Category: Corona Virus

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UC Davis Launches Clinical Trials to Treat a Deadly Coronavirus Disease in Cats (Not the One that Causes COVID-19) – YubaNet

August 11, 2022

August 10, 2022 Scientists from the University of California, Davis, School of Veterinary Medicine have launched new clinical trials focused on improving treatments for feline infectious peritonitis, or FIP, and are currently enrolling patients at the UC Davis veterinary hospital.

FIP is a serious disease caused by a feline coronavirus variant, though not the one that causes COVID-19. The virus will spread through a cats body causing systemic inflammation. Up to 95% of cats diagnosed with FIP die without treatment. Cats can develop FIP at any age, but it is usually diagnosed in cats between 6 months and 2 years of age. It is one of the most common causes of death in young cats with infectious diseases. Currently there is no successful treatment approved for veterinarians in the United States.

Previous research conducted by UC Davis Professor Emeritus Niels Pedersen uncovered several promising treatments for this disease, including an antiviral drug that is not available to veterinarians in the U.S. Associate Professor Amir Kol, Professor Brian Murphy and Assistant Professor Krystle Reagan with the School of Veterinary Medicine are expanding on Pedersens research to further improve FIP treatment. They are seeking cats in the early to mid-stage of FIP disease for inclusion in clinical trials.

Trials will examine antiviral drugs, stem cell therapy

One trial will compare whether cats improve when treated with one of two closely related antiviral drugs. The first drug, remdesivir, is an antiviral drug with emergency use authorization from the FDA to treat COVID-19. If fully licensed, veterinarians could prescribe it to affected cats in the future. The second drug, GS-441524 is closely related to remdesivir. Pedersen found it safe and effective in treating cats with FIP. Currently veterinarians cannot prescribe it in the U.S. In this study, cats will receive either oral GS-441524 or oral remdesivir for comparison. Cats eligible for the study must be diagnosed with the wet form of FIP, in which obvious fluid build-up is present within the abdomen and chest.

The other trial, funded by the National Institute of Child Health and Development, will examine if antiviral drugs combined with a new stem cell therapy using mesenchymal stem cells, or MSCs, improve response to treatment for FIP. The goal of the study is to see if cell therapy can direct a more effective antiviral immune response and help regenerate the cats compromised immune system post-infection. For this study, one group will receive antiviral drugs along with infusions of MSCs, and the other will receive an antiviral drug and placebo infusions.

FIP, as many other chronic viral infections, is characterized by a dysfunctional immune system that is unable to clear the virus, said Kol, associate professor in the schools Department of Pathology, Microbiology and Immunology. Our study explores a novel cellular therapy that may help cats with FIP to better fight infection, clear the virus, and regenerate their injured immune systems. Results from our study will be highly impactful with immediate translatable potential.

Potential to help children

The trial could help humans as well. It is part of a larger study looking into new treatments for multisystem inflammatory syndrome in children, or MIS-C, a condition that causes organs and other body parts to become inflamed. FIP is similar to MIS-C and provides a clinically relevant model to investigate this novel, multipronged therapeutic approach. While the exact causes of MIS-C remain unclear, it is known that children diagnosed with it had the virus that causes COVID-19 or had been in contact with someone who was COVID-19 positive.

Owners interested in enrolling their cats in these clinical trials must live in Northern California or close by because cats will need several trips to UC Davis. Cats will need to meet the medical criteria. To learn more, visit UC Davis Veterinary Clinical Trials.

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UC Davis Launches Clinical Trials to Treat a Deadly Coronavirus Disease in Cats (Not the One that Causes COVID-19) - YubaNet

Hawaii Department of Health reports 3,189 new infections, 14 coronavirus-related deaths – Honolulu Star-Advertiser

August 11, 2022

The Hawaii Department of Health today reported 3,189 new COVID-19 infections over the past week, lower than reported the previous week, bringing the total number of cases since the start of the pandemic to 332,822.

The states seven-day average of new cases also fell to 452, down from 528 reported on Aug. 3, representing a decline for three weeks in a row. DOHs daily average reflects new cases per day from July 30 to Aug. 5, which is an earlier set of days than the new infections count.

Actual numbers are estimated to be at least five to six times higher since these figures do not include home test kit results.

DOH also reported 14 more deaths, bringing the states coronavirus-related death toll to 1,606.

The states average positivity rate, meanwhile, continued its downward trend to 12.4%, compared to 13.8% reported the previous week, representing tests performed between Aug. 2 to 8.

By island, there were 2,262 new infections reported on Oahu, 369 on Hawaii island, 342 on Maui, 162 on Kauai, and six on Molokai. Another 48 infections were reported for out-of-state Hawaii residents.

There are 142 patients with COVID in Hawaii hospitals today, according to the Healthcare Association of Hawaii, with 11 in intensive care.

For the past week, HAH reported an average of 141 COVID patients hospitalized, and an average of 23 new COVID admissions per day.

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Hawaii Department of Health reports 3,189 new infections, 14 coronavirus-related deaths - Honolulu Star-Advertiser

Time to Recovery of Severely Ill COVID-19 Patients and its Predictors: | JMDH – Dove Medical Press

August 11, 2022

Introduction

COVID-19 is one of the leading causes of morbidity and mortality globally. It is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and was first identified in Wuhan, China in early December 2019. It can cause fever, headache, shortness of breath, coughing, body weakness, sore throat, pain, and severe respiratory syndrome in human beings and is mainly transmitted by respiratory droplets and close contact with an infected human being.1 On January 30, 2020, the outbreak was declared a public health emergency of international concern by the WHO. According to the WHO daily situation report, currently the transmission is classified as community transmission and the total cases of COVID-19 are increasing worldwide; there were a total of 538,321,874 confirmed cases and 6,320,599 deaths as of June 22, 2022.2

In Ethiopia, the first case of COVID-19 was confirmed on March 13, 2020 and the infection has been spreading to all parts of the country, including Tigray region, wherein this research was conducted. According to the WHO, Ethiopia reported a total of 484,536 confirmed cases and 7524 deaths as of June 22, 2022.2

The infection fatality rates of COVID-19 patients, patient outcomes and related complications reported so far have varied considerably between countries. Previous studies showed that the overall mortality rate of COVID-19 patients is 3.77% 5.4%,35 and 41.1% - 61.5%68 among critical ill and severe patients. To reduce the infection fatality rate, understanding the factors associated with the duration of viral ribonucleic acid (RNA) shedding, the time from infection to viral RNA-negative conversion in COVID-19 patients is urgently needed.9 Moreover, it is also important to evaluate the testing time in order to reduce the infection fatality rate.10

Reports from previous studies indicated that the median duration of viral shedding in COVID-19 patients ranged from 847 days.9,1117 Most of the studies conducted on the duration of SARS-COV-2 shedding among COVID-19 patients are from China and Europe. The recovery time among severely ill patients is limited and different factors might hasten recovery or delay of the disease. Evidences reveal that older age, the time lag from illness onset to hospital admission and underlying comorbidities are associated with prolonged duration of viral RNA shedding in COVID-19 patients.9,1620 However, the epidemic in high income countries seems to be different from that of low and middle income countries in the risk factors, speed of the spread of the virus, and the record of the death toll related to the duration of SARS-COV-2 shedding.

Understanding the average time of recovery and its predictors is crucial for the decision making process at national and international levels in order to formulate preventive measures and optimize treatment options. Different studies have shown that the median time to recovery from COVID-19 patients varies across settings and disease status. The present study aimed to estimate the time to recovery and identify its associated factors among severely ill COVID-19 patients admitted to treatment centers in Tigray, Northern Ethiopia. This study provided useful information to predict the recovery time of severely ill COVID-19 patients through this retrospective cohort study.

A retrospective cohort study was analyzed that involved 139 severely ill COVID-19 patients admitted to isolation and treatment centers in Tigray, northern Ethiopia. Regardless of signs or symptoms development, all individuals with laboratory confirmed SARS-CoV-2 infection were admitted to the isolation and treatment centers within 24 hours. Anyone who has contact with confirmed COVID-19 case was being isolated for 14 days. Persons who failed to develop symptoms within 14 days were discharged from the isolation centers. Cases were confirmed by polymerase chain reaction (PCR) in the treatment centers.

All laboratory-confirmed positive COVID-19 severely ill patients admitted to treatment centers in the region between May 7 and October 28, 2020 with a definite outcome (recovered or dead) were designated as study participants.

The data were collected using a standardized form from electronic medical records. The data set contains demographic characteristics such as age, gender and occupation, clinical information of the patients contains temperature at admission, sign and symptoms status (such as fever, cough, shortness of breath, pain, sore throat, headache, body weakness), and presence of comorbidity (such as cardiovascular disease, diabetes mellitus, renal disease, respiratory disease) and patient outcomes (recovered or died). All severely ill COVID-19 patients admitted to the treatment centers between May 7 and October 28, 2020 were included in this study. Those severely ill patients with incomplete demographic and treatment outcome were excluded from the study.

In this study, the dependent variable was time to recovery from COVID-19 among severely ill patients and recovery is the event of interest. The time was estimated in days and recovery time was defined as the number of days it takes from the day the PCR test was positive until the patient is diagnosed negative for COVID-19 and discharged from treatment centers. The confirmed COVID-19 patients in the treatment centers were retested when symptoms subside and the body temperature remains at the normal range for at least three days and they were considered as recovered only after receiving two consecutive laboratory tests negative.

The independent variables considered in this study were sex, age, occupation, symptoms, comorbidity and type of comorbidity, temperature, travel history and source of infection.

The COVID-19 cases were all individuals tested positive for SARS-CoV-2 by PCR. Symptomatic cases were defined as any SARS-CoV-2 positive individual by PCR with at least one sign or symptom for COVID-19, including but not limited to: cough, fever, shortness of breath, headache, sore throat, and pain. Cases with comorbidity are COVID-19 patients with at least one known preexisting chronic medical illness. Severely ill COVID-19 patients: These patients with clinical signs of pneumonia and have at least one of the following conditions i) respiratory rate interval > 30 breaths/min; ii) SpO2 (saturation of peripheral oxygen) < 93% at rest; iii) severe respiratory distress, and iv) oxygenation index (artery partial pressure of oxygen/inspired oxygen fraction, PaO2/FiO2) < 300 mmHg.

The data were coded, cleaned, and checked for inconsistencies and completeness. STATA version 16 software was used for data processing and data analysis. Summary measures such as counts, percentages, means, medians and IQRs were calculated. The Log rank test was applied to compare the survival time between different predictors. A cox proportional hazard regression model was used to determine the potential risk factors associated with the duration time to recovery among severely ill COVID-19 patients. Factors associated with outcome at p-value < 0.20 in bivariate Cox regression were selected for multivariable Cox regression analysis. An adjusted hazard ratio (AHR) with 95% confidence interval was computed and statistical significance was declared at p-value < 0.05. Cox proportional hazards assumption was checked using the Schoenfeld residual test.

The ethics committee of Mekelle University, College of Health Sciences approved the current study with the ethical clearance registration number of IBR1826/2021. The study was conducted in accordance with the Declaration of Helsinki. Consent to participate was fully waived as the study participants were not directly involved in the study (ie an already existing data were utilized for analysis in the current study). The confidentiality of data was kept as there were no personal identifiers used and neither the raw data nor the extracted data were passed to a third person.

A total of 139 severely ill COVID-19 patients were included in this study that was reported from May 7, 2020 to October 28, 2020. The median age of the patients was 35 years (IQR, 2760). A total of 55.4% of patients were younger than 40 years, and 25.9% were older than 59 years. The patients in the non-survivor group were much older than those in the survivor group [median = 57 years (IQR, 29.572 years) versus median = 30 years (IQR, 2540 years), p-value < 0.001]. Of the non-survival patients (56 (40.3%) of 139), 48.2% of the patients were older than 59 years. The majority of COVID-19 patients (77.0%) were males and 73.2% of COVID-19 deaths were in men. Majority (60.4%) of the severely ill COVID-19 patients their sources of infection were from the community and 18% were imported. Among the study patients in our study, 20.1% of the patients had travel history and 40.3% were died (Table 1).

Table 1 Background Characteristics of 139 Severely Ill COVID-19 Patients Admitted to Treatment Centers of Tigray, Northern Ethiopia, 2020

Of the total study patients, 61.2% were symptomatic. The most common symptoms at the onset of disease reported were shortness of breath 57.5%, and cough 52.5%. This is followed by body weakness 36.7%, fever 32.4% and pain 28.1%. Among the non-survival patients (56 (40.3%) of 139), 78.6% had shortness of breath and 71.4% had cough symptoms. Moreover, 28.8% patients had one or more coexisting medical conditions alongside COVID-19. The comorbidity rate in the non-survivor group was higher than that of the survivor group (44.6% versus 18.1%, p-value < 0.001). Based on the body temperature on admission, 71.9% of the patients had temperature < 37.3C and 28.1% had elevated temperature 37.3C (Table 2). The most frequent comorbidities were cardiovascular diseases (50%), diabetes mellitus (20%) and respiratory diseases (18%) (Figure 1).

Table 2 Clinical Characteristics of 139 Severely Ill COVID-19 Patients in Tigray, Northern Ethiopia, 2020

Figure 1 Types of underline comorbidity of severely ill COVID-19 patients in Tigray, 2020. *Cardiovascular diseases included hypertension and heart failure. **Other diseases include traumatic injury, HIV, malignancy, hepatitis, cancer, rabies, smoker, peptic ulcer disease.

A total of 139 severely ill COVID-19 patients were followed for a minimum of 1 and a maximum of 37 days with median follow-up of time 18 days (IQR: 1127). Eighty-three patients were recovered with median time of 26 days (95% CI: 2327 days). The overall incidence recovery rate was 3.1 (95% CI: 2.5 3.9) per 100 person-days of observations. The incidence recovery rate among male and female severely ill patients was 3.1 per 100 person-day (95% CI: 2.54.0) and 3.2 per 100 person-day (95% CI: 2.05.1) respectively. In this study, the recovery rate from COVID-19 among severely ill patients with and without comorbidity was found to be 2.1 (95% CI: 1.33.5) and 3.5 (95% CI: 2.84.4) per 100 person-day respectively. Log Rank test was used to compare survival time between categories of different predictors. The survival estimates of severely ill patients varied in relation to age, fever, cough, shortness of breath, headache, body weakness, pain, and underline comorbidity (Tables 1 and 2). The survival status of severely ill COVID-19 patients was also estimated by the KaplanMeier survival curve. The overall graph of KaplanMeier survival function depicted that the curve tends to decrease rapidly in between 18 and 26 days indicating that most severely ill COVID-19 patients recovered within this time (Figure 2). A separate KaplanMeier survivor functions curve was constructed to estimates the survival time based on different covariates to see the existence of difference in recovery rate between categories of individual covariates. There was a significant difference in the time of recovery between patients with and without previous medical conditions or comorbidity, where patients without comorbidity recovered faster (Figure 3). A significant difference in the recovery rate among the two groups is also found by the Log rank test (Table 2). The median recovery times of the patients with and without comorbidity were 32 days and 24 days, respectively.

Figure 2 Kaplan-Meier survival estimate for time to recovery among severely ill COVID-19 patients in Tigray, Northern Ethiopia.

Figure 3 Kaplan-Meier survival estimate for time to recovery among patients with and without comorbidity.

Predictors that had association at a p-value of <0.20 in bivariate Cox regression were included in multivariable Cox regression. Age, fever, coughing, shortness of breath, sore throat, headache, body weakness, pain, comorbidity, and temperature were statistically significant at a p-value of < 0.20 level of significance. In the multivariable cox regression model only age, shortness of breath, body weakness and comorbidity were found to have statistically significant association with recovery time among the severely ill COVID-19 patients. Severely ill COVID-19 patients who were aged < 40 years had 4.1 times higher rate of recovery as compared to patients who were aged 60 and above years (AHR=4.09, 95% CI: 1.5810.61). In addition, the recovery rate was higher for patients who had no underline comorbidity diseases (AHR = 2.48, 95% CI: 1.185.24), shortness of breath (AHR = 2.07, 95% CI: 1.083.98) and body weakness (AHR = 2.62, 95% CI: 1.205.72) (Table 3). The Schoenfeld residual test results confirmed that the proportional hazard assumption satisfies.

Table 3 Predictors of Time to Recovery Among Severely Ill COVID-19 Patients in Tigray Region, 2020

This study comprised 139 severely ill COVID-19 patients who were admitted to treatment centers in Tigray region. Our study shows that the overall median time to recovery among severely ill COVID-19 patients was 26 days, which is consistent with some previous research study.11,2123 However, the median recovery time was lower in many other previous studies. For instance, a study done in Eka Kotebe General Hospital, Ethiopia (19 days),20 Guangzhou Eighth Peoples Hospital, China (12 days),9 Singapore (12 days),24 University of California San Diego (7 days)25 and Wollega Referral Hospital, Ethiopia (18 days).26 The discrepancy of the findings could be the differences in the composition of study participants, sample size and severity of the disease. In addition, the fact that the recovery time was shorter among patients treated in China, Singapore and the United States of America could be due to the availability of advanced medical technologies and medications and effective COVID-19 patients management approach and conducive hospital setting. The selected study participants in most of these studies were all COVID-19 cases, whereas our study was conducted among severely ill COVID-19 patients admitted to intensive care units. Evidences have shown that severely ill patients stay longer to recover from COVID-19.27 The time at which the first swab is taken and the criteria for considering patient recovered can also influence the recovery time. Moreover, in the current study, a significant number of the patients had previous medical conditions or comorbidity, which might have affected to delay recovery.

This study revealed that cardiovascular diseases and diabetes mellitus were the most common comorbidities, which is consistent with the previously reported research studies.5,2834 Moreover, in this study 61% of the patients had signs and symptoms on admission. The most common symptoms were shortness of breath and cough. This finding is in line with most previous studies.3538 The result of this study showed that there was no difference between males and females in the recovery period in bivariate analysis. This was consistent with some previous studies.39,40 However, other studies have found that male patients had longer duration of viral RNA shedding than female patients with COVID-19.17,41

The multivariable cox proportional hazard regression analysis demonstrated that age, comorbidity, shortness of breath and body weakness were risk factors for time to recovery among severely ill COVID-19 patients. We found that older age was associated with high risk of delayed viral clearance. The younger patients recovery rate is significantly higher than those older than 59 years. This finding was in line with previous studies.9,17,27,4246 This might be attributed to the severity progression of COVID-19 among older age cases compared to the younger cases which in turn leads to either death or delayed duration of viral clearance in elderly patients.42 Moreover, it could be due to the life style of old aged patients in that they might not have a regular physical exercise or could have additional underlying disease conditions like chronic illnesses and may also have the habit of consuming lifesaving and life prolonging drugs.

The current study has demonstrated that patients with comorbidity condition had higher risk of delayed viral clearance from COVID-19 compared to their counterparts. The existing facts are supporting the present study finding that comorbidity conditions majorly cardiovascular diseases attributed to the high risk of delayed viral clearance from COVID-19 cases.17,37,42,47 Moreover, this study revealed that the recovery rate was higher for patients who had no shortness of breath and body weakness. The limitation of the present study is the retrospective study design and finding the whole array of COVID-19 patient information from the electronic medical record was a challenge.

The median of recovery time from severely ill COVID-19 patients was long. The study revealed that older age, having at least one comorbid condition, shortness of breath and body weakness were significant factors related with the time to recovery among the severely ill COVID-19 patients. Therefore, elders and individuals with at least one comorbid condition has to get due attention to prevent infection by the virus. Moreover, attention should be given in the treatment practice for individuals who had shortness of breath and body weakness symptoms.

The findings of this research were extracted from the data gathered and analyzed based on the stated methods and materials. The dataset supporting this finding can be obtained from the corresponding author upon request.

Ethics approval to conduct this study was obtained from the institutional research review committee of College of Health Sciences, Mekelle University with the ethical clearance registration number of IBR1826/2021. The study was conducted in accordance with the Declaration of Helsinki. Consent to participate was fully waived as the study participants were not directly involved in the study (ie, already existing data were utilized for analysis in the current study).

No funding was obtained for this study.

The authors declare no conflicts of interest in relation to this work.

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44. Wu J, Li W, She X, et al. Early antiviral treatment contributes to alleviate the severity and improve the prognosis of patients with novel coronavirus disease (COVID-19). J Intern Med. 2020;288(1):128138. doi:10.1111/joim.13063

45. Das AK, Gopalan SS. Epidemiology of COVID-19 and predictors of recovery in the Republic of Korea. Pulm Med. 2020;2020:7291698. doi:10.1155/2020/7291698

46. Muhammad LJ, Islam MM, Usman SS, Ayon SI. Predictive data mining models for novel coronavirus (COVID-19) infected patients recovery. SN Comput Sci. 2020;1(4):206. doi:10.1007/s42979-020-00216-w

47. Chinnadurai R, Ogedengbe O, Agarwal P, et al. Older age and frailty are the chief predictors of mortality in COVID-19 patients admitted to an acute medical unit in a secondary care setting-a cohort study. BMC Geriatr. 2020;20(1):409. doi:10.1186/s12877-020-01803-5

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Coronavirus Omicron variant, vaccine, and case numbers in the United States: Aug. 10, 2022 – Medical Economics

August 11, 2022

Patient deaths: 1,034,020

Total vaccine doses distributed: 794,231,535

Patients whove received the first dose: 261,591,428

Patients whove received the second dose: 223,035,566

% of population fully vaccinated (both doses, not including boosters): 67.2%

% tied to Omicron variant: 100%

% tied to Other: 0%

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Coronavirus Omicron variant, vaccine, and case numbers in the United States: Aug. 10, 2022 - Medical Economics

Biden Emerges From Isolation Again After Second Negative Coronavirus Test – The New York Times

August 8, 2022

WASHINGTON President Biden left isolation on Sunday morning after a weeklong rebound case of Covid-19, heading to Rehoboth Beach in Delaware for a short getaway before resuming official travel.

The president appeared in good spirits as he emerged from the White House in the early morning hours without a tie and headed to Marine One for the flight to the beach. Im feeling good, he told reporters.

The White House said that Mr. Biden had tested negative for the coronavirus for a second consecutive day before leaving the White House. He will safely return to public engagement and presidential travel, Dr. Kevin C. OConnor, the White House physician, said in a memo released by the White House.

Mr. Biden originally tested positive for the coronavirus on July 21 and experienced a sore throat, a runny nose, a cough, body aches and fatigue. After five days of isolation and a regimen of the antiviral treatment Paxlovid, he tested negative and returned to the Oval Office, only to test positive again several days later and go back into isolation. He tested negative again on Saturday, and Dr. OConnor said the president would wait until a second negative result to emerge from isolation.

While he has tried to maintain a schedule of public appearances via video feed from the White House residence, Mr. Biden has been eager to return to the political fray in person at a time when he has scored some significant successes and wants to translate them into public support heading into the fall midterm campaigns.

The Senate was in session overnight as it moved toward passage of a long-delayed, slimmed-down version of Mr. Bidens domestic legislation, which will be a major victory if it reaches his desk.

The president expressed confidence that the Senate would approve the measure, which includes the nations largest investment in climate change and energy initiatives as well as a plan to lower the cost of prescription drugs, expanded health care subsidies and a minimum tax on corporations that have otherwise paid little to nothing. I think its going to pass, Mr. Biden told reporters.

The presidents beach trip will not last long. Anticipating a second negative test result, the White House had already scheduled a trip for the president and the first lady to visit Kentucky on Monday to examine flood damage.

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Biden Emerges From Isolation Again After Second Negative Coronavirus Test - The New York Times

Add the coronavirus pandemic, and Minnesotans with chronic and terminal illnesses are even more isolated – MinnPost

August 8, 2022

One of the most significant impacts of the pandemic has been the isolation that so many people have experienced. Local psychologists report an increase in clients suffering from the anxiety and depression that such isolation can produce.

But there is one underreported, yet significant group that has been even more severely impacted by the pandemic and its resulting restrictions: people with life-threatening or chronic health conditions.

Imagine being someone with cancer, or debilitating diabetes, COPD or Parkinsons disease. And then imagine not being able to leave your home, except for periodic doctors appointments many of which gravitated online as you face your illness and the fear of contracting COVID-19.

These folks are clients of ours at Pathways, A Healing Center.

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Our organizationwas established in 1988 to provide free wellness and complementary health care services and programs like acupuncture, grief circles, massage and guided movement to people with life-threatening and chronic illnesses.

As the early days of the pandemic forced the closing of our doors, we grappled with what to do, fearing that our clients would experience a high degree of isolation. In my 13 years of serving as Pathways executive director, we had never experienced a large-scale crisis like the one we were facing. Fortunately, with the full support of the staff and our board, we were able to launch a virtual services platform for our free wellness and complementary health care services and programs.

I was glad that we could pivot, yet I worried: Would this meet the needs of our unusual client base? Before the pandemic, our research showed that our in-person services significantly improved peoples quality of life by reducing pain, anxiety and fatigue.

Now two and half years into a pandemic that never seems to end with each new variant more transmissible than the last we wanted to understand how effective we were being at meeting our clients needs.

New research conducted by a researcher from the University of Arizona on the effectiveness of Pathways virtual service offerings shows that our virtual programs (Tai Chi, meditation, writing for healing and life coaching, to name just a few), like those offered in person (energy healing, yoga) achieved equally strong outcomes, positively and significantly impacting peoples quality of life.

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The new research findings currently under peer review and slated to be published later this year showed Pathways participants progressing from depressed to joyful and overwhelmed to empowered, plus 16 more before-and-after pairings such as hopeless to hopeful and broken to whole. Positive shifts like these are associated with healthy lifestyle changes for disease management, pain reduction and fewer hospitalizations.

Tim Thorpe

But its not just in the research; our numbers also tell the same story. In 2020, 4,088 services were scheduled through Pathways virtual programming platform; in 2021, 5,345 services were scheduled a 31% increase in virtual services usage. And so far in 2022, that trend is continuing, with an 18% increase this June compared to last June.

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Pathways offered me a space to be with other people who were also suffering, learning and healing, said Kate Jackson, a cancer survivor and former Pathways participant who switched careers to be a health and wellbeing coach after her cancer diagnosis and now leads Pathways classes. Accessibility is whats key. People with chronic and terminal illnesses often dont feel well but virtual services mean they dont have to leave home to stay connected and receive support and care.

As the latest phase of the pandemic continues to escalate, its important to let people with chronic or life-threatening illnesses who are feeling the effects of isolation know that they are not alone. And that there is a free resource available to them, and its right here at http://www.pathwaysminneapolis.org.

In person or online, we are and will be here for them.

Tim Thorpe is the executive director at Pathways, A Healing Center.

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Add the coronavirus pandemic, and Minnesotans with chronic and terminal illnesses are even more isolated - MinnPost

The COVID endgame: When and how will businesses and schools be able to treat the virus like the flu – WFAA.com

August 8, 2022

Case counts spiked and flattened, but at-home tests have made spread tough to gauge. Experts are looking to wastewater and hospitals.

DALLAS Its been two and a half years since COVID-19 shut down the country, and its still in the front of many Americans lives.

But, that may be changing even as cases have surged.

Its going to be with us for the long-term like flu is with us for the long-term, said Dr. James McDeavitt, the vice president and dean of clinical affairs at Baylor College of Medicine.

McDeavitt believes COVID is moving into a new endemic stage and may already be there. With at-home testing results rarely, if ever, being reported to health officials, hes looking at wastewater surveillancewhich is now set up across the country as well as hospitalizations as a gauge of spread.

Both have risen but lately leveled off.

The case rate numbers are incredibly unreliable now, McDeavitt said. We really havent seen the death rate increase and we havent seen hospitalizations increase to the same extent.

He says 99% of ICU COVID patients at the hospital are unvaccinated. The Dallas-Fort Worth Hospital Council estimated around 85% of COVID patients overall are unvaccinated. Treatments like Paxlovid are effective and widely available, but the disease likely isnt going away.

I think for the foreseeable future, were going to be chasing it to a degree, McDeavitt said.

That doesnt mean it has to dominate life, though. Flu kills between 20,000 and 80,000 Americans a year. McDeavitt expects COVID to settle in around 100,000 deaths per year and remain a top-ten cause of death in the country.

Its going to be a significant public health problem for some time to come, he said. We need to still think about the most vulnerable in our populations and help to protect them.

For the first time since the first COVID case was reported, a school year begins with every student and teacher able to be vaccinated, though many still arent.

Im very concerned the way this new variant, the BA.5, continues to spread that once kids get back and cluster in school, were going to see another increase, Dr. David Winter at Baylor Scott & White said. Only half of kids are vaccinated so I think parents should consider that.

The current TEA guidance is for kids with symptoms must wait at least five days since they started, have symptoms improving and be fever free. Students who test positive but dont have symptoms must wait five days since the positive test.

I think weve moved into a phase of the pandemic where this is largely about managing individual risk, McDeavitt said. For sort of the rank and file people, get vaccinated, be careful, if you get sick, dont expose other people.

The current variant is more contagious and less severe, but theres no promise that wont change in the future.

Two and a half years later, COVID still dictates life, but before long, itll become just another part of it.

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The COVID endgame: When and how will businesses and schools be able to treat the virus like the flu - WFAA.com

Another Way the Coronavirus Is Outsmarting Us – The Atlantic

August 5, 2022

By the time a cell senses that its been infected by a virus, it generally knows it is doomed. Soon, it will be busted up by the bodys immunological patrol or detonated by the invader itself. So the moribund cell plays its trump card: It bleats out microscopic shrieks that danger is nigh.

These intercellular messages, ferried about by molecules called interferons, serve as a warning signal to nearby cellsYou are about to be infected; its time for you to set up an antiviral state, says Juliet Morrison, an immunologist at UC Riverside. Recipient cells start battening down the hatches, switching on hundreds of genes that help them pump out suites of defensive proteins. Strong, punchy interferon responses are essential to early viral control, acting as a first line of defense that comes online within minutes or hours, says Mario Santiago, an immunologist at the University of Colorado Anschutz Medical Campus. At their best, interferons can contain the infection so quickly that the rest of the immune system hardly needs to get involved.

Viruses, of course, arent content to let that happen. Pretty much all of them, SARS-CoV-2 included, are darn good at impairing interferon signaling, or finding their way around the virus-blocking shields that cells raise after heeding those molecular calls. And as new coronavirus variants arise, they may be steadily improving their ability to resist interferons punchmaking it easier, perhaps, for the microbes to spread within and between bodies, or spark more serious disease.

Read: How long can the coronavirus keep reinfecting us?

This development may sound kind of familiar: As the coronavirus has evolved, one of its main moves has been to repeatedly dodge the antibodies that vaccines and past infections raise. But theres a key difference. Although antibodies are powerful, most are able to recognize and latch onto only a super-specific sliver of a single pathogens physique. Interferons, meanwhile, are the ultimate generalists, a set of catch-all burglar alarms. Even if the body has never seen a particular pathogen before and no relevant antibodies are present, cells will make interferons as soon as they realize a virus is aroundany and all viruses, says Eleanor Fish, an immunologist at the University of Toronto. It doesnt matter what the virus is, it doesnt matter where it comes in.

Once warned, interferon-ized cells leap into action. They will reinforce their exteriors; sharpen molecular scissors that can hack the microbe to bits, should it get inside; and conjure up sticky substances that can stop the viruss progeny from exiting. All that buys the immune system time to rouse, again with interferons help, more precise fighters, such as B cells and T cells.

But this system isnt foolproof. Some viruses will cloak their innards from cellular sensors, so the relevant alarm wires never get tripped. Others destroy the gears that get the interferon system cranking, so the warning signals never get sent. Particularly resilient viruses may not even mind if interferon messages go out, because theyre able to steel themselves against the many defenses that the molecules marshal in other cells. Strategies such as these are pretty much ubiquitous because theyre so crucial to pathogen success. I defy you to identify any virus that doesnt have in its genome factors to block the interferon response, Fish told me.

This, from our perspective, is not ideal. Derail these early responses, and theres a domino effect, says Vineet Menachery, a coronavirologist at the University of Texas Medical Branch. More cells get infected; antibody and T-cell responses hang back, even as viral particles continue to spread. Eventually, the body may get wise and try to catch up. But by then, it may be too late. The brunt of viral replication might be over, leaving the immune frenzy to misdirect much of its havoc onto our own tissues instead.

Interferons, then, can make or break a hosts fate. Researchers have found that people whose interferons are weak or laggy after catching the coronavirus are far more likely to get very seriously sick. Others experience similar problems when their immune system churns out misguided antibodies that attack and destroy interferons as they try to ferry messages among cells. Interferons also play a very dramatic role in counteracting the viruses that cause dengue and yellow fever. Those pathogens are rapidly wrangled by rodent interferons and never make those animals sick, Morrison told me. In people, though, the microbes have cooked up ways to muffle the moleculesa big reason they cause such debilitating and deadly disease.

Read: Could genetics be the key to never getting the coronavirus?

Coronaviruses in general are pros at interferon sabotage. Among the most powerful is MERS, which just shuts down everything in the interferon assembly line, says Susan Weiss, a coronavirologist at the University of Pennsylvania. That essentially ensures that almost no interferons are released, even when gobs of virus are roiling about, a dismantling of defenses that likely contributes to MERS substantial fatality rate. Weiss doesnt think SARS-CoV-2 is likely to copy its cousin in that respect anytime soon. The virus does have some ability to gum up interferon production, but it would take a lot more, she told me, to silence the system as MERS has.

Still, SARS-CoV-2 seems to be taking its own small, tentative steps toward interferon censorship. For months, several groups of researchers, CU Anschutzs Santiago among them, have been studying how well the virus can invade and replicate inside of cells that have been exposed to interferons. Recent variants such as Delta and Omicron, theyve found, seem to be better at infiltrating those reinforced cells compared with some versions that preceded thema hint that this resistance might be helping new iterations of the virus sweep the globe and cause repeated rounds of disease.

The bump in SARS-CoV-2s resilience doesnt appear to be massivemore at the margins of enhancing infective success, Menachery told me. Antibody evasion, for instance, might be playing the more dominant role in helping the virus spread and sicken more people. Still, the pattern thats unfolding raises a discomfiting question, Santiago told me. Interferons potency against the virus already seems to be getting slowly but surely undermined; what if at some point in the future, the virus becomes a lot more resistant? The challenge of managing COVID, whether through vaccines or antivirals, might disproportionately balloon. And unlike antibody evasion, with interferon resistance, theres not anything we can do to vaccinate against this, Menachery told me.

Read: The BA.5 wave is what COVID normal looks like

Still, theres probably a ceiling to how interferon-resistant the coronavirus can become. Eventually, repeated attempts to disarm our alarm systems may come at a cost to the viruss infective potential, or the speed at which it spreads, Morrison told me. Interferons are also extremely diverse, and have redundancies among them. Should one flavor get flummoxed by a pathogen, another would likely help fill in the gaps.

Many researchers, such as Fish, are also testing interferon-based treatments in people who have very recently been infected by or exposed to the coronavirus. Several of these trials have produced mixed or disappointing results. Even so, I think theres every reason to think that interferons are still going to be effective in some form, once scientists nail the timing, recipe, and dose, says Eric Poeschla, Santiagos collaborator at CU Anschutz. The molecules are, after all, natures DIY antivirals.

For a gamble like that to pay off, though, viral evolutionand thus, viral transmissionwill need to be kept in some check. SARS-CoV-2 has immense wiggle room in its genome; giving it less practice at infecting us is one of the most straightforward ways to halt its self-improvement kick. Every replication cycle is an opportunity, Menachery told me, for the virus to further fine-tune its MO.

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Another Way the Coronavirus Is Outsmarting Us - The Atlantic

Long covid: One in 8 have symptoms months after coronavirus infection – New Scientist

August 5, 2022

Researchers estimated the prevalence of long covid using survey data from the Netherlands in the early stages of the pandemic

By Jason Arunn Murugesu

A man recovering from covid-19 at a hospital in The Hague, the Netherlands, in April 2020

REMKO DE WAAL/ANP/AFP via Getty Images

One in 8 adults who had a covid-19 infection during the early stages of the pandemic developed long covid symptoms, according to survey data from the Netherlands.

Long covid is defined by the World Health Organization (WHO) as an illness that usually occurs within three months from the onset of covid-19, with symptoms that last for at least two months. These cannot be explained by an alternative diagnosis and can include chest pain, loss of smell and painful muscles.

The symptoms have many causes, so it is hard to determine how many people experience these long-term effects resulting from covid-19 infection.

Aranka Ballering at the University of Groningen and her colleagues surveyed more than 76,000 adults between 31 March 2020 and 2 August 2021 in Drenthe, Friesland and Groningen in the north of the Netherlands.

The researchers initially surveyed people weekly about their health. They then surveyed participants every two weeks from June 2020 and then just once a month from August 2020.

During the study period, 4251 people were diagnosed with covid-19 for the first time. The team matched each of these people to two others of the same age and sex who didnt get infected.

By comparing the people who had covid-19 with the matched controls on the same dates, the researchers could better determine which symptoms experienced three to five months after infection were caused by long covid.

They defined long covid as a condition in which at least one symptom increased to moderate severity three to five months after a person developed covid-19. According to this definition, 1 in 8 people in the study who got covid-19 developed long covid. Loss of smell and taste, painful muscles and general tiredness were the most prevalent long covid symptoms.

The team also found that it took longer for long covid symptom severity to return to baseline levels in women compared with men. Some studies suggest that women face greater barriers to healthcare and so seek out help for symptoms later, and this may affect the severity of long covid, says Ballering.

The researchers couldnt say whether these symptoms lasted beyond five months, nor could they say how badly they interfered with daily life.

The ancestral and alpha SARS-CoV-2 variants were most prevalent during the study period, so the findings may not extend to people infected with other variants. The study also doesnt show what effect vaccines may have had on long covid. Just 10 per cent of the participants had been fully vaccinated by the end of the study, as most of the data was collected before vaccines were available.

About 98 per cent of those studied were white and they were all in the Netherlands, so these results may not extend to other ethnic and national groups. It is also unclear how long covid risk changes when people are infected with the virus multiple times, says Ballering.

I think these figures are an underestimate, says Danny Altmann at Imperial College London. What I can say from my research is that I think were undercounting long covid, not overcounting it.

He says this study highlights the gaps in our knowledge regarding long covid. What were not good at yet is working out the nuances of long covid after different variants, such as delta.

Journal reference: The Lancet, DOI: 10.1016/S0140-6736(22)01214-4

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Long covid: One in 8 have symptoms months after coronavirus infection - New Scientist

Covid-19s Origins Are More Complicated Than Once Thought – WIRED

August 5, 2022

In October 2014, virologist Edward Holmes took a tour of the Huanan Seafood Wholesale Market in Wuhan, a once relatively overlooked city of about 11 million people in the central Chinese province of Hubei. The market would have presented a bewildering environment for the uninitiated: rows of stalls selling unfamiliar creatures for food, both dead and alive; cages holding hog badgers and Siberian weasels, Malayan porcupines and masked palm civets. In the southwest corner of the market, Holmes found a stall selling raccoon dogs, stacked in a cage on top of another housing a species of bird he didnt recognize. He paused to take a photo.

Eight years on, that photo is a key piece of evidence in the painstaking effort to trace the coronavirus pandemic back to its origins. Of course, its been suspected since the early days of the pandemicsince before it was even a pandemicthat the Wuhan wet market played a role, but its been difficult to prove it definitively. In the meantime, other origin theories have flowered centered on the Wuhan Institute of Virology, a biological research lab which, its argued, accidentally or deliberately unleashed the virus on the city and the world.

The overwhelming scientific consensus is that Covid originated in a similar way to related diseases such as SARS, which jumped from bats to humans via an intermediate animal. Figuring out exactly what happened with Covid-19 could prove immensely valuable both in terms of finally disproving the lab leak theory and by providing a source of information on how to stop the next pandemic. This is not about placing blame, says Kristian Andersen, a professor of immunology and microbiology at the Scripps Research Institute in California. This is about understanding in as much detail as we can the origins of the Covid-19 pandemic.

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For the last two years, an international team of scientists including Andersen and Holmes has been trying to pinpoint the epicenter of the pandemic, using methods ranging from genetic analysis to social media scraping. Their research, which attracted widespread coverage in preprint before being published in its final form last week, reads as much like a detective report as an academic study.

First: the scene of the crime. Where exactly in this city of 11 million people did the virus first jump from animals to humans? To find out, the teamled by University of Arizona biologist Michael Worobeyscoured a report published by the World Health Organization in the summer of 2021, which was based on a joint investigation the public health body conducted with Chinese scientists. By cross-referencing the different maps and tables within the report, the researchers obtained coordinates for 155 of the earliest Covid cases in Wuhan, people who were hospitalized from the disease in December 2019.

Most of those cases were clustered around central Wuhan, particularly on the west bank of the Yangtze riverthe same area as the Huanan market. There was this extraordinary pattern where the highest density of cases was both extremely near to and very centered on the market, says Worobey, lead author on the paper, which was published in Science. Statistical analysis confirmed that it was extremely unlikely that the pattern of cases seen in the early days of the pandemic would have been so clustered on the market if Covid had originated anywhere else: A random selection of similar people from around Wuhan were very unlikely to have lived so close to the market.

Even early patients who didnt work or shop at the market were more likely to live close to it. This is an indication that the virus started spreading in people who worked at the market, but then started to spread into the local community, as vendors went to local shops, infected people who worked in those shops, and then local community members not linked to the market started getting infected, says Worobey.

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