Research Roundup: COVID-19 Outbreak in NYC Earlier than Believed and More

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Every week there are numerous scientific studies published. Here’s a look at some of the more interesting ones.

New York City COVID-19 Outbreak Began Earlier Than Thought

Investigators with NYU Langone Health/NYU School of Medicine leveraged gene testing to trace the origins of COVID-19 through the New York City region in the spring. Their data demonstrated that the virus first developed in late February, “seeded” by a minimum of 109 different sources that then spread, instead of from a single “patient zero.” They also found that more than 40% of people who tested positive did not have any known contact with another person before contracting the disease. They published their research in the journal Genome Research.

“Our findings show that New York’s early screening test methods missed the onset and roots of the outbreak by several days at the minimum,” said study co-lead author Matthew Maurano, assistant professor in the Department of Pathology at NYU Langone Health. “The work strongly suggests that to nip future outbreaks in the bud, we need a system of rapid, plentiful real-time genetic surveillance as well as traditional epidemiologic indicators.”

The study also showed that more than 95% of New Yorkers with COVID-19 had a viral strain that was highly contagious, which explains why it spread so aggressively. The research team collected viral genetic data on 864 nasal swabs collected from New Yorkers who tested positive for COVID-19 between March 12 and May 10. They were mostly from Manhattan, Brooklyn, and Nassau County on Long Island. They then compared the gene sequences of the virus from those samples to ones observed in the original strain analyzed last winter from patients in Wuhan, China. They found that the New York strains more closely matched those originating from Europe or the U.S. instead of from China. They also found some of the early infection chains, meaning person to person infections, ran at least 50 people long.

The sequences analyzed in this study made up about 10% of COVID-19 patients within a single hospital system in New York. The community infection scale was probably much higher, with the original introduction of the virus to New York City possibly earlier.

The Evolution of COVID-19 Viral Mutations

Researchers at the University of Illinois College of Agricultural, Consumer and Environmental Sciences tracked the mutation rate of the SARS-CoV-2 proteins, the proteome, through time, beginning with the first genome published in January 2020 and ending more than 15,300 genome iterations later in May. The team discovered some regions are still actively mutating, while the mutation rate in other regions appears to be slowing, with primarily single versions of key proteins continuing to mutate. On the one hand, the higher mutation rate appears to be bad news, suggesting that the virus is continuing to change and adapt to its environment. But the slower mutation rate in some regions suggests that the stabilization of specific proteins may be good news for the development of treatment. The team did observe what appeared to be a general slowing of the mutation rate beginning in April, which included stabilization within the spike (S) protein.

How Cancer Remodels Chromosomes

Studies by scientists at the University of Virginia found that cancer remodels the architecture of chromosomes so cancer can establish itself and spread. They found that cancer depends on a protein known as “CCCTC-binding factor” (CTCF), which occurs naturally in cells. In normal, healthy cells CTCF maintains chromosome structure and plays a role in turning genes on and off as needed. Cancer highjacks CTCF, causing it to appear in locations where it shouldn’t and inhibiting its binding. This changes the three-dimensional structure of chromosomes and how genes function. They identified CTCF remodeling in six different cancers, including T-cell acute lymphoblastic leukemia, acute myeloid leukemia, breast cancer, colorectal cancer, lung cancer, and prostate cancer. 

Potent Antibody Against COVID-19 Virus Mapped

Quite a number of therapeutic antibodies are in clinical trials against SARS-CoV-2, the virus that causes COVID-19, including those being developed by Eli Lilly and Regeneron Therapeutics. Both of those companies have requested emergency use authorization from the U.S. Food and Drug Administration. Investigators at Fred Hutchinson Cancer Research Center in Seattle have mapped a potent antibody from a COVID-19 survivor,  describing how it interferes with the spikes on the virus’s surface and induces pieces of those spikes to break off. They also indicate that the antibody, CV30, was 530 times more potent than any of the others they identified. The antibody functions in two ways, overlapping the virus’s target site on human cells, and the second to induce dissociation of part of the spike. They plan to begin preclinical tests with hopes of moving it to human trials.

How Exercise Stalls Cancer Growth

Anecdotally, people who exercise have been observed to have a better cancer prognosis than inactive people. But why that was the case wasn’t really understood. Researchers at Sweden’s Karolinska Institutet believe they have found an explanation. Physical exercise changes the metabolism of cytotoxic T cells in the immune system, which improves their ability to attack cancer cells. Cytotoxic T cells specialize in killing cancer cells. Working in laboratory mice, one group that exercised regularly on a spinning wheel and another that did not, they then studied the cytotoxic T cells in the animals by injecting antibodies that remove the T cells in both groups of mice. They also transferred cytotoxic T cells from the fit mice into unfit mice with tumors and found it improved their prospects compared to the cancerous mice who received cells from unfit mice.

“Our research shows that exercise affects the production of several molecules and metabolites that activate cancer-fighting immune cells and thereby inhibit cancer growth,” said Helene Rundqvist, senior researcher at the Department of Laboratory Medicine, Karolinska Institutet, and the study’s first author. “We hope these results may contribute to a deeper understanding of how our lifestyle impacts our immune system and inform the development of new immunotherapies against cancer.”

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