Both the US and Europe lost coronavirus in January. Then piel a second time

An analysis of small genetic changes in the SARS-CoV-2 virus from the United States and Europe shows how during the first month of this year, both continents managed to prevent the first waves of the virus. Even though the widows thought the opposite then.

nsk Wu-chan is only a few hours away from the rest of the world. It was therefore inevitable that the SARS-CoV-2 virus would spread to other countries soon after the epidemic was stopped.

The first case appeared in the United States on January 15. At that time in Washington, an unnamed citizen pistol, known only as WA1, flew from Wuhan. He developed pneumonia, and because he was in contact with the risk area, WA1 was tested for the presence of a new coronavirus (which was not even labeled SARS-Cov-2 at the time). Epidemiologists then traced all the patient’s contacts and came to the conclusion that the virus was most likely to be prevented.

Europe was in a similar situation. On January 20, she arrived from the engagement of employees of a supplier to the automotive industry, who was briefly introduced by her native from Wuhan before departure (the anti-movement people were introduced in the city on January 23). She suffered from a snout (she snorted, took whites without a prescription) and her story led to the first proven case of contagion between two foreign (unrelated) people outside the country. A total of 16 people were proclaimed.

What was it according to?

In both cases, the hygienists were quite sure that they had managed to intercept all the contacts and stop the virus in the new locality. One hundred percent certainty is never possible, so logically, the questions arose as to whether the virus really did not live up to these first patients.

It was about Europe, but especially the USA. There, molecular geneticist Trevor Bedford published on March 29 a widely cited analysis comparing the genetic information (genome) of a virus from patient WA1 with a virus from a patient known as WA2 (the second patient with a diagnosed disease in Washington). The type of virus sample came from the 24th of February, and patient WA2 was demonstrably infected directly in the USA, he was not present. He did not even come into contact with anyone who traveled to this country.

The viruses in the bodies of both patients were genetically similar. Bedford and colleagues came to the conclusion that they were a very high probability (95 percent) of viruses from a single line. Otherwise, the virus from patient WA1 somehow escaped the attention of the epidemiologist and hid for Washington for a week.

From the reactions of the representative of the state of Washington, it seems that the information contributed to this American state of the jet to intensify the efforts in the fight against the contagion. It always seemed likely that an epidemic of invisibility was going on in Washington for several weeks, and sweat could be really high. Washington was not the best at it, the disease penetrated into several homes for the elderly and the total number of people who died with the proven SARS-CoV-2 virus is over 1,100 (does not mean that they all died because of the virus, so give them soon and tm urit it will never be completely accurate).

In Europe, the situation was similar in some respects. Even in this case, there were opinions in the scientific literature that the virus could not be stopped in Germany, and it reached the Alps in Italy. It was again the bottom, especially since the strain that spread so much in Lombardy, the so-called line B.1, differed only slightly from the samples obtained from German patients.

From both cases, it might seem that the virus is unstoppable and the virus can do so despite the best efforts of hygienists and epidemiologists. But this is a mistake, a hard new analysis carried out by experts from several American and European universities, who looked at samples of the virus from Germany and the USA new and armed with new knowledge. (It is now available as a preprint on BiorXiv.org, the first author is Michael Worobey of the University of Arizona.)

An error has occurred

The authors of the analysis are now able to compare the original samples: today we have more than 25,000 samples of the SARS-CoV-2 virus from various cities around the world. Including the USA and Italy, of course.

Comparison is not easy. It is based on simulations that try to fill the empty space in the virus history. Otherwise, find out how the paths from point A (first cases of the virus) to point B (samples from later) are possible. Whether it is probable that it is really a follower, ie viruses, which come from one evolution of the line. Or viruses that drank from the outbreak of separtn and developed in Europe and the United States.

The analysis is complicated mainly by the lack of data: virus samples are not taken and analyzed from each patient, and these gaps are filled back only slightly. The proven case of infection are millions (not to mention the unproven ones), petench sample to the plate thousands.

The fact that SARS-CoV-2 is relatively stable also plays a role. It does not mutate extremely quickly (according to Soni Pekov, according to me, this virus changes very quickly, it is unique in the world and there is no support in this literature for scientific claims). The whole virus has about 30,000 letters of the genetic code (first of all).

Today, according to the analysis of samples taken from all over the world, it is stated (see, for example, the Nextstrain project) that the SARS-CoV-2 virus changes one of a thousand letters of its RNA within one year. For lace, the rate of change is about two per thousand bz per year, for HIV only one thousand. This is one of the reasons why there may be differences in the genetic status of a virus from different parts of the world. (On the other hand, in terms of vaccination development, the slow pace of change is good at first.)

He was in a hurry before the great catastrophe

Even knowing that the data, and therefore the results, are not entirely certain, the authors estimate that, in fact, the Bavarian and Washington cases were most likely to be well-received by hygienists and epidemiologists. For some typical genetic variants, they appear in other formulas only sporadically and not at all (those sporadically appearing could easily have formed naturally, but if there were pm offspring, they would appear more often). It is not entirely certain, but it seems that in the first cases of the virus, Europe and the USA actually managed to resist and stop it.

She wasn’t so dense that she would slip through in the end. In the case of the European, the virus probably arrived in Italy directly from Wuchan. This is indicated by both epidemiological (ie the movement of people) and genetic analysis. According to them, the Lombard virus B.1 is especially a descendant of the high voltage high voltage virus, which got into Italy sometime between 31 January and 14th standards. Soon the sweat (sometimes between the 14th and 26th standards) then got from Europe to New York.

An attempt to reconstruct the entry of SARS-CoV-2 virus in Europe

An attempt to reconstruct the entry of the SARS-CoV-2 virus in Europe according to Michael Worobey and colleagues. At the bottom left (green) had an episode of entry into Bavaria, which managed to stop (hence the sample genome of the virus known as BavPat1). Then, between the 7th and 14th standards, the virus, according to them, got to Italy and from there to other parts of Europe. And very soon from Italy he also went to New York (blue area on the top right).

In the burrow at the same time, the virus also entered the United States from behind. A new genetic analysis states that the virus in the body of patient WA2 (the second in Washington state) came from a line that could have entered the United States sometime between the 7th and 19th standards of 2020, again directly from Wuhan. The carrier could be any of the roughly 40,000 people, mainly American citizens, who traveled to the United States for the past two years from the United States to the United States. Alternatively, Canada, specifically the province of British Columbia, may have been the site of entry, where the virus was gradually discovered very close to that of a WA2 patient.

Of course, the analysis may not be true. It does not provide a certain answer, it is just probability. For example, it is possible that in fact Trevor Bedford was right, and in fact the patient’s WA1 virus was hidden for weeks.

According to the author, however, the probability of such an event was very small, not less than one percent. And neither does Bedford. He wrote it in a long post on Twitter, in which he comments and explains the work, and he assumes it.

He said he changed his mind about the new work and that his original assumption that the virus had been invisible since Washington in January was wrong. I’m sorry I caused the confusion. Although I think I did the right thing, given the available information, I ended the thread on Twitter.

It must be added that the confusion was not so great and so great. When he published his analysis at the end of the burrow, the virus was said to have been in the United States. At the same time, it generally indicates that the virus was definitely not unstoppable. Whether the bag was only a matter of time, the disease did not develop, or it was really possible to stop it in the sweat, SARS-CoV-2 genome analyzes cannot answer this.