The coronavirus mutating increased contagiousness United States, according to a new genetic study: One of the latest mutations in the coronavirus could be making it more contagious.
This is stated by the latest study of the Houston Hospital after analyzing more than 5,000 COVID-19 genetic sequences spread throughout the United States, the country that has managed the worst crisis of the disease and which today has the largest contagion data in the world.
The paper, published by The Washington Post and appeared on the Health website medrxiv, revealed a genome sequence of 30,000 characters of the coronavirus since early March, when the virus first appeared in the Houston metropolitan area (Texas), whose population is estimated to be about 7 million.
Viruses, as a rule, accumulate genetic mutations over time, but most are insignificant. Coronaviruses, in particular, are relatively stable because they have a correction mechanism when replicating; that is, drastic mutations are rare, but with the immense rate of contagion in the US, the chances of it changing with problematic consequences are increasing.
"We have given this virus many opportunities," says James Musser, author of the study, to The Washington Post. In this case, one of the consequences of this finding would be an increase in the rates of infection of SARS-CoV-2 and, therefore, of COVID-19 disease within the United States.
According to the report, which is yet to be peer reviewed, the infection would have spread across the region in two waves: the first, with older people and high purchasing power groups; the second, to younger people and lower-income neighborhoods, mainly Latin Americans.
So far, Musser's study is the largest set of genetic sequences in the United States, only surpassed internationally by the one published earlier this month in the United Kingdom. So, the results were similar to those of today, with a virus that mutated the structure of the Spyke protein as it spread through Houston's ZIP codes. This protein is COVID-19's gateway to the body.
Coronavirus mutating increased contagiousness United States
The virus, says David Morens, a virologist and advisor at the National Institute of allergies and Infectious Diseases (USA), could potentially be responding, through random mutations, to interventions such as the use of masks and social distancing, among other prevention measures.
"Wearing masks, washing hands and all those things are barriers to transmissibility or contagion, but as the virus becomes more contagious it also becomes more effective in overcoming those barriers," he says. Also in developing vaccines: as immunity is gained, SARS-CoV - 2 could be under pressure to evade the immune response. It's only a matter of time before I figure it out.
If that happened, we'd be in the same situation as the flu, chasing the virus as it mutates to change the vaccine.
Although a peer review of the Houston study is still pending, many experts are already keeping their backs on the news that, in less than a year, the virus that has upset the world has been able to change its "attitude" and evolve into a more fatal version.
In the second wave of the outbreak in Houston, the study found a variant of the Chinese outbreak that had jumped to a prevalence of 99.9%. Thus, the researchers deduced that people infected with the strain had higher virus loads in their upper respiratory tracts, a potential factor in causing the strain to spread more effectively than it had in Wuhan, for example.
Research suggests that this small change, affecting 3 identical amino acid chains, extended the transmissibility of the virus by spreading through Houston, although it does not rule out similar developments elsewhere. However, the study clarifies that it did not find that the mutations "made the virus more lethal" or altered clinical outcomes.
"There's something biologically different about this strain, about this family of strains," Kristian Andersen, an immunologist at the Scripps Research Institute in California, told the same newspaper.
For the UK study, based on some 25,000 genomes, the research found 285 separate mutation sites that changed the structure of the protein in what could be further evolution. According to this clue, as the virus interacts with our bodies and immune systems, it may be learning new tricks to help it respond to its host.
The actual mutations of viruses, at least in this case, occur randomly when they make mistakes in trying to copy their genome into our cells. However, each new contagion gives the opportunity for more mutations to occur, which in turn increases the chance that one of them will be useful to the virus and eventually prevail, as seems to be the case.
Given the changes that are already occurring in the genetic code of the virus, a key conclusion of Musser is that we are not sequencing it enough if we want to be able to anticipate what it will do next. Even in Houston, the study estimates that only about 10% of known cases have been sequenced.
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Senolytic, the Spanish startup that seeks the recipe of eternal youth to live at 80 as if you were 30
Among the most outstanding scientists in longevity is Manuel Serrano, a Spanish expert in the field of senescent cells.
When our body ages, it loses the ability to eliminate these types of cells and their accumulation causes various pathologies associated with age.
In 2016, Manuel Serrano met Marc Ramis, a biotech industry guru who has driven numerous startups in the sector and launched together with Serrano Senolytic Therapeutics to combat aging by creating molecules that target senescent cells.
"What we focus on is the biology of aging," explains Ramis, CEO of Senolytic, in an interview.
That is, for now, the startup is not focused on achieving the potima of immortality or extending our life expectancy to 300 years.
"From around the age of 40, the decline of our body begins," explains Ramis. The idea of understanding the biology of these processes allows us to manipulate them in order to achieve "that you are in your 30s to your 80s, and then the decline is faster".
Basically, not necessarily more years of life, but yes quality of life for more years.
The company immediately caught the attention of the United States. In particular, Life Biosciences-the company led by David Sinclair and specialized in the science of longevity - that made the company pack and move to Boston, although most of the scientific research is still carried out in Spain, in the Parc Cientific of Barcelona.
Life Biosciences has a portfolio of six startups that operate semi-independently and work on different projects, but all related to the science of aging.
Senolytic develops molecules that function as drugs capable of eliminating senescent cells and, ideally, avoid the pathology associated with aging.
Although this has the potential to treat a large number of related disorders, the Ramis startup is associated with fibrosis.
Fibrosis is a disease that is characterized by the pathological formation of fibrous tissue in an organ of the body and can be of various types. Senolytic began highly focused on pulmonary fibrosis, but has advanced toward the kidney.
The molecules developed by the startup-which are still in a state "between discovery and pre-clinical", as Ramis warns— reach fibrotic tissue and eliminate senescence.
Recently, the longevity biotechnology industry (and specifically the senescence-focused sector) suffered a setback when Unity, a company backed by Jeff Bezos, failed with its first clinical trial.
The American biotechnologist develops a whole portfolio of drugs based on the eradication of accumulated senescent cells, under the theory is that these therapies can cut these senescent cells to slow down or even reverse the age-associated disease and restore tissue. That is, the same idea as Senolytic.
Unity was the first biotech company to conduct human trials to test whether its drug UBX0101, a treatment for ostearthritis, was able to reduce knee pain.
In August, the startup announced the results of Phase 2 of its trial in 183 patients and with the announcement came disappointment: UBX0101 showed no significant results compared to the group that had received the placebo.
Among the founders of Unity is researcher Judith Campisi, who together with Manuel Serrano and scientist James Kirkland, make up the podium of the greatest experts in senescence, says Ramis.
The CEO says Unity's clinical failure is "a learning experience" for the entire industry, especially on " how we can improve target identification and improve biomarker control."
"We don't see it as a failure, "insists the CEO, who also notes that Senolytic's approach is"totally different."
In addition, Ramis suggests that perhaps the rating of Unity, which took the leap to parquet in 2018 and plummeted after the August announcement, was too high.
Looking ahead, Senolytic aims to bring its anti-fibrosis molecules to clinical trials.