting of SARS coronavirus. Nucleic Acids Res. 33, 42654275 (2005).

Article CAS PubMed PubMed Central Google Scholar

Zhang, K. et al. Cryo-EM and antisense targeting of the 28-kDa frameshift stimulation element from the SARS-CoV-2 RNA genome. Nat. Struct. Mol. Biol. 28, 747754 (2021).

Article CAS PubMed PubMed Central Google Scholar

Brierley, I., Digard, P. & Inglis, S. C. Characterization of an efficient coronavirus ribosomal frameshifting signal: requirement for an RNA pseudoknot. Cell 57, 537547 (1989).

Article CAS PubMed PubMed Central Google Scholar

Sun, Y. et al. Restriction of SARS-CoV-2 replication by targeting programmed 1 ribosomal frameshifting. Proc. Natl Acad. Sci. USA 118, e2023051118 (2021).

Article CAS PubMed PubMed Central Google Scholar

Osipiuk, J. et al. Structure of papain-like protease from SARS-CoV-2 and its complexes with non-covalent inhibitors. Nat. Commun. 12, 743 (2021).

Article CAS PubMed PubMed Central Google Scholar

Jin, Z. et al. Structure of Mpro from SARS-CoV-2 and discovery of its inhibitors. Nature 582, 289293 (2020).

Article CAS PubMed Google Scholar

Ziebuhr, J., Snijder, E. J. & Gorbalenya, A. E. Virus-encoded proteinases and proteolytic processing in the Nidovirales. J. Gen. Virol. 81, 853879 (2000).

Article CAS PubMed Google Scholar

Thoms, M. et al. Structural basis for translational shutdown and immune evasion by the Nsp1 protein of SARS-CoV-2. Science 369, 12491256 (2020). Thoms et al. (2020) and Schubert et al. (2020) elucidate the binding of SARS-CoV-2 nsp1 to the ribosome and cause translational shutdown.

Article CAS PubMed PubMed Central Google Scholar

Schubert, K. et al. SARS-CoV-2 Nsp1 binds the ribosomal mRNA channel to inhibit translation. Nat. Struct. Mol. Biol. 27, 959966 (2020).

Article CAS PubMed Google Scholar

Fisher, T. et al. Parsing the role of NSP1 in SARS-CoV-2 infection. Cell Rep. 39, 110954 (2022).

Article CAS PubMed PubMed Central Google Scholar

Snijder, E. J., Decroly, E. & Ziebuhr, J. The nonstructural proteins directing coronavirus RNA synthesis and processing. In Advances in Virus Research Vol. 96 (ed. Ziebuhr, J.) 59126 (Academic Press, 2016).

Cortese, M. et al. Integrative imaging reveals SARS-CoV-2-induced reshaping of subcellular morphologies. Cell Host Microbe 28, 853866.e5 (2020).

Article CAS PubMed PubMed Central Google Scholar

Snijder, E. J. et al. A unifying structural and functional model of the coronavirus replication organelle: tracking down RNA synthesis. PLoS Biol. 18, e3000715 (2020).

Article CAS PubMed PubMed Central Google Scholar

Wolff, G., Melia, C. E., Snijder, E. J. & Brcena, M. Double-membrane vesicles as platforms for viral replication. Trends Microbiol. 28, 10221033 (2020).

Article CAS PubMed PubMed Central Google Scholar

Klein, S. et al. SARS-CoV-2 structure and replication characterized by in situ cryo-electron tomography. Nat. Commun. 11, 5885 (2020).

Article CAS PubMed PubMed Central Google Scholar

Ricciardi, S. et al. The role of NSP6 in the biogenesis of the SARS-CoV-2 replication organelle. Nature 606, 761768 (2022).

Article CAS PubMed PubMed Central Google Scholar

Twu, W. I. et al. Contribution of autophagy machinery factors to HCV and SARS-CoV-2 replication organelle formation. Cell Rep. 37, 110049 (2021).

Article CAS PubMed PubMed Central Google Scholar

Tabata, K. et al. Convergent use of phosphatidic acid for hepatitis C virus and SARS-CoV-2 replication organelle formation. Nat. Commun. 12, 7276 (2021).

Article CAS PubMed PubMed Central Google Scholar

Excerpt from:

SARS-CoV-2 biology and host interactions - Nature.com

Is It COVID-19, a Cold, or the Flu? What to Do as COVID and Flu Cases Surge – Boston University

January 16, 2024

Heading out on a crowded bus or train? It might be time to wear a mask after a recent surge in COVID cases, according to BU infectious diseases researcher David Hamer. Photo via iStock/sibway

COVID-19

Here we go again. Another winter, another COVID-19 wave. As many Americans try their best to move on from or ignore the coronaviruscalling quits on masking, skipping vaccinations, not bothering to testCOVID-19 is surging in the United States.

Current data suggests virus levels in Massachusetts recently hit peaks unseen since the Omicron variant burst onto the scene two years ago. According to the latest numbers from Massachusetts Department of Public Health, COVID-19 cases in the state jumped from around 2,000 a week in early November to nearly 6,000 a week by the end of December. Local physicians reported a continued rise in cases into January. The upswing has been driven by a new highly transmissible coronavirus variant, JN.1an Omicron offshoot thats now the dominant strain of the virus in the US.

Throw in flu and RSV, plus the usual wintry sniffles from colds, and we have all the ingredients for a lousy, laid-up winter. Just 18 percent of Massachusetts residents are up-to-date with their COVID vaccinations; 37 percent have had a flu shot.

To get the latest on the surge, whether we all need to dig out those masks again, and how to tell whether its COVID, the flu, or a cold causing that runny nose and sore throat, The Brink spoke with Boston University infectious diseases expert David Hamer. A BU School of Public Health and Chobanian & Avedisian School of Medicine professor of global health and medicine, Hamer is also a core director and researcher at BUs Center on Emerging Infectious Diseases.

Hamer: We are seeing more COVID cases nationwide, but its complicated. Part of the problem is the quality of the data that feeds into this. It used to be when everybody was doing active testing and using PCR tests, all that data fed into the public health systems. But now lots of people are doing home tests, and those dont end up being captured, so the data arent as good as they were two years ago at the heart of the pandemic.

But, that said, theres definitely a substantial increase of reported cases in Massachusetts, and the wastewater data had been creeping up, as well, so a lot of signs that theres more transmission. This has been the biggest spike weve had since Omicron. And compounding that, theres more flu being transmitted also. I think were looking at sort of a syndemic of multiple diseases. What to me is really interesting is that we havent had a big surge in COVID for a whileis it now starting to settle into more of a respiratory season pattern?

Hamer: Yes, is the short answer. Many hospitals in the Northeast, including Boston Medical Center [BUs primary teaching hospital], have gone back to masks. I have a clinic todayI had not been using a mask consistently, but I think its advisable [now], because theres a higher risk.

And then public transportation, less than 5 percent of people wear masks in my experience, but I started masking more about a month ago because I was watching the numbers, thinking I dont want to get COVIDor other respiratory viruses, for that matter. In crowded places where theres likely to be inadequate ventilation, right now is a good time to think about having a mask.

Hamer: The level of boosting is really pretty woeful relative to what it should be. The JN.1 variant has been on the risethe CDC estimated that almost two-thirds of COVID cases in the US now are due to this subvariant. The bivalent vaccine, the modified vaccine that we have available, was designed for other Omicron subvariants, but it cross-protects against this. People really should be thinking about having a booster if they havent had it.

Hamer: Its really hard to tell. Between more immunity among individuals due to COVID vaccines or having had natural COVID infections, possibly the evolution of the virus toward a milder [disease], causing more upper respiratory symptoms, theres so much overlap between the common cold, COVID, RSV, andsomewhatinfluenza. Usually, you have a fever with influenza, but not always now with COVID. A lot of patients Ive seen will only have a stuffy or runny nose, a little bit of a cough. They may not necessarily have a fever, severe fatigue, and other symptoms that would be more suggestive of COVID, or loss of sense of smell, which were not seeing as commonly anymore.

Any respiratory symptoms should trigger testing, because SARS-CoV-2 is so easily transmissible. You dont want your coworkers, your family members, to become sick, so its important to know.

Hamer: They should spend five days in relative isolationat home, if they canbefore they resurface. And then when they start going back out in public, or if they go back to work, they should ideally wear a mask with all external contacts for the next five days. This goes back to studies we did here at BU among studentsbut also in studies that colleagues of ours did at Mass General with an older population. On average, young healthy BU students would shed virus and, by day five, many of them had gotten down to levels where they had undetectable or very low levels of viral load. But some were still shedding virus out to day seven, eight, nine, or even 10. Usually, it was around seven or eight that they finished up. So, people are still infected for at least five to seven or eight days after an episode. And thats in young, healthy students; in an older population, the duration of viral shedding is more prolonged.

Hamer: There are still people who have long COVID. Theres a lot of evidence that suggests vaccination and treatments like Paxlovid may help reduce the likelihood of long COVID developing. The flip side of that is theres a lot of evidence that people arent accessing the treatments, theyre not using them. Theyre not for everybody, but for those who are older, have underlying diseases or certain risk factors, they should be used.

Hamer: Yeah, unfortunately, its not over. A lot of people I knew that were very, very careful for three years, when it seemed like everything was good, they started going back to their usual liveshaving more social interactions, not wearing masks in public placesand many people that had never become infected had their first infection. And Im one of them.

Hamer: Theres still a fair amount of COVID circulating. Theres also a rising risk of influenza, as well as other regular respiratory viruses, and people should be thinking about doing things that help reduce their risk. So, vaccination. If they become infected, testing; if they test positive, isolating. Also, if theyre at higher risk, speaking with their physician about having oral treatment. The public health service message is if you have cold symptoms, you should, if at all possible, try not to come to work or go to school.

This interview has been edited for length and clarity.

Need a COVID-19 rapid test? BUs City Convenience is now offering two rapid antigen tests for $9.99. Need a flu shot? Student Health Services will be hosting immunization clinics on January 24, 25, and 26check its website for details.

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Is It COVID-19, a Cold, or the Flu? What to Do as COVID and Flu Cases Surge - Boston University

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