Nearly half, or 47 percent, of U.S. adults have one of five underlying medical conditions associated with increased risk for severe COVID-19–associated illness, the Centers for Disease Control and Prevention (CDC) reported in its Morbidity and Mortality Weekly Report.
The agency estimated disease risk for 3,142 U.S. counties.
Counties with the highest prevalence were concentrated in the Southeast and Appalachian region. The estimated number of people with these conditions followed population distributions, but the prevalence was higher in more rural counties.
According to numerous previous studies, the risk for severe COVID-19–associated illness (illness requiring hospitalization, admission to an intensive care unit (ICU), mechanical ventilation, or resulting in death) increases with age, as well as the presence of underlying medical conditions, including chronic obstructive pulmonary disease (COPD), cardiovascular disease, diabetes, chronic kidney disease, and obesity, the CDC said.
The overall weighted prevalence of these conditions was 30.9 percent for obesity, 11.4 percent for diabetes, 6.9 percent for COPD, 6.8 percent for heart disease, and 3.1 percent for chronic kidney disease. Counties with the highest prevalence of any condition were concentrated in Southeastern states, particularly in Alabama, Arkansas, Kentucky, Louisiana, Mississippi, Tennessee, and West Virginia, as well as some counties in Oklahoma, South Dakota, Texas, and northern Michigan, among others.
The estimated median prevalence of any condition generally increased as the location became more rural, ranging from 39.4 percent in large central metropolitan counties to 48.8 percent in non-core counties, while the estimated median number of people with any underlying condition ranged from 4,300 in non-core counties to almost 302,000 in large central metropolitan counties.
To reach these findings, the CDC used a small-area estimation approach to determine county-level prevalence of selected conditions associated with severe COVID-19 disease among U.S. adults aged 18 years and older using self-reported data from the 2018 Behavioral Risk Factor Surveillance System (BRFSS), as well as population data from the U.S. Census. Overall, 437,500 people participated in BRFSS, which is a random digit-dialed phone survey.
Antibodies promising in fight against COVID-19
Based on positive results in recent preclinical studies, potently neutralizing antibodies identified by researchers are showing promise as a potential therapy for preventing and treating COVID-19, according to scientists at Vanderbilt University Medical Center (VUMC). The monoclonal antibodies were isolated from the blood of a couple from Wuhan, China, who were diagnosed with COVID-19 after traveling to Toronto, Canada, in late January. They were two of the earliest confirmed cases of COVID-19 in North America.
During the past two years, VUMC researchers led by James Crowe, Jr., MD, and Robert Carnahan, PhD, have developed ultra-fast methods for discovering highly potent antiviral human monoclonal antibodies and validating their ability to protect small animals and non-human primates, all in less than three months.
Reporting in the journal Nature Medicine, the researchers and colleagues from across the country describe how they used this rapid antibody discovery platform to isolate hundreds of human monoclonal antibodies against the surface spike (S) protein that enables SARS-CoV-2, the virus that causes COVID-19, to infect lung cells.
In a separate report published in the journal Nature, VUMC scientists and their colleagues describe how two of the antibodies, COV2-2196 and COV2-2130, bind to distinct sites on the S protein and either alone or in combination reduce the viral “burden” in infected mice and protect them from weight loss and lung inflammation.
They also found that COV2-2196 and another potent antibody, COV2-2381, given alone protected rhesus macaques from SARS-CoV-2 infection. Collectively these results suggest that these monoclonal antibodies, either alone or in combination, “are promising candidates for prevention or treatment of COVID-19,” the researchers concluded.
Drug that calms cytokine storm associated with lower mortality risk among COVID-19 patients
Critically ill COVID-19 patients who received a single dose of a drug that calms an overreacting immune system were 45 percent less likely to die overall, and more likely to be out of the hospital or off a ventilator one month after treatment, compared with those who didn’t receive the drug, according to a new study by a team from the University of Michigan.
The lower risk of death in patients who received intravenous tocilizumab happened despite the fact that they also had twice the risk of developing an additional infection, on top of the novel coronavirus. The study is published in Clinical Infectious Diseases after being available as a preprint last month.
It suggests a benefit from timely and targeted efforts to calm the “cytokine storm” caused by the immune system’s overreaction to the coronavirus. Tocilizumab, originally designed for rheumatoid arthritis (RA), has already been used to calm such storms in patients receiving advanced immunotherapy treatment for cancer.
The researchers base their conclusions on a thorough look back at data from 154 critically ill patients treated at Michigan Medicine, U-M’s academic medical center, during the first six weeks of the pandemic’s arrival in Michigan from early March to late April. The analysis looked at patients’ records through late May.
During that time, when little was known about what would help COVID-19 patients on ventilators, about half of the studied patients received tocilizumab and half did not. Most received it within the 24-hour period surrounding their intubation. This created a natural opportunity for comparing the two groups’ outcomes in an observational study, though clinical trials are still needed to truly see if the drug provides a benefit, the authors say.
Simple blood test can predict severity of COVID-19 for some patients
An early prognosis factor that could be a key to determining who will suffer greater effects from COVID-19, and help clinicians better prepare for these patients, may have been uncovered by researchers at The University of Texas Health Science Center at Houston (UTHealth). Results of the findings were published in the International Journal of Laboratory Hematology.
The severity of COVID-19 infections can range from little or no symptoms for some patients to fighting for their lives in the intensive care unit (ICU) for others. Little is known about what causes these differences.
“Because of the uncertainty surrounding the implications of this virus, we knew there needed to be a prognostic factor that could aid hospital workers in managing COVID-19,” said Ahmad Farooq, MD, corresponding author on the study, and assistant professor of gastroenterology at McGovern Medical School at UTHealth. “In this study, we discovered evidence of a relationship between lymphocytopenia and disease severity that could really help clinicians prepare for critically ill patients.”
Lymphocytopenia is the condition of having an abnormally low levels of white blood cells, called lymphocytes, which are key components of the immune system. Using a cohort of 57 patients from a local Houston hospital, researchers analyzed basic, clinical, and laboratory data from a simple blood draw and found that patients who were admitted into an ICU showed signs of lymphocytopenia compared to patients who were not in the ICU.
At the time of hospital admission, patients who ended up in the ICU had lymphocytopenia in comparison to those not needing ICU admission, revealing that blood lymphocyte count could be a predictive marker in identifying who may be admitted into the ICU and suffer severe implications. Additionally, researchers found that patients with lymphocytopenia were more likely to develop an acute kidney injury (AKI) during admission. According to Farooq, mortality rates are higher in patients who have both COVID-19 and AKI compared to those without AKI.
Antibodies against SARS-CoV-2 may diminish over time in mild cases of infection
A study by UCLA researchers shows that in people with mild cases of COVID-19, antibodies against SARS-CoV-2 — the virus that causes the disease — drop sharply over the first three months after infection, decreasing by roughly half every 36 days. If sustained at that rate, the antibodies would disappear within about a year, according to a news release from UCLA.
Previous reports have suggested that antibodies against the novel coronavirus are short-lived, but the rate at which they decrease has not been carefully defined.
The researchers studied 20 women and 14 men who recovered from mild cases of COVID-19. Antibody tests were conducted at an average of 36 days and 82 days after the initial symptoms of infection.
The findings raise concerns about antibody-based “immunity passports,” the potential for herd immunity and the reliability of antibody tests for estimating past infections. In addition, the findings may have implications for the durability of antibody-based vaccines.
Genetic factors may influence COVID-19 susceptibility
A new Cleveland Clinic study has identified genetic factors that may influence susceptibility to COVID-19, which could guide personalized treatment. In this study, a team of researchers led by Feixiong Cheng, PhD, Genomic Medicine Institute, investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms (variations in DNA sequences) in the ACE2 and TMPRSS2 genes. ACE2 and TMPRSS2 produce enzymes (ACE2 and TMPRSS2, respectively) that enable the virus to enter and infect human cells.
Looking at 81,000 human genomes from three genomic databases, they found 437 non-synonymous single-nucleotide variants in the protein-coding regions of ACE2 and TMPRSS2. They identified multiple potentially deleterious polymorphisms in both genes (63 in ACE2; 68 in TMPRSS2) that offer potential explanations for different genetic susceptibility to COVID-19, as well as for risk factors.
Several ACE2 variants were found to be associated with cardiovascular and pulmonary conditions by potentially altering the angiotensinogen-ACE2 interaction. In addition, germline deleterious variants in the coding region of TMPRSS2, a key gene in prostate cancer, were found to occur in different cancer types, suggesting that oncogenic roles of TMPRSS2 may be linked to poor outcomes with COVID-19.
These findings demonstrate a possible association between ACE2 and TMPRSS2 polymorphisms and COVID-19 susceptibility and indicate that a systematic investigation of the functional polymorphisms in ACE2 and TMPRSS2 among different populations could pave the way for precision medicine and personalized treatment strategies for COVID-19. However, all investigations in this study were performed in general populations, not with COVID-19 patient genetic data.
“Because we currently have no approved drugs for COVID-19, repurposing already approved drugs could be an efficient and cost-effective approach to developing prevention and treatment strategies,” Dr. Cheng said. “The more we know about the genetic factors influencing COVID-19 susceptibility, the better we will be able to determine the clinical efficacy of potential treatments.”
