COVID-19 CENTRAL @THEU

COVID-19 is unlikely to be spread through semen, according to University of Utah Health scientists who participated in an international study of Chinese men who recently had the disease. The researchers found no evidence of the virus that causes COVID-19 in the semen or testes of the men.

The study was not comprehensive enough to fully rule out the possibility that the disease could be sexually transmitted. However, the chances of it occurring, based on this limited finding, appear to be remote.

“The fact that in this small, preliminary study that it appears the virus that causes COVID-19 doesn’t show up in the testes or semen could be an important finding,” says James M. Hotaling, M.D., a co-author of the study and a U of U Health associate professor of urology specializing in male fertility. “If a disease like COVID-19 were sexually transmittable that would have major implications for disease prevention and could have serious consequences for a man’s long-term reproductive health.”

The study appears in Fertility & Sterility, a peer-reviewed journal published by the American Society of Reproductive Medicine.

The international team of researchers from China and the United States launched the study in response to concerns that SARS-CoV-2, the virus that causes COVID-19, could be sexually transmitted like Ebola, Zika and other emerging viral pathogens. To find out, they collected semen samples from 34 Chinese men one month (on average) after they were diagnosed with mild to moderate cases of COVID-19. Laboratory tests did not detect SARS-CoV-2 in any of the semen samples.

But just because the virus wasn’t present in the existing semen didn’t necessary rule out that it hadn’t entered the testes where sperm cells are formed.

“If the virus is in the testes but not the sperm it can’t be sexually transmitted,” says Jingtao Guo, Ph.D., a postdoctoral scientist at the Huntsman Cancer Institute at the University of Utah who also co-authored the study. “But if it is in the testes, it can cause long-term damage to semen and sperm production.”

To sort this part of the puzzle out, the researchers analyzed a dataset generated from a single cell mRNA atlas from healthy young organ donors that was available from prior work. This atlas allows them to examine mRNA, the genetic material used to make proteins, in any single testicular cell. In this case, scientist used it to examine the expression of a pair of genes associated with SARS-CoV-2. These two genes, angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) act as receptors, allowing SARS-CoV2 to penetrate cells and replicate. In order for the virus to access cells effectively, both receptors must be present in the same cell.

When the scientists examined the dataset, they found that genes encoding these two proteins were only found in four of the 6,500 testicular cells, suggesting that SARS-CoV-2 is unlikely to invade human testicular cells, Guo says

Despite these findings, the researchers acknowledge that their study has several important limitations including a small sample size and the fact that none of the donors had been severely ill with COVID-19.

“It could be that a man who is critically ill with COVID-19 might have a higher viral load, which could lead to a greater likelihood of infecting the semen. We just don’t have the answer to that right now,” Hotaling says. “But knowing that we didn’t find that kind of activity among the patients in this study who were recovering from mild to moderate forms of the disease is reassuring.”

However, Hotaling warns that intimate contact can still increase the risk of spreading the disease through coughing, sneezing and kissing. In addition, some infected people are asymptomatic and can appear healthy, even as they pass the virus along to others.

In addition to Drs. Hotaling and Guo, other U of U Health researchers involved in this study titled, “No Evidence of SARS-CoV-2 in Semen of Males Recovering from COVID-19,” were Darshan  Patel, MD, and Adam Spivak, MD. The research was supported by the National Natural Science Foundation of China and the Huazhong University of Science & Technology.

See original press release here.

Amniotic fluid, the clear liquid that helps nourish and protect fetuses before birth, isn’t just for babies. In fact, for nearly 100 years, doctors have used the mixture to help heal skin wounds, burns, and leg ulcers as well as provide protection for surgical adhesions.

Now, in a first-of-its-kind effort, University of Utah Health researchers are investigating whether human amniotic fluid (HAF) can reduce lung inflammation caused by COVID-19 and promote the recovery of patients who have contracted the disease.

“If successful, our research could shorten or mitigate the intensity of COVID-19 and have a lot of downstream effects including reducing the need for critical care, improving patient outcomes, and getting them home faster,” says Craig Selzman, MD, the study’s senior investigator and chief of U of U Health’s Division of Cardiothoracic Surgery.

Selzman and his colleagues first became interested in amniotic fluid as a possible treatment for COVID-19 after reading about a small study conducted in China. The study found that four pregnant women who were ill with the virus gave birth to healthy babies who didn’t have any covid-19 symptoms.

Intrigued, Selzman’s team, working in conjunction with the School of Medicine’s Cell Therapy and Regenerative Medicine program, treated 10 COVID-19 patients with HAF. Preliminary results in this small group suggest there was a 40% reduction of inflammation in some patients’ lungs. This reduction was measured by changes in C-reactive protein (CRP), a substance produced in the liver that is considered a biomarker of body’s inflammatory response.

“Theoretically, amniotic fluid is probably halting the progression of the disease by impeding its ability to cause inflammatory responses in the heart, lungs and other organs,” Selzman says.

But why HAF, which is composed of a mixture of electrolytes (salts), proteins, carbohydrates, lipids and urea, triggered this effect still isn’t clear and will required additional study.

In the meantime, Selzman and his colleagues are getting ready to conduct a phase 2 clinical trial involving 60 COVID-19 patients with varying severity of the illness. Half will receive HAF treatment; the other 30 will get standard care.

In addition to monitoring the patients for acute symptoms, the researchers hope HAF treatment will diminish the risk that these patients will develop pulmonary fibrosis (scarring and stiffening of the lungs) and other chronic respiratory conditions.

“If we can halt this inflammatory process early on, we could actually prevent the onset of advance lung disease in the months and years ahead,” Selzman says. “So, it’s not just trying to get people better right now. It’s also trying to stave off what could be long-term consequences of this viral infection.”

This research is supported, in part, by the University of Utah’s Immunology, Inflammation & Infectious Disease Initiative (3i) See original press release here. 

Diagnosing respiratory illness associated with vaping has always been challenging. But add the current COVID-19 pandemic to the mix and it becomes extremely difficult since both illnesses share many symptoms.

There are no tests for e-cigarette, or vaping, product use-associated lung injury, known by the acronym, EVALI, which has sickened 2,800 people and killed 68 Americans as of February. Physicians can only diagnose EVALI by first ruling out other conditions that it’s not, a task that is further complicated by patients not always disclosing that they vape.

While cases of EVALI have dropped since their peak in September 2019, they are now once again climbing, and the COVID-19 pandemic has made diagnosing the condition even more difficult since both illnesses share symptoms.

“EVALI is still happening, and on the rise again as people use vaping to cope with pandemic stress,” said Denitza Blagev, a pulmonary medicine physician at Intermountain Healthcare. “It’s important for clinicians to keep EVALI in mind as they are considering COVID. EVALI has a different prognosis and therapies that we can use to treat these patients, as long as we can diagnose them.”

This comes on the heels of a new study by researchers at Stanford University this week that found vaping is linked to a substantially increased risk of COVID-19 among teenagers and young adults, according to a new study led by researchers at the Stanford University School of Medicine.

The study, which published online Aug. 11 in the Journal of Adolescent Health, is the first to examine connections between youth vaping and COVID-19 using U.S. population-based data collected during the pandemic.

The study found that among young people who were tested for the virus that causes COVID-19, those who vaped were five to seven times more likely to be infected than those who did not use e-cigarettes.

“Patients who contract EVALI or COVID and suffer the same levels of respiratory failure tend to have divergent outcomes,” said Sean J. Callahan, assistant professor of pulmonary and critical care medicine at University of Utah Health. “Patients with EVALI require a high level of oxygen, but still tend to do well, whereas someone with COVID needing the same level of oxygen support may not do as well. Getting the diagnosis right is vital.”

In a new study published in the journal CHEST, researchers from Intermountain Healthcare and University of Utah Health looked at all patients diagnosed with EVALI at their institutions since March 2020, when COVID tests were readily available in Utah. They found a total of 12 people, who were diagnosed with EVALI who had a negative flu test and at least one negative COVID-19 test between March 1 and May 15.

They found that both illnesses showed similar symptoms: respiratory failure, gastrointestinal distress and/or ground glass opacities in the lungs.

Making accurate EVALI diagnoses even more difficult are patients who didn’t admit that they vaped, even after being asked repeatedly. In some cases, clinicians didn’t know someone’s true vaping history until well into the hospital course.

“This is a situation in which you’ve got to ask the patient repeatedly and hope they eventually volunteer the truth,” said Dr. Callahan. “It’s crucial for diagnosis.”

Researchers did, however, find two important differences that can help differentiate between EVALI and COVID-19.

First, COVID-19 often leads to normal or low white blood cell counts, while 11 of the 12 EVALI patients showed an increased white blood cell count. Second, patients with severe EVALI tended to be young, with a mean age of 30.8 years old. While COVID-19 can severely affect younger adults, it’s relatively uncommon.

While treatments for COVID-19 are being evaluated, EVALI patients typically respond well to established treatments, such as to corticosteroids. Drs. Blagev and Callahan said this is why physicians should consider EVALI when evaluating patients who test negative for COVID-19.

“The risk of missing other diseases that can present with similar and non-specific symptoms, such as a cough or shortness of breath, remains during this time,” said Dr. Blagev.

She said while it’s more challenging to diagnose in the time of COVID, EVALI remains an important diagnosis to consider in patients, particularly after an initial negative COVID test.

“First, and foremost, it’s important to keep EVALI in mind because that diagnosis has different treatment and prognosis than COVID. Equally important during a pandemic is ruling out COVID before making the diagnosis of EVALI,” she added.

See original post here.

The Utah Health and Economic Recovery (HERO) Project— a collaboration between the David Eccles School of Business at the University of Utah, University of Utah Health, Study Design and Biostatistics Core of the Center for Clinical and Translational Science, the Governor’s Office of Management and Budget, Utah Department of Health and the Hope Corps—has concluded phase one of a large-scale undertaking to test 10,000 Utahns from across four counties. In phase one, field workers collected data from 8,500 Utahns aged 12 and older from Davis, Salt Lake, Summit and Utah counties. The data gathered will inform decision-makers in the state as they work to help keep residents safe and get people back to work.

Phase One of the two-phase project aims to measure the proportion of people who have antibody to SARS-CoV-2, the virus that causes COVID-19 infection, in order to understand prevalence within the population (that is the total number of infections that have occurred over time) and other factors associated with the virus . Phase Two will extend the same work to Utah’s other counties, assess communities that may have high viral activity, focus on students/children to help guide best practices for returning to school, and monitor changes in antibody prevalence over time.

Phase One Main Findings:

Results were analyzed for blood samples and nasopharyngeal tests collected between May 4^th and June 10^th, 2020. This project used the best available tests to yield accurate estimates. A random sampling scheme called cluster sampling was used to get a representative sample. The estimated seroprevalence accounts for sampling design, non-response, and test error.

• It is estimated that the overall 4-county seroprevalence (or the proportion of members of the population with detectable antibodies to SARS-CoV-2) is 0.96% (95% confidence interval: 0.42% – 1.81%). This means that about 1 in 100 residents of these counties showed evidence of prior infection.
• For every case that was detected by some other means, there were approximately another 2.4 cases that were not detected.This is lower than case count ratios reported in community seroprevalence studies conducted in other states and suggests that testing was comparatively comprehensive during the early months of the pandemic In Utah.
• Roughly 30% of participants who were seropositive (i.e., had COVID-19 antibodies) reported having a prior positive COVID test, which is consistent with the detected fraction estimated at the population level, as reported above. To re-emphasize, more people have had COVID-19 infection than what clinical diagnosis, contact tracing, and screening indicate.
• We estimate the infection fatality rate (or ratio) in Utah to be approximately 0.29% (with an approximate 95% confidence interval of 0.16% to 0.67%). The case fatality rate, the proportion of fatalities among diagnosed cases, is approximately 0% in Utah. Note: the term “case fatality rate (ratio)” refers to COVID-19 related deaths among reported cases of COVID-19 infection while the term “infection fatality rate (ratio)” includes both detected and undetected COVID-19 infections. Hence, the case fatality rate can be expected to be larger than the infection fatality rate, proportional to the seroprevalence to case count ratio.
• When one member of a household had antibody to SARS-CoV-2, the proportion of other members of the household that were seropositive was 12.4%. This figure is a rough estimate of the secondary attack rate of COVID-19 infection within households.
• Overall, 0.2% of nasopharyngeal swabs were positive by viral PCR testing.

Implications: Phase One has two implications. First, the low seroprevalence and the relatively high detection fraction indicate that Utah’s early efforts to monitor and limit SARS-CoV-2 infections were successful. Second, the low seroprevalence indicates our population is highly susceptible to COVID-19. As efforts to restore economic and social activities are underway, it is imperative that recommended preventive measures are followed to retain the benefits achieved through substantial statewide efforts over the past few months. NOTE: the data in this report largely reflect infections that occurred up until the beginning of June, before current increases in detected cases.

Overview of project design: Utah HERO provides the first randomized, representative estimate of seroprevalence in Utah using two different systematic sampling designs. The project’s primary sampling design targeted 10,694 randomly selected households and used an intensive sampling process including both in-person visits and mailings to maximize the response rate across these households. Because of the need to conduct in-person visits and obtain laboratory testing, the primary design used a clustered sampling approach in which the targeted households were sampled from 23 of 229 compact geographic areas (defined by two or more adjacent Census tracts) which were themselves randomly selected across the four-county area. An additional 10,040 households across the same four counties were recruited by mailings, but did not receive in-person visits.

This “letter only” sampling design was able to broadly sample across all geographic areas within the four counties, but the less intensive sampling led to a higher rate of non-response. Both the primary and secondary designs utilized stratified random sampling based on 15 strata defined by combinations of  the COVID-19 cumulative case count at the start of the study, median age, and the proportion of individuals self-identifying as Hispanic to the Census. The stratified sampling plan assured adequate representation in the project across the different ethnicity, age, and COVID-19 case-count groups. By taking into account the relative proportions of individuals within each stratum, our data analyses are able to make inferences to the full population across these strata, as well as to important subgroups of individuals.

See original press release here.