#GISAID

[biglisbonnews]

Scientists bicker over who was first to identify covid's genome The Global Initiative on Sharing Avian Influenza Data (GISAID), a large database launched in 2008 to collect and share the genome information of influenza viruses, is a key tool for scientific cooperation at the international level. Through it, scientists have been able to access genetic information of the latest…Read more... https://qz.com/covid-genome-sequence-gisaid-debate-1850284511

[suchananewsblog]

New COVID-19 origins data point to raccoon dogs in China market

Genetic material collected at a Chinese market near where the first human cases of COVID-19 were identified show raccoon dog DNA comingled with the virus, adding evidence to the theory that the virus originated from animals, not from a lab, international experts say. “These data do not provide a definitive answer to how the pandemic began, but every piece of data is important to moving us closer…

[covid-safer-hotties]

Also preserved on our archive (Thousands of reports, sources, and resources! Daily updates!)

By Robert Stevens

A COVID wave fuelled by the XEC variant is leading to hospitalisations throughout Britain.

According to the UK Health Security Agency (UKHSA), the admission rate for patients testing positive for XEC stood at 4.5 per 100,000 people in the week to October 6—up significantly from 3.7 a week earlier. UKHSA described the spread as “alarming”.

Last week, Dr. Jamie Lopez Bernal, consultant epidemiologist at the UKHSA, noted of the spread of the new variant in Britain: “Our surveillance shows that where Covid cases are sequenced, around one in 10 are the ‘XEC’ lineage.”

The XEC variant, a combination of the KS.1.1 and KP.3.3 variants, was detected and recorded in Germany in June and has been found in at least 29 countries—including in at least 13 European nations and the 24 states within United States. According to a New Scientist article published last month, “The earliest cases of the variant occurred in Italy in May. However, these samples weren’t uploaded to an international database that tracks SARS-CoV-2 variants, called the Global Initiative on Sharing All Influenza Data (GISAID), until September.”

The number of confirmed cases of XEC internationally exceeds 600 according to GISAID. This is likely an underestimation. Bhanu Bhatnagar at the World Health Organization Regional Office for Europe noted that “not all countries consistently report data to GISAID, so the XEC variant is likely to be present in more countries”.

Another source, containing data up to September 28—the Outbreak.info genomic reports: scalable and dynamic surveillance of SARS-CoV-2 variants and mutations—reports that there have been 1,115 XEC cases detected worldwide.

Within Europe, XEC was initially most widespread in France, accounting for around 21 percent of confirmed COVID samples. In Germany, it accounted for 15 percent of samples and 8 percent of sequenced samples, according to an assessment from Professor Francois Balloux at the University College London, cited in the New Scientist.

Within weeks of those comments the spread of XEC has been rapid. Just in Germany, it currently accounts for 43 percent of infections and is therefore predominant. Virologists estimate that XEC has around twice the growth advantage of KP.3.1.1 and will be the dominant variant in winter.

A number of articles have cited the comments made to the LA Times by Eric Topol, the Director of the Scripps Research Translational Institute in California. Topol warns that XEC is “just getting started”, “and that’s going to take many weeks, a couple months, before it really takes hold and starts to cause a wave. XEC is definitely taking charge. That does appear to be the next variant.”

A report in the Independent published Tuesday noted of the make-up of XEC, and its two parent subvariants: “KS.1.1 is a type of what’s commonly called a FLiRT variant. It is characterised by mutations in the building block molecules phenylalanine (F) altered to leucine (L), and arginine (R) to threonine (T) on the spike protein that the virus uses to attach to human cells.

“The second omicron subvariant KP.3.3 belongs to the category FLuQE where the amino acid glutamine (Q) is mutated to glutamic acid (E) on the spike protein, making its binding to human cells more effective.”

Covid cases are on the rise across the UK, with recent data from the UK Health Security Agency (UKHSA) indicating a 21.6 percent increase in cases in England within a week.

There is no doubt that the spread of XEC virus contributed to an increase in COVID cases and deaths in Britain. In the week to September 25, there were 2,797 reported cases—an increase of 530 from the previous week. In the week to September 20 there was a 50 percent increase in COVID-related deaths in England, with 134 fatalities reported.

According to the latest data, the North East of England is witnessing the highest rate of people being hospitalised, with 8.12 people per 100,000 requiring treatment.

Virologist Dr. Stephen Griffin of the University of Leeds has been an active communicator of the science and statistics of the virus on various public platforms and social media since the start of the pandemic. He was active in various UK government committees during the height of the COVID-19. In March 2022, he gave an interview to the World Socialist Web Site.

This week Griffin spoke to the i newspaper on the continuing danger of allowing the untrammelled spread of XEC and COVID in general. “The problem with COVID is that it evolves so quickly,” he said.

He warned, “We can either increase our immunity by making better vaccines or increasing our vaccine coverage, or we can slow the virus down with interventions, such as improving indoor air quality. But we’re not doing those things.”

“Its evolutionary rate is something like three or four times faster than that of the fastest seasonal flu. So you’ve got this constant change in the virus, which accelerates the number of susceptible people.

“It’s creating its own new pool of susceptibles every time it changes to something that’s ‘immune evasive’. Every one of these subvariants is distinct enough that a whole swathe of people are no longer immune to it and it can infect them. That’s why you see this constant undulatory pattern which doesn’t look seasonal at all.”

There are no mitigations in place in Britain, as is the case internationally, to stop the spread of this virus. Advice for those with COVID symptoms is to stay at home and limit contact with others for just five days. The National Health Service advises, “You can go back to your normal activities when you feel better or do not have a high temperature”, despite the fact that the person may well still be infectious. Families are advised that children with symptoms such as a runny nose, sore throat, or mild cough can still “go to school or childcare' if they feel well enough.

The detection and rapid spread of new variants disproves the lies of governments that the pandemic is long over and COVID-19 should be treated no differently to influenza.

Deaths due to COVID in the UK rose above 244,000 by the end of September. It is only a matter of time before an even deadlier variant emerges. Last month, Sir Chris Whitty, England’s chief medical officer, told the ongoing public inquiry into COVID-19 “We have to assume a future pandemic on this scale [the global pandemic which began in 2020] will occur… That’s a certainty.”

[allthebrazilianpolitics]

New Sars-CoV-2 variant identified in three Brazilian states

A new strain of the Sars-CoV-2 virus, currently spreading worldwide, has been detected in Brazil. Named XEC, this sublineage of the Omicron variant has been identified in the states of Rio de Janeiro, São Paulo, and Santa Catarina.

The Oswaldo Cruz Institute (IOC/Fiocruz) made the first discovery of the variant in samples from two patients residing in Rio de Janeiro. Both were diagnosed with COVID-19 in September.

The decoded genetic sequences were uploaded to the Gisaid platform on September 26 and October 7. Following the data from Rio de Janeiro, additional XEC lineage genomes from São Paulo, based on samples collected in August, and from Santa Catarina, from two samples taken in September, were also submitted by other research groups.

Continue reading.

[partisan-by-default]

XEC is a "recombinant" COVID-19 variant, which means it's a mix of two previous Omicron subvariants called KS 1.1 and KP 3.3.

A recombinant variant is created when someone is infected with two strains of a virus that go on reproduce and create another strain.

There are conflicting reports about where the strain originated, but most suggest it was first detected in Germany in May or June.

XEC is a recombinant variant made from the KS 1.1 and KP 3.3 strains. (Unsplash: Medakit Ltd)

Cases have been reported in 29 countries, according to GISAID, including Brazil, Canada, China, France, Spain and Japan.

The World Health Organization (WHO) classified XEC as a variant under monitoring in September so health authorities could give it more attention and investigate whether it presented an additional threat to global public health.

University of Queensland infectious diseases physician Paul Griffin told the ABC that XEC could become the dominant variant by the end of October.

[wumblr]

well i've said it once already this month but 500 covid/ml in wastewater with 5+ strains circulating, neither of which are things that have gone well in the past

(currently circulating are the six XBB strains and EG5)

deaths appear to be rising very slowly (from 470 to 550/wk), still remaining at an all time low. hospitalizations more clearly rising (to 12k/wk), which seems to suggest that the proportion of people with severe cases remains lower than any other point during the pandemic, at the moment

biobot, gisaid, cdc

[canisvesperus]

Raw milkers are cooked (no pun intended).

[moontyger]

We’ve learned that the viral load in milk from infected cows is especially high. This suggests that infection might be spread through milking machines or when the milking rooms are power washed, aerosolizing infected milk. This is why workers should wear protective gear.

Another huge problem is that cattle in the U.S. are fed poultry “litter,” a euphemism for leftover feathers, bird droppings, spilled seed, and the occasional dead mouse or rat mixed in. There is supposed to be a 15-day period before cattle are slaughtered when the broiler litter is not to be used. Because of this two-week “weaning period” before human consumption, dairy cows are not supposed to be fed bird litter.

Cow manure—based on poultry litter—is widely spread on fields as a fertilizer, including on organic farms. So, our whole agricultural supply chain could be at risk of spreading infection. At least with limited testing, it doesn't look like cows are shedding virus thru their stool.

There are other possible routes of transmission. For example, house flies and blow flies can transmit H5N1 and other avian influenza viruses. During an HPAI (H5N1) epidemic in Thailand in 2005, blood-engorged mosquitoes collected at poultry farms tested positive for H5N1 by reverse transcription-PCR. Windborne spread could explain up to 24% of the transmission over distances up to 25 km in the 2003 outbreak.

There is now apparently spread of infection from cows back to birds. Grackles, blackbirds, and chickens all showed mutations from mammals, suggesting this route.

Gaps In Response

The government’s response to this potential biothreat has been reactive and limited.

The strongest initial criticism is that, despite calls for data and sample sharing as a foundation of pandemic preparedness, the USDA has not fully shared their data. When it finally shared genetic sequences with GISAID, the international database widely used by scientists since 2008, the USDA did not say where the samples originated nor include critical timing data.

Another problem is that the testing of cows is limited to dairy cows before they are moved to a different state. We don’t know if beef cattle are infected.

Surprisingly, the government apparently has had no power to restrict the movement of cattle or to require testing or reporting of infected herds or workers. A number of farmers are reluctant to allow testing. We know how voluntary reporting and restrictions will work…

However, on April 24, the USDA’s Animal and Plant Health Inspection Service announced that dairy cows would have to be tested before interstate transport and that labs and vets would have to report positive tests in cows. APHIS also announced finding H5N1 in a lung tissue sample from an asymptomatic dairy cow in an affected herd.

While there was one recently reported case of conjunctivitis in a person, there is likely to be considerable underreporting. There have been anecdotal reports of other symptomatic workers with fever, cough, and lethargy—and who do not want to be tested or seen by doctors. Many workers are likely undocumented and have no trust in the government. Dairy owners won’t want to risk prices falling or calls to cull their herds. Cattle veterinarian Dr. Barb Petersen said there has been underreporting and fear. She told Bovine Veterinarian’s journalist Rhonda Brooks, “But every dairy that I've worked with has – with the exception of one – had sick human beings at the same time they had sick cows.” She also reported infections in people with no direct contact with dairy cows. “I'm talking owners and feeders who don't usually touch cows.”

[fox-bright]

Me: "I'm feeling like maybe we'll actually get ahead of the H5N1 thing, as long as people aren't stupid about it. We're paying a lot of attention to it, and while a really quite upsetting number of people who should know better are just handwaving it, I feel hopeful."

GISAID: "Look at this nifty E627K substitution!"

Me: "...okay, so maybe I do some more canning this weekend."

[girlfriendsofthegalaxy]

this is my very favorite shit- database drama and people who can’t keep their email aliases straight

When Jeremy Kamil started to sequence samples of the rapidly spreading pandemic coronavirus in the spring of 2020, it was clear where he should deposit the genetic data: in GISAID, a long-running database for influenza genomes that had established itself as the go-to repository for SARS-CoV-2 as well.

Kamil, a virologist at Louisiana State University’s (LSU��s) Health Sciences Center Shreveport, says he quickly struck up a friendly relationship with a Steven Meyers, who used a gisaid.org email address. The two often exchanged emails and talked on the phone, sometimes for hours, about the pandemic and data sharing—but also about music, beer, and Saturday Night Live. Meyers said he had previously worked at Time Warner and had changed jobs after his boss at that company, Peter Bogner, launched GISAID in 2008. Meyers was born in Germany and living in Santa Monica, California, just like Bogner, whom he would call “our big boss” and “the Big Cheese.”

Over time, things got a little weird, Kamil says. Emails he sent to Meyers were sometimes answered from Bogner’s email account. “I used Peter’s account as writing on my little gadget was too treacherous,” was the explanation Meyers gave in one case. “I did ask though, first 😊.” Sometimes Bogner emailed Kamil about a topic he was discussing with Meyers at that very moment. Kamil offered to come to Santa Monica to meet Meyers on one of his trips to see his parents in Los Angeles, where they lived. But Meyers never seemed keen.

On 24 December 2022, when Kamil was again in Los Angeles, Meyers wrote that he would be “lucky this time around”: Kamil would have a chance to meet Bogner, along with GISAID in-house lawyer Ben Branda, in Santa Monica. Meyers himself couldn’t make it. Five days later, at a restaurant named R+D Kitchen, Kamil says he noticed Bogner had the same voice—with a hint of a German accent—as Meyers. “It wasn’t similar,” Kamil says. “It was identical.” It was the final nail, Kamil says: “I was duped.”

[excalculus]

Here we are, heading into another COVID winter.  The fucker’s still here and sadly we aren’t likely to get rid of it any time soon.  You kill diseases by cutting off transmission and slowly strangling them to death.  We tried that.  We locked down the whole world and it didn’t work.

I won’t deny that things look really ugly right now, especially with other respiratory diseases coming back.  But as the sequencing results keep coming in, it’s really starting to look like something incredible happened.

Sure, the lockdowns didn’t succeed in killing COVID.  That doesn’t mean they killed nothing.

Hey, I wonder how the influenza viruses are holding up?

There are two types of influenza that cause the epidemics we get every winter: A and B.  (C and D don’t really get up to the same level of mischief so let’s ignore them for now.)  Type A infects both animals and people, and includes things like the H1N1 bird flu pandemic strain, swine flu, et al.  The H[number]N[number] format points out which subtype of two important viral proteins it has, and usually strains are reported with that code, what animal they jumped into humans from, and where they were first sequenced.  Type B only affects humans, especially children.  It doesn’t have subtypes like Type A.  Instead it has two distinct lineages: B/Victoria and B/Yamagata. 

Today’s best flu vaccines are called “quadrivalent” because they target B/Victoria, B/Yamagata, and our best guess at which two Type A’s are going to blow up this year.  The guess is based on global sequencing of flu infections, so we have at least a decent idea of both past and current circulation logged in databases like GISAID and the WHO’s FluNet. 

Cases went way down during the lockdowns - masking and social distancing pushed spread down to a fraction of what it usually is.  Influenza in general is now back in force as people go back to their normal behavior.  There’s plenty of Type A flying around.  There’s been B/Victoria.

B/Yamagata has not been conclusively identified since March of 2020.

As early as 2021, flu researchers noticed the lack of new B/Yamagata sequences coming in and started to suspect something was fishy.  Look at this graph of GISAID flu data by lineage:

[GISAID] [paper]

Let’s, uh, check FluNet maybe?  That shows that in a typical year you see tens of thousands of cases of B/Yamagata on PCR tests.  2017 had 30,552; 2018 had 51,524.  Then... 3,464 in 2019.  364 in 2020 in only 9 countries.  It does seem like there are still signs of life in 2021 with 8 hits, but keep in mind these detections are based on simple PCR tests like what we do for COVID.  PCR tests are exquisitely sensitive, to the point where it’s been shown that giving flu vaccines and then later using the same room to give flu tests can throw a weak positive by picking up viral RNA from the vaccine.  More specifically, as of March 2022 there’s been a case of this exact thing happening with what looked like a B/Yamagata detection.  So it’s going to be more reliable to look at only the results from full sequencing, where you can yeet anything that matches the vaccine ingredients and only look at wild viruses. 

[paper]

Zero.  Nothing.  All signs point to we shot at COVID and blew up an entire flu lineage as collateral damage!  What the fuck!  We’re probably going to have to change how we do flu vaccines because fully a quarter of what they aim at looks to be gone from the face of the earth!

True, influenza B/Yamagata could still be out there somewhere that hasn’t been sequenced.  Proving absence is hard.  But the fact that Type A and its sibling B/Victoria are back and easy to find really does suggest it’s gone, or stomped down so far it’s near impossible to find.  Time to watch and wait and feed every sample we can into the sequencers, but if we keep not finding it...

A disease is considered eradicated when we’re sure there’s no more transmission “in the wild”.  For smallpox, which was also wildly contagious and also had no nonhuman reservoir, that was three years from the last known case. 

Clock’s ticking.

[kaelio]

On 24 December 2022, when Kamil was again in Los Angeles, Meyers wrote that he would be “lucky this time around”: Kamil would have a chance to meet Bogner, along with GISAID in-house lawyer Ben Branda, in Santa Monica. Meyers himself couldn’t make it. Five days later, at a restaurant named R+D Kitchen, Kamil says he noticed Bogner had the same voice—with a hint of a German accent—as Meyers. “It wasn’t similar,” Kamil says. “It was identical.” It was the final nail, Kamil says: “I was duped.” Karthik Gangavarapu, a post-doctoral fellow at the University of California (UC), Los Angeles, who had many lengthy calls with Meyers—but never with Bogner—also suspected they were one and the same. When Science sent Gangavarapu an audio clip of Bogner talking, he replied: “This is definitely the same voice as Steven Meyers.” No one Science has spoken to in the virology community—including members of GISAID’s science advisory board—recalls ever meeting Meyers, or even seeing a picture of him.

Rest assured this isn't an anti-vax post etc. Just some absolutely insane things going on with GISAID.

[min-phone-pyae]

COVID FLiRT variants KP.3 and XEC: What you need to know

KP.3 was the 'predominant' SARS-CoV-2 variant in the US. It was also spreading in Europe. It's now joined with another variant and become XEC.

Over the European summer, the number of COVID-19 infections rose again, with test positivity for SARS-CoV-2 above 20%. Globally, test positivity was about 10%.

The US also saw a rise in hospitalizations, apparently after a wave of COVID-19 infections in Singapore.

Now, as we in the northern hemisphere move into autumn and winter, there is concern about two new variants.

The first one is known as KP.3 and its sub-variant KP.3.1.1. The second is XEC, a "recombinant" variant which is related to KP.3.

KP.3 is considered a global Variant of Concern (VOC) in the US by The US Center for Disease Control and Prevention (CDC) because KP.3 was "predominant" there in August. VOCs may spread more easily or cause more severe illness.

It's important to note that KP.3 is not a global VOC, only in the US.

The CDC recommended people get an updated 2024–2025 COVID-19 vaccine.

What are the KP.3 and XEC variants?

KP.3 is one of a group of SARS-CoV-2 variants known as FLiRT variants. SARS-CoV-2 is the base virus that causes COVID, the illness.

As the name KP.3 suggests, there are also KP.1 and KP.2 sub-variants. KP.3 became predominant because it is more infectious than other circulating sub-variants.

KP.3 and other FLiRT variants descend from the omicron variant of SARS-CoV-2.

Now, think of a family tree: The KP variants are children of the JN.1 variant. And JN.1 is, in turn, a child of omicron variant BA.2.86.

How omicron evolved into the subvariants KP.3. and XEC

This is important to know because of all the major COVID variants, omicron remains dominant, globally. You'll recall, other major variants are alpha, beta, delta, and gamma.

But omicron keeps evolving or mutating into new variants and sub-variants.

XEC the sub-variant is believed to have formed when KP.3 joined with KS.1.1. But we don't know for sure.

As Francois Balloux, Professor of Computational Systems Biology and Director at the UCL Genetics Institute, UK, told the Science Media Centre, "XEC is a likely recombinant between the subvariants KP.3.3 and KS.1.1."

XEC COVID variant in Germany

XEC has been reported as being first detected in Germany in June. But it is yet to appear on the Robert Koch Institute's COVID Dashboard.

As a spokesperson from the Robert Koch Institute implied via email, XEC may never appear on the dashboard because it is "impossible to predict how individual variants will spread."

Since June, the number of XEC cases in Germany has been in double-digits, but the spokesperson did not specify further. The RKI's doesn't even mention XEC on its weekly assessment, published September 18, 2024.

The focus in Germany remains on KP.3.1.1, which is dominant and considered more infectious than previous variants.

In an interview with the DPA news agency, virologist Sandra Ciesek said it was no surprise that KP.3.1.1 was more infectious.

"The virus keeps mutating in search of new ways to infect people […] but that doesn't mean that the variant causes a more severe illness," said Ciesek, who's based at the German Center for Infection Research.

How prevalent are KP.3.1.1, KS.1.1 and XEC? Up to September 3, KP.3.1.1 remains the most dominent variant, according to data provided by GISAID, the Global Initiative on Sharing All Influenza Data, and presented by outbreak.info.

KP.3.1.1 was detected worldwide 14,396 times

KP.3.3 was detected worldwide 9,157 times

KS.1.1 was detected worldwide 2,650 times

XEC was detected worldwide 95 times

[covid-safer-hotties]

Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes - Published July 29, 2024

You read that right: Covid infections can result in AIDS. I've been following this preprint since 2022, and I'm so excited to see it finally published! You might remember the preprint from the original Milf-Adjacent or covidsafehotties blogs.

Highlights •Genotypes N/120 and N/152 of SARS-CoV-2 have been identified in the acquired immuno-deficiency scope caused by Sarbecovirus.

•A new binding site for the Sarbecovirus N protein is proposed as the main route of infection of lymphocytes through CD147 receptors.

•Immune dysregulation caused by infection of CD147 lymphocytes is consistent with clinical data of severe and Long Covid cases.

Abstract Background Epigenetics and clinical observations referring to Betacoronavirus lead to the conjecture that Sarbecovirus may have the ability to infect lymphocytes using a different way than the spike protein. In addition to inducing the death of lymphocytes, thus drastically reducing their population and causing a serious immune deficiency, allows it to remain hidden for long periods of latency using them as a viral reservoir in what is named Long-Covid Disease. Exploring possibilities, the hypothesis is focused on that N protein may be the key of infecting lymphocytes.

Method The present article exhibits a computational assay for the latest complete sequences reported to GISAID, correlating N genotypes with an enhancement in the affinity of the complex that causes immune deficiency in order to determine a good docking with the N protein and some receptors in lymphocytes.

Results A novel high-interaction coupling of N-RBD and CD147 is presented as the main way of infecting lymphocytes, allowing to define those genotypes involved in their affinity enhancement.

Conclusion The hypothesis is consistent with the mutagenic deriving observed on the in-silico assay, which reveals that genotypes N/120 and N/152 are determinant to reduce the Immune Response of the host infecting lymphocytes, allowing the virus persists indefinitely and causing an Acquire Immune Deficiency Syndrome.

Graphical abstract

[schoje]

Pesquisadores de cinco estados brasileiros sequenciaram amostras que indicam uma possível nova linhagem do novo coronavírus (SARS-CoV-2) em circulação no país, segundo informou hoje (12) o Laboratório Nacional de Computação Científica, um instituto do Ministério da Ciência e Tecnologia, Inovações (MCTI) localizado em Petrópolis, no Rio de Janeiro. Além da linhagem identificada no Reino Unido, o Brasil já tem casos confirmados de duas variantes (P.1 e P.2), que surgiram a partir de cepas que circulavam no país.  A possível nova linhagem foi encontrada no sequenciamento de três amostras, em um universo de 195 que foram analisadas por pesquisadores do Amazonas, Rio Grande do Norte, Paraíba, Bahia e Rio de Janeiro. Essa identificação, entretanto, permitiu descobrir que já havia outras amostras com as mesmas características sequenciadas. O trabalho foi organizado pelo Laboratório de Bioinformática (Labinfo) do LNCC, e também participaram quatro universidade públicas: Universidade Federal do Rio Grande do Norte (UFRN), Universidade Federal da Paraíba (UFPB), Universidade Estadual de Santa Cruz (UESC) e Universidade do Estado do Rio de Janeiro (UERJ). Ao todo, 22 pesquisadores assinam a publicação, que foi submetida a um periódico científico ao mesmo tempo em que os sequenciamentos foram depositados em uma base de dados públicos internacionais (Gisaid).  A coordenadora do Labinfo, Ana Tereza Vasconcelos, explica que os dados compartilhados serão analisados por outros pesquisadores ao redor do mundo para que a identificação da nova linhagem seja confirmada pela comunidade científica. Segundo a cientista, as amostras em que a mutação foi encontrada são de Natal, no Rio Grande do Norte, e do interior da Bahia. "Essas mutações não interferem na vacina, mas demonstram que o vírus está mudando o tempo inteiro, e quanto mais as pessoas estiverem na rua sem máscara e sem medidas de proteção individual, mais o vírus vai mudar e mais variantes vão surgir. É mais uma demonstração de que o vírus está circulando livremente", diz Ana Tereza Vasconcelos, que reforça o pedido pelo respeito às medidas de prevenção, como evitar aglomerações, usar máscaras e higienizar as mãos.  A possível nova linhagem teria se originado da linhagem B.1.1.33, já presente no Brasil desde o início de 2020. A mutação apresentada é a E484K, na proteína S, estrutura que forma a coroa de espinhos que dá nome ao novo coronavírus. Essa mutação é associada ao escape do sistema imunológico, o que, segundo a coordenadora do Labinfo, ainda precisa ser confirmado por mais estudos. "Essa mutação já foi relacionada a vírus que conseguem escapar do sistema imunológico do hospedeiro. Os vírus estão tentando sobreviver, e eles têm mecanismos de escape. A gente acredita que essa nova linhagem pode ter esse mesmo mecanismo", afirma a pesquisadora. Essa mesma mutação já foi identificada nas variantes P.1 e P.2, originadas no Brasil a partir da linhagem B.1.1.28, e também também está entre as modificações genéticas encontradas nas variantes descobertas no Reino Unido e na África do Sul.  A mutação é um processo comum na reprodução dos vírus, que se multiplicam rapidamente e podem produzir versões geneticamente diferentes nesse processo. A maior circulação do vírus faz com que mais organismos se multipliquem, o que aumenta as chances de uma mutação ocorrer. Para que uma nova linhagem surja, no entanto, é necessário que essa mutação seja identificada em diversos indivíduos de uma determinada linhagem.