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Scientists are seeing signs of lasting immunity to COVID-19, among survivors with even mild infections – Firstpost

Posted: August 21, 2020 at 8:57 pm

The New York TimesAug 19, 2020 14:24:20 IST

To the immune system, not all germs are equally memorable. But our bodys cells seem to be seriously studying up on the coronavirus.

Scientists who have been monitoring immune responses to the virus are now starting to see encouraging signs of strong, lasting immunity, even in people who developed only mild symptoms of COVID-19, a flurry of new studies suggests. Disease-fighting antibodies, as well as immune cells, called B cells and T cells that are capable of recognizing the virus, appear to persist months after infections have resolved an encouraging echo of the bodys enduring response to other viruses.

Things are really working as theyre supposed to, said Deepta Bhattacharya, an immunologist at the University of Arizona and an author on one of the new studies, which has not yet been peer-reviewed.

Although researchers cannot forecast how long these immune responses will last, many experts consider the data a welcome indication that the bodys most studious cells are doing their job and will have a good chance of fending off the coronavirus, faster and more fervently than before, if exposed to it again.

This is exactly what you would hope for, said Marion Pepper, an immunologist at the University of Washington and an author on another of the new studies, which is currently under review at the journal Nature. All the pieces are there to have a totally protective immune response.

Protection against reinfection cannot be fully confirmed until there is proof that most people who encounter the virus a second time are actually able to keep it at bay, Pepper said. But the findings could help quell recent concerns over the viruss ability to dupe the immune system into amnesia, leaving people vulnerable to repeat bouts of disease.

Researchers have yet to find unambiguous evidence that coronavirus reinfections are occurring, especially within the few months that the virus has been rippling through the human population. The prospect of immune memory helps to explain that, Pepper said.

Face shields and masks for sale in New York on March 23, 2020. The clear plastic guards may be easier to wear, disinfect and reuse than cloth or surgical face coverings, although they dont entirely replace the need for masks. (Marian Carrasquero/The New York Times)

In discussions about immune responses to the coronavirus, much of the conversation has focused on antibodies Y-shaped proteins that can latch onto the surfaces of pathogens and block them from infecting cells. But antibodies represent just one wing of a complex and coordinated squadron of immune soldiers, each with its own unique modes of attack. Viruses that have already invaded cells, for instance, are cloaked from antibodies but are still vulnerable to killer T cells, which force infected cells to self-destruct. Another set of T cells, nicknamed helpers, can coax B cells to mature into antibody-making machines.

(Yet another sector of the immune system assails pathogens within minutes of their arrival while sending out signals called cytokines to mobilize forces from elsewhere in the body. Some evidence suggests that severe cases of COVID-19 may stem from this early process going awry.)

Antibodies also come with an expiration date: Because they are inanimate proteins and not living cells, they cant replenish themselves, and so disappear from the blood just weeks or months after they are produced. Hoards of antibodies appear shortly after a virus has breached the bodys barriers, then wane as the threat dissipates. Most of the B cells that produce these early antibodies die off as well.

But even when not under siege, the body retains a battalion of longer-lived B cells that can churn out virus-fighting antibodies en masse, should they prove useful again. Some patrol the bloodstream, waiting to be triggered anew; others retreat into the bone marrow, generating small amounts of antibodies that are detectable years, sometimes decades, after an infection is over. Several studies, including those led by Bhattacharya and Pepper, have found antibodies capable of incapacitating the coronavirus lingering at low levels in the blood months after people have recovered from COVID-19.

The antibodies decline, but they settle in what looks like a stable nadir, which is observable about three months after symptoms start, Bhattacharya said. The response looks perfectly durable.

Seeing antibodies this long after infection is a strong indication that B cells are still chugging away in the bone marrow, Pepper said. She and her team were also able to pluck B cells that recognize the coronavirus from the blood of people who have recovered from mild cases of COVID-19 and grow them in the lab.

Multiple studies, including one published Friday in the journal Cell, have also managed to isolate coronavirus-attacking T cells from the blood of recovered individuals long after symptoms have disappeared. When provoked with bits of the coronavirus in the lab, these T cells pumped out virus-fighting signals, and cloned themselves into fresh armies ready to confront a familiar foe. Some reports have noted that analyses of T cells could give researchers a glimpse into the immune response to the coronavirus, even in patients whose antibody levels have declined to a point where they are difficult to detect.

This is very promising, said Smita Iyer, an immunologist at the University of California, Davis, who is studying immune responses to the coronavirus in rhesus macaques but was not involved in the new studies. This calls for some optimism about herd immunity, and potentially a vaccine.

Notably, several of the new studies are finding these powerful responses in people who did not develop severe cases of COVID-19, Iyer added. Some researchers have worried that infections that take a smaller toll on the body are less memorable to the immune systems studious cells, which may prefer to invest their resources in more serious assaults. In some cases, the body could even jettison the viruses so quickly that it fails to catalog them. This paper suggests this is not true, Iyer said. You can still get durable immunity without suffering the consequences of infection.

A resident wears a mask to curb the spread of the coronavirus, while browsing meat products at a Beijing supermarket on 15 June 2020. The capital is bracing for a resurgence of the coronavirus after more than 100 new cases were reported in recent days in the city, which hadnt seen a case of local transmission in more than a month. Image: AP

What has been observed in people who fought off mild cases of COVID-19 might not hold true for hospitalized patients, whose bodies struggle to marshal a balanced immune response to the virus, or those who were infected but had no symptoms at all. Research groups around the world are continuing to study the entire range of responses. But the vast majority of the cases are these mild infections, said Jason Netland, an immunologist at the University of Washington and an author on the paper under review at Nature. If those people are going to be protected, thats still good.

This new spate of studies could also further assuage fears about how and when the pandemic will end. On Friday, updated guidance released by the Centers for Disease Control and Prevention was misinterpreted by several news reports that suggested immunity against the coronavirus might last only a few months. Experts quickly responded, noting the dangers of propagating such statements and pointing to the wealth of evidence that people who previously had the virus are probably at least partly protected from reinfection for at least three months, if not much longer.

Considered with other recent reports, the new data reinforce the idea that, Yes, you do develop immunity to this virus, and good immunity to this virus, said Dr. Eun-Hyung Lee, an immunologist at Emory University who was not involved in the studies. Thats the message we want to get out there.

Some illnesses, like the flu, can plague populations repeatedly. But that is at least partly attributable to the high mutation rates of influenza viruses, which can quickly make the pathogens unrecognizable to the immune system. Coronaviruses, in contrast, tend to change their appearance less readily from year to year.

Still, much remains unknown. Although these studies hint at the potential for protectiveness, they do not demonstrate protection in action, said Cheong-Hee Chang, an immunologist at the University of Michigan who was not involved in the new studies. Its hard to predict whats going to happen, Chang said. Humans are so heterogeneous. There are so many factors coming into play.

Research in animals could help fill a few gaps. Small studies have shown that one bout of the coronavirus seems to protect rhesus macaques from contracting it again.

But tracking long-term human responses will take time, Pepper said. Good immune memory, she added, requires molecules and cells to be abundant, effective and durable and scientists cannot yet say that all three conditions have been definitively met.

As peoples bodies settle into their post-coronavirus state, were just now hitting the point of relevance to take the long view on immunity, Bhattacharya said. Things may change a few months or years down the line. Or they may not.

Theres no shortcuts here, Bhattacharya said. We just have to follow it out.

Katherine J. Wuc.2020 The New York Times Company

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Studies show positive signs of strong, lasting Covid-19 immunity – The Irish Times

Posted: August 21, 2020 at 8:57 pm

To the immune system, not all germs are equally memorable. But our bodys cells seem to be seriously studying up on the coronavirus.

Scientists who have been monitoring immune responses to the virus are now starting to see encouraging signs of strong, lasting immunity, even in people who developed only mild symptoms of Covid-19, a flurry of new studies suggests.

Disease-fighting antibodies, as well as immune cells called B cells and T cells that are capable of recognising the virus, appear to persist months after infections have resolved an encouraging echo of the bodys enduring response to other viruses.

Things are really working as theyre supposed to, said Dr Deepta Bhattacharya, an immunologist at the University of Arizona and an author on one of the new studies, which has not yet been peer-reviewed.

Although researchers cannot forecast how long these immune responses will last, many experts consider the data a welcome indication that the bodys most studious cells are doing their job and will have a good chance of fending off the coronavirus, faster and more fervently than before, if exposed to it again.

This is exactly what you would hope for, said Dr Marion Pepper, an immunologist at the University of Washington and an author on another of the new studies, which is currently under review at the journal Nature. All the pieces are there to have a totally protective immune response.

Protection against reinfection cannot be fully confirmed until there is proof that most people who encounter the virus a second time are actually able to keep it at bay, Dr Pepper said. But the findings could help quell recent concerns over the viruss ability to dupe the immune system into amnesia, leaving people vulnerable to repeat bouts of disease.

Researchers have yet to find unambiguous evidence that coronavirus reinfections are occurring, especially within the few months that the virus has been rippling through the human population. The prospect of immune memory helps to explain that, Dr Pepper said.

In discussions about immune responses to the coronavirus, much of the conversation has focused on antibodies Y-shaped proteins that can latch on to the surfaces of pathogens and block them from infecting cells. But antibodies represent just one wing of a complex and co-ordinated squadron of immune soldiers, each with its own unique modes of attack.

Viruses that have already invaded cells, for instance, are cloaked from antibodies, but are still vulnerable to killer T cells, which force infected cells to self-destruct.

Another set of T cells, nicknamed helpers, can coax B cells to mature into antibody-making machines. (Yet another sector of the immune system assails pathogens within minutes of their arrival, while sending out signals called cytokines to mobilise forces from elsewhere in the body. Some evidence suggests that severe cases of Covid-19 may stem from this early process going awry.)

Antibodies also come with an expiration date: Because they are inanimate proteins and not living cells, they cant replenish themselves, and so disappear from the blood just weeks or months after they are produced. Hoards of antibodies appear shortly after a virus has breached the bodys barriers, then wane as the threat dissipates. Most of the B cells that produce these early antibodies die off as well.

But even when not under siege, the body retains a battalion of longer-lived B cells that can churn out virus-fighting antibodies en masse, should they prove useful again. Some patrol the bloodstream, waiting to be triggered anew; others retreat into the bone marrow, generating small amounts of antibodies that are detectable years, sometimes decades, after an infection is over.

Several studies, including those led by Dr Bhattacharya and Dr Pepper, have found antibodies capable of incapacitating the coronavirus lingering at low levels in the blood months after people have recovered from Covid-19.

The antibodies decline, but they settle in what looks like a stable nadir, which is observable about three months after symptoms start, Dr Bhattacharya said. The response looks perfectly durable.

Seeing antibodies this long after infection is a strong indication that B cells are still chugging away in the bone marrow, Dr Pepper said. She and her team were also able to pluck B cells that recognise the coronavirus from the blood of people who have recovered from mild cases of Covid-19 and grow them in the lab.

Multiple studies, including one published last Friday in the journal Cell, have also managed to isolate coronavirus-attacking T cells from the blood of recovered individuals long after symptoms have disappeared. When provoked with bits of the coronavirus in the lab, these T cells pumped out virus-fighting signals, and cloned themselves into fresh armies ready to confront a familiar foe.

Some reports have noted that analyses of T cells could give researchers a glimpse into the immune response to the coronavirus, even in patients whose antibody levels have declined to a point where they are difficult to detect.

This is very promising, said Dr Smita Iyer, an immunologist at the University of California, Davis, who is studying immune responses to the coronavirus in rhesus macaques but was not involved in the new studies. This calls for some optimism about herd immunity, and potentially a vaccine.

Notably, several of the new studies are finding these powerful responses in people who did not develop severe cases of Covid-19, Dr Iyer added. Some researchers have worried that infections that take a smaller toll on the body are less memorable to the immune systems studious cells, which may prefer to invest their resources in more serious assaults.

In some cases, the body could even jettison the viruses so quickly that it fails to catalogue them.

This paper suggests this is not true, Dr Iyer said. You can still get durable immunity without suffering the consequences of infection.

What has been observed in people who fought off mild cases of Covid-19 might not hold true for hospitalised patients, whose bodies struggle to marshal a balanced immune response to the virus, or those who were infected but had no symptoms at all.

Research groups around the world are continuing to study the entire range of responses. But the vast majority of the cases are these mild infections, said Jason Netland, an immunologist at the University of Washington and an author on the paper under review at Nature. If those people are going to be protected, thats still good.

Some illnesses, like the flu, can plague populations repeatedly. But that is at least partly attributable to the high mutation rates of influenza viruses, which can quickly make the pathogens unrecognisable to the immune system. Coronaviruses, in contrast, tend to change their appearance less readily from year to year.

Still, much remains unknown. Although these studies hint at the potential for protectiveness, they do not demonstrate protection in action, said Cheong-Hee Chang, an immunologist at the University of Michigan who was not involved in the new studies. Its hard to predict whats going to happen, Chang said. Humans are so heterogeneous. There are so many factors coming into play.

Research in animals could help fill a few gaps. Small studies have shown that one bout of the coronavirus seems to protect rhesus macaques from contracting it again.

But tracking long-term human responses will take time, Dr Pepper said. Good immune memory, she added, requires molecules and cells to be abundant, effective and durable and scientists cannot yet say that all three conditions have been definitively met.

As peoples bodies settle into their post-coronavirus state, were just now hitting the point of relevance to take the long view on immunity, Dr Bhattacharya said. Things may change a few months or years down the line. Or they may not.

Theres no shortcuts here, Dr Bhattacharya said. We just have to follow it out. New York Times

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Inconsistencies in data presentation could harm efforts against COVID-19 and future outbreak preparedness – PRNewswire

Posted: August 20, 2020 at 10:54 am

WASHINGTON, Aug. 20, 2020 /PRNewswire/ --Since COVID-19 emerged late last year, there's been an enormous amount of research produced on this novel coronavirus disease. But the content publicly available for this data and the format in which it's presented lack consistency across different countries' national public health institutes, greatly limiting its usefulness, Children's National Hospital scientists report in a new study. Their findings and suggestions, published online August 19 in Science & Diplomacy, could eventually help countries optimize their COVID-19-related data and data for future outbreaks of other diseases to help further new research, clinical decisions and policy-making around the world.

Recently, explains study senior author Emmanule Dlot, Ph.D., research faculty at Children's National Research Institute, she and her colleagues sought data on sex differences between COVID-19 patients around the world for a new study. However, she says, when they checked the information available about different countries, they found a startling lack of consistency, not only for sex-disaggregated data, but also for any type of clinical or demographic information.

"The prospects of finding the same types of formats that would allow us to aggregate information, or even the same types of information across different sites, was pretty dismal," says Dr. Dlot.

To determine how deep this problem ran, she and colleagues at Children's National, including Eric Vilain, M.D., Ph.D., the James A. Clark Distinguished Professor of Molecular Genetics and the director of the Center for Genetic Medicine Research at Children's National, and Jonathan LoTempio, a doctoral candidate in a joint program with Children's National and George Washington University, surveyed and analyzed the data on COVID-19.

The research spanned data reported by public health agencies from highly COVID-19 burdened countries, viral genome sequence data sharing efforts, and data presented in publications and preprints.

At the time of study, the 15 countries with the highest COVID-19 burden at the time included the US, Spain, Italy, France, Germany, the United Kingdom, Turkey, Iran, China, Russia, Brazil, Belgium, Canada, the Netherlands and Switzerland. Together, these countries represented more than 75% of the reported global cases. The research team combed through COVID-19 data presented on each country's public health institute website, looking first at the dashboards many provided for a quick glimpse into key data, then did a deeper dive into other data on this disease presented in other ways.

The data content they found, says LoTempio, was extremely heterogenous. For example, while most countries kept running totals on confirmed cases and deaths, the availability of other types of data such as the number of tests run, clinical aspects of the disease such as comorbidities, symptoms, or admission to intensive care, or demographic information on patients, such as age or sex differed widely among countries.

Similarly, the format in which data was presented lacked any consistency among these institutes. Among the 15 countries, data was presented in plain text, HTML or PDF. Eleven offered an interactive web-based data dashboard, and seven had comma-separated data available for download. These formats aren't compatible with each other, LoTempio explains, and there was little to no documentation about where the data that supplies some formats such as continually updated web-based dashboards was archived.

Dr. Vilain says that a robust system is already in place to allow uniform sharing of data on flu genomes the World Health Organization's (WHO) Global Initiative on Sharing All Influenza Data (GISAID) which has been readily adapted for the virus that causes COVID-19 and has already helped advance some types of research. However, he says, countries need to work together to develop a similar system for harmonized sharing other types of data for COVID-19. The study authors recommend that COVID-19 data should be shared among countries using a standardized format and standardized content, informed by the success of GISAID and under the backing of the WHO.

In addition, the authors say, the explosion of research on COVID-19 should be curated by experts who can wade through the thousands of papers published on this disease since the pandemic began to identify research of merit and help merge clinical and basic science.

"Identifying the most useful science and sharing it in a way that's usable to most researchers, clinicians and policymakers, will not only help us emerge from COVID-19 but could help us prepare for the next pandemic," Dr. Vilain says.

Other researchers who contributed to this study include D'Andre Spencer, MPH, Rebecca Yarvitz, BA, and Arthur Delot-Vilain.

About Children's National HospitalChildren's National Hospital, based in Washington, D.C., celebrates150yearsof pediatric care, research and commitment to community. Volunteers opened the hospital in 1870 with 12 beds for children displaced after the Civil War. Today, 150 years stronger, it is among the nation's top 10 children's hospitals. It is ranked No. 1 fornewborn carefor the fourth straight year and ranked in all specialties evaluated by U.S. News & World Report. Children's National is transforming pediatric medicine for all children. In 2020, construction will be complete on the Children's National Research & Innovation Campus, the first in the nation dedicated to pediatric research. Children's National has been designated twice as a Magnethospital, demonstrating the highest standards of nursing and patient care delivery. This pediatric academic health system offers expert care through a convenient, community-based primary care network and specialty outpatient centers in the D.C., metropolitan area, including the Maryland and Northern Virginia suburbs. Children's National is home to theChildren's National Research InstituteandSheikh Zayed Institute for Pediatric Surgical Innovationand is the nation's seventh-highest NIH-funded children's hospital. It is recognized for its expertise and innovation in pediatric care and as a strong voice for children through advocacy at the local, regional and national levels.

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SOURCE Childrens National Hospital

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OpGen Announces CE-IVD Marking and Commercial Launch in Europe of its Own Developed Molecular Diagnostic SARS-CoV-2 Kit with PULB for Detection of the…

Posted: August 20, 2020 at 10:54 am

- Own developed SARS-CoV-2 Kit with PULB for COVID-19 uses real-time PCR (RT-PCR) technology on open PCR platforms, designed to provide results in approximately one hour

- 100% Sensitivity and 97.3% Specificity demonstrated in isolated RNA

- Inclusion of PCR-Compatible Universal Lysis Buffer (PULB) in the kit as a workflow option allows labs to circumvent the need for extraction equipment and reagents

GAITHERSBURG, Md., and HOLZGERLINGEN, Germany, Aug. 20, 2020 (GLOBE NEWSWIRE) -- OpGen, Inc. (Nasdaq: OPGN, OpGen), a precision medicine company harnessing the power of molecular diagnostics and bioinformatics to help combat infectious disease, announced today that its subsidiary Curetis GmbH has obtained the CE mark certification in the European Union for its own SARS-CoV-2 Kit with PULB for the detection of SARS-CoV-2, the virus that causes COVID-19.

Developed and manufactured by Curetis team in Germany, the SARS-CoV-2 Kit with PULB uses real-time reverse transcription polymerase chain reaction (RT-PCR) technology for qualitative detection of the SARS-CoV-2 virus isolated from oropharyngeal and nasopharyngeal swab specimens from individuals suspected of COVID-19 by their healthcare provider or for screening of asymptomatic individuals. This kit can be used with RNA isolated by performing standard RNA isolation processes, as well as with oropharyngeal or nasopharyngeal swabs collected in PCR compatible viral transport medium treated with PCR-Compatible Universal Lysis Buffer (PULB) provided in the kit. Including PULB in the kit as a workflow option allows labs to circumvent the need for extraction equipment and extraction kits/reagents, thereby providing operational and workflow efficiencies, time and cost savings. The kit is designed to provide time to results in approximately one hour, and it runs on open real-time PCR instruments such as the QuantStudio 5 Real-Time PCR System and the Bio-Rad CFX96 Real-Time PCR Detection System.

The CE-IVD Marking is an important step in advancing our efforts to support critical COVID-19 testing; the Curetis SARS-CoV-2 Kit with PULB provides additional testing capacity in countries that recognize the CE Mark to test patients, said Johannes Bacher, COO of OpGen.

By launching this new product in Europe, we are committed to helping our distributors and customers to expand the availability of SARS-CoV-2 diagnostic testing, and our own-developed CE-IVD marked SARS-CoV-2 Kit with PULB is expected to help increase availability of these much-needed tests," said Oliver Schacht, PhD, CEO of OpGen. Our customers will benefit from an optimized workflow and a test that delivers great performance and significantly shorter time-to-result at favorable economics compared to many of the commercially available open PCR platform COVID-19 tests including the BGI SARS-CoV-2 kit. Having access to our own SARS-CoV-2 kit allows us to have that product distributed rather than the BGI test kit which we will cease distributing effective immediately.

About OpGen, Inc.OpGen, Inc. (Gaithersburg, MD, USA) is a precision medicine company harnessing the power of molecular diagnostics and bioinformatics to help combat infectious disease. Along with subsidiaries, Curetis GmbH and Ares Genetics GmbH, we are developing and commercializing molecular microbiology solutions helping to guide clinicians with more rapid and actionable information about life threatening infections to improve patient outcomes, and decrease the spread of infections caused by multidrug-resistant microorganisms, or MDROs. OpGens product portfolio includes Unyvero, Acuitas AMR Gene Panel and Acuitas Lighthouse, and the ARES Technology Platform including ARESdb, using NGS technology and AI-powered bioinformatics solutions for antibiotic response prediction.

For more information, please visit http://www.opgen.com.

Forward-Looking Statements by OpGenThis press release includes statements regarding the commercial launch of a SARS-CoV-2 Kit by OpGens subsidiary, Curetis GmbH. These statements and other statements regarding OpGens SARS-CoV-2 test kits, their commercialization and launch, future plans and goals constitute "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934 and are intended to qualify for the safe harbor from liability established by the Private Securities Litigation Reform Act of 1995. Such statements are subject to risks and uncertainties that are often difficult to predict, are beyond our control, and which may cause results to differ materially from expectations. Factors that could cause our results to differ materially from those described include, but are not limited to, our ability to successfully, timely and cost-effectively develop, seek and obtain regulatory clearance for and commercialize our product and services offerings, the rate of adoption of our products and services by hospitals and other healthcare providers, the success of our commercialization efforts, the impact of COVID-19 on the Companys operations, financial results, and commercialization efforts as well as on capital markets and general economic conditions, the realization of expected benefits of our business combination transaction with Curetis GmbH, the effect on our business of existing and new regulatory requirements, and other economic and competitive factors. For a discussion of the most significant risks and uncertainties associated with OpGen's business, please review our filings with the Securities and Exchange Commission. You are cautioned not to place undue reliance on these forward-looking statements, which are based on our expectations as of the date of this press release and speak only as of the date of this press release. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise.

OpGen Contact:Oliver SchachtCEOInvestorRelations@opgen.com

Press Contact:Matthew BretziusFischTank Marketing and PRmatt@fischtankpr.com

Investor Contact:Megan PaulEdison Groupmpaul@edisongroup.com

Source: OpGen, Inc.

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Will Rice College O-Week moves online after two advisors test positive for COVID-19 – The Rice Thresher

Posted: August 20, 2020 at 10:54 am

Photo Courtesy Jeff Fitlow

By Rishab Ramapriyan 8/18/20 9:18pm

On Tuesday, Will Rice College announced that the remainder of Orientation Week activities will be conducted fully online. The announcement came after a second Will Rice O-Week advisor tested positive for COVID-19 this morning.

According to the Dean of Undergraduates Bridget Gorman, this decision was not mandated by the Rice University administration, but rather reached locally by the Will Rice magisters and O-Week coordinator team. In their email to the Will Rice advising team and new student cohort, the coordinators said that this decision was made out of an abundance of caution.

We take this action to minimize the risk to your own health and to limit further spread of the virus, the coordinators wrote.

Advisors and new students living on-campus are restricted to their floors as mandated campus-wide, but they are still able to use outdoor spaces, according to Rahul Popat, the Will Rice College President. As long as students follow the guidelines set by the Culture of Care Agreement, they are free to exit their rooms.

Vice President of Administration Kevin Kirby, who chairs the Crisis Management Advisory Committee, said that Rices team of 17 contact tracers promptly responded to both Will Rice cases. Any individuals who met the Centers for Disease Control and Prevention criteria for close contact (within 6 feet for more than 15 minutes) were quarantined and tested using a molecular test (polymerase chain reaction test). A few additional advisors who believed that they had been in contact with the COVID-19-positive students voluntarily quarantined themselves, according to Kirby. All of the quarantined students have tested negative and there have been no additional cases in the Will Rice community as of this morning.

New students and advisors had all received an antigen rapid test from CVS on move-in day, but antigen tests have a lower sensitivity and specificity than molecular tests. As such, all O-Week participants will undergo a follow-up molecular test by the end of this week. However, the entire Will Rice advising team and new student cohort will be tested via the molecular test either today or tomorrow as a precaution, according to Kirby. Results from Rices molecular tests, which are provided by Houston Methodist and Baylor Genetics, are returned within 48 hours, but Kirby said that the tests are often being returned in 24 hours.

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We'll go through the whole college and test everybody, Kirby said. We'll see if there are any [COVID-19 positive students] that have been missed or any new infections and sort of sweep through and get everybody today or tomorrow. And these tests are very accurate.

According to Kirby, there was an additional Will Rice advisor who tested positive for COVID-19, however this student had fully recovered from a previous COVID-19 infection and Student Health Services determined that they did not pose any risk for transmission, according to Kirby. The CDC notes this possibility in their guidance on discontinuing isolation measures.

Recovered persons can continue to shed detectable SARS-CoV-2 RNA in upper respiratory specimens for up to 3 months after illness onset, albeit at concentrations considerably lower than during illness, in ranges where replication-competent virus has not been reliably recovered and infectiousness is unlikely, the CDC writes. Studies have not found evidence that clinically recovered persons with persistence of viral RNA have transmitted SARS-CoV-2 to others.

Following this guidance, Kirby said that this additional Will Rice advisor was not isolated, but continues to be monitored.

Kirby said that 833 new students were given rapid tests on Saturday and Sunday, and three students tested positive. Those who tested positive could either move in to Sid Richardson College, the designated isolation housing, or return home. No more than two students have occupied Sid Rich at any point thus far, Kirby noted.

Campuswide, there have been 4,595 tests administered between August 1 and August 17, and 11 people (3 staff, 7 undergraduates, 1 graduate student) have tested positive, based on a recent update from Crisis Management. Kirby said that Rice will be administering 4,500 tests per week by the first week of classes.

Gorman said that two restrictions have been added to the campuswide O-Week program as precautionary measures. First, all remaining cross-college events have been canceled for the week. Second, students will not be allowed to eat meals together in the college commons, and must eat meals in their dorm rooms or outdoors in a physically-distanced manner.

We're testing everybody this week, as we're doing every week, Gorman said. So we're going to know in the next couple of days whether we're seeing any more spread or whether it's just these two cases at Will Rice.

Gorman said that she hopes to remove the restriction on college commons dining after O-Week, but will decide after more test results are returned.

I think by the weekend after we've gone through and gotten the test results back on everybody on campus and we get a sense about where we're at, we will make a decision at that point, Gorman said. But in preparation, just in case, we are going to ramp up our outside furniture.

Kirby said that while the COVID-19 positivity rate is substantially lower on campus than in Houston, it is important to continue all safety precautions and adapt to changing conditions.

We have to be very careful and wary right about that and we need to not have a false sense of optimism here, Kirby said. That's why it's important that we continue to do all the safety precautions ... and we continue to do our testing rigorously and often. We're prepared to make changes like we already have. I'm sure we'll continue to make changes over the course of the fall semester.

[8/18/2020 at 11:15 p.m.] The story was updated with correct information about the movement of on-campus students. Will Rice President Rahul Popat clarified that on-campus students are not restricted to their rooms.

[8/18/2020 at 11:45 p.m.] The story was updated with information about an additional Will Rice advisor who tested positive for COVID-19, but was determined to not pose any risk for transmission.

[8/19/2020 at 3:10 p.m.] The story was updated with statistics from on-campus COVID-19 testing.

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Will Rice College O-Week moves online after two advisors test positive for COVID-19 - The Rice Thresher

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Whitby student welcomes A-level U-turn – but still left in limbo over his future – Whitby Gazette

Posted: August 20, 2020 at 10:54 am

A-level student Kilian Robinson.

Kilian Robinson, 18, of Egton, consistently achieved the highest possible grades for his subjects Biology, Chemistry and Maths over the past two years.

But he was horrified on Thursday to discover that his centre assessment grades had been reduced from A*A*A* to ABB by the controversial Government algorithm, despite him not once attaining anything lower than an A.

He said today (Tues) that Imperial College London had indicated they would keep his place on a Biological Scienes course open to him if he successfully appealed.

Yesterday's Governments U-turn means Kilian has attained his grades and fulfilled his side of the bargain.

He is now waiting to hear back from Imperial College London, having emailed them after the dramatic climbdown was announced.

They said they would honour my offer if I got the grades now Ive got them," he said.

The fight isnt over. Everyone is anxious about it and what if the course is full?

Its a massive problem, yes Ive got my grades but its still to be resolved.

Kilian was offered a place on a Molecular Genetics course in Edinburgh, despite not his results being initially downgraded, but he declined as he has set his heart on a place at Imperial College London.

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Whitby student welcomes A-level U-turn - but still left in limbo over his future - Whitby Gazette

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The Newest Label Coming to a Grocery Store Near You – The Regulatory Review

Posted: August 20, 2020 at 10:53 am

Starting in 2022, food producers will be required to label genetically engineered foods.

Nearly 70 percent of processed foods at U.S. grocery stores contain at least one genetically engineered ingredient. Even though most scientists believe that genetically engineered foods pose no health risks, around half of Americans polled by Pew Research Center think genetically engineered foods are worse for ones health.

After decades of controversy, many genetically engineered foods will require labels in the United States starting in 2022, due to the national bioengineered food disclosure standard adopted by the U.S. Department of Agriculture (USDA) in 2018.

Almost 80 percent of Americans polled by the Mellman Group in 2015 strongly favor mandatory labeling of what is commonly known as genetically modified organisms, or GMOs. But for years, members of Congress had attempted to pass GMO labeling laws with no success. In 2014, however, Vermont was the first state in the United States to pass a GMO labeling law.

Given fear that other states would follow Vermonts example and subject food producers to a variety of requirements nationally, congressional gridlock eventually thawed. In July 2016, the same month the Vermont labeling requirements were slated to take effect, President Barack Obama signed federal legislation that now preempts states from imposing labeling requirements. That legislation also directed the USDA to develop a federal labeling standard.

USDA officials compiled a list of bioengineered foods to help delineate exactly what needs to be labeled under this program. For a food to be added to this list, it needs to be food authorized for and in commercial production somewhere in the world. Thirteen different foods currently meet these criteria, including at least one type of pineapple, salmon, corn, and soybean. USDA officials review and update this list annually.

A food manufacturer may choose between three different labeling options to comply with this standard. The first option, which is similar to requirements of the preempted Vermont law, calls for food to be labeled with the phrase bioengineered food. If the food product is a multigradient food, the regulation requires the label to state that the product contains a bioengineered food ingredient.

A second option allows for manufacturers to use a new bioengineered symbol. This symbol, designed specifically not to disparage biotechnology, depicts a stem growing from a field with a sun in the background. Around the symbol appears the word bioengineered.

A third option allows manufacturers to use an electronic label, like a QR code, which a consumer can scan using a smartphone to obtain more information.

The USDA labeling standard does not address the question of whether or how food manufacturers can label foods to indicate the absence of genetically engineered ingredients. The USDA maintains that the U.S. Food and Drug Administration retains regulatory authority over absence claims. Currently, the Non-GMO Project remains a popular private labeling regime that privately certifies food that reportedly does not contain genetically engineered ingredients.

While the USDA program allows food manufacturers to choose from a variety of labeling options, there are a few exemptions that allow manufacturers to bypass labeling. First, any food served at a restaurant or similar establishment, such as a salad bar or food truck, is exempt from the program. Second, very small food manufacturers, specifically those with annual receipts less than $2.5 million, are exempt from the program. Third, any food labeled as USDA organic will also be presumptively free of genetically engineered food under this program and will not require a label. Finally, meat or dairy products derived from animals fed genetically engineered crops will not require a label.

Although this program finally establishes a nationwide genetic engineering label for food, something critics have long fought for, some stakeholders argue that the requirements fall short.

Advocates from the Non-GMO Project argue that the USDA program is misleading given that the categorical exemption for meat and dairy products derived from animals fed genetically engineered crops prevents the program from providing meaningful disclosure.

Groups such as the Organic Trade Associationargue that the National Bioengineered Food Disclosure Standard falls short of fully informing U.S. consumers. The association argues that, among other things, the option to include an electronic label without the need for on-pack language is misleading to consumers. Similarly, the Environmental Working Group opposes the electronic labeling option and argues that rural consumers without expensive phones or living with irregular service will be unable to use these kinds of labels.

Both of these major criticisms, however, concern parts of the statutory mandate under the 2016 Act. Specifically, the 2016 Act calls for the USDA to permit an electronic label option and forbids the labeling of meat derived from animals fed with genetically engineered crops.

The USDA labeling requirements will become mandatory in January, 2022.

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How viruses shape the world – The Economist

Posted: August 20, 2020 at 10:53 am

Aug 22nd 2020

HUMANS THINK of themselves as the worlds apex predators. Hence the silence of sabre-tooth tigers, the absence of moas from New Zealand and the long list of endangered megafauna. But SARS-CoV-2 shows how people can also end up as prey. Viruses have caused a litany of modern pandemics, from covid-19, to HIV/AIDS to the influenza outbreak in 1918-20, which killed many more people than the first world war. Before that, the colonisation of the Americas by Europeans was abettedand perhaps made possibleby epidemics of smallpox, measles and influenza brought unwittingly by the invaders, which annihilated many of the original inhabitants.

The influence of viruses on life on Earth, though, goes far beyond the past and present tragedies of a single species, however pressing they seem. Though the study of viruses began as an investigation into what appeared to be a strange subset of pathogens, recent research puts them at the heart of an explanation of the strategies of genes, both selfish and otherwise.

Viruses are unimaginably varied and ubiquitous. And it is becoming clear just how much they have shaped the evolution of all organisms since the very beginnings of life. In this, they demonstrate the blind, pitiless power of natural selection at its most dramatic. Andfor one group of brainy bipedal mammals that viruses helped createthey also present a heady mix of threat and opportunity.

As our essay in this weeks issue explains, viruses are best thought of as packages of genetic material that exploit another organisms metabolism in order to reproduce. They are parasites of the purest kind: they borrow everything from the host except the genetic code that makes them what they are. They strip down life itself to the bare essentials of information and its replication. If the abundance of viruses is anything to go by, that is a very successful strategy indeed.

The world is teeming with them. One analysis of seawater found 200,000 different viral species, and it was not setting out to be comprehensive. Other research suggests that a single litre of seawater may contain more than 100bn virus particles, and a kilo of dried soil ten times that number. Altogether, according to calculations on the back of a very big envelope, the world might contain 1031 of the thingsthat is ten followed by 31 zeros, far outnumbering all other forms of life on the planet.

As far as anyone can tell, virusesoften of many different sortshave adapted to attack every organism that exists. One reason they are powerhouses of evolution is that they oversee a relentless and prodigious slaughter, mutating as they do so. This is particularly clear in the oceans, where a fifth of single-celled plankton are killed by viruses every day. Ecologically, this promotes diversity by scything down abundant species, thus making room for rarer ones. The more common an organism, the more likely it is that a local plague of viruses specialised to attack it will develop, and so keep it in check.

This propensity to cause plagues is also a powerful evolutionary stimulus for prey to develop defences, and these defences sometimes have wider consequences. For example, one explanation for why a cell may deliberately destroy itself is if its sacrifice lowers the viral load on closely related cells nearby. That way, its genes, copied in neighbouring cells, are more likely to survive. It so happens that such altruistic suicide is a prerequisite for cells to come together and form complex organisms, such as pea plants, mushrooms and human beings.

The other reason viruses are engines of evolution is that they are transport mechanisms for genetic information. Some viral genomes end up integrated into the cells of their hosts, where they can be passed down to those organisms descendants. Between 8% and 25% of the human genome seems to have such viral origins. But the viruses themselves can in turn be hijacked, and their genes turned to new uses. For example, the ability of mammals to bear live young is a consequence of a viral gene being modified to permit the formation of placentas. And even human brains may owe their development in part to the movement within them of virus-like elements that create genetic differences between neurons within a single organism.

Evolutions most enthralling insight is that breathtaking complexity can emerge from the sustained, implacable and nihilistic competition within and between organisms. The fact that the blind watchmaker has equipped you with the capacity to read and understand these words is in part a response to the actions of swarms of tiny, attacking replicators that have been going on, probably, since life first emerged on Earth around 4bn years ago. It is a startling example of that principle in actionand viruses have not finished yet.

Humanitys unique, virus-chiselled consciousness opens up new avenues to deal with the viral threat and to exploit it. This starts with the miracle of vaccination, which defends against a pathogenic attack before it is launched. Thanks to vaccines, smallpox is no more, having taken some 300m lives in the 20th century. Polio will one day surely follow. New research prompted by the covid-19 pandemic will enhance the power to examine the viral realm and the best responses to it that bodies can mustertaking the defence against viruses to a new level.

Another avenue for progress lies in the tools for manipulating organisms that will come from an understanding of viruses and the defences against them. Early versions of genetic engineering relied on restriction enzymesmolecular scissors with which bacteria cut up viral genes and which biotechnologists employ to move genes around. The latest iteration of biotechnology, gene editing letter by letter, which is known as CRISPR, makes use of a more precise antiviral mechanism.

The natural world is not kind. A virus-free existence is an impossibility so deeply unachievable that its desirability is meaningless. In any case, the marvellous diversity of life rests on viruses which, as much as they are a source of death, are also a source of richness and of change. Marvellous, too, is the prospect of a world where viruses become a source of new understanding for humansand kill fewer of them than ever before.

This article appeared in the Leaders section of the print edition under the headline "The aliens among us"

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How viruses shape the world - The Economist

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CRISPR and CRISPR-Associated (Cas) Genes Market Analysis Growth Opportunities and Trends by Forecast To 2025 – Scientect

Posted: August 20, 2020 at 10:53 am

Global CRISPR and CRISPR-Associated (Cas) Genes Market: Snapshot

Over the years, biomedical researchers have increasingly focused on developing efficient and reliable methods for precise and targeted changes to virtually any point of genome of any living cell. Recent advances in the genome engineering has triggered several biological researches and translational applications. Economical manipulation and modification of genomic sequences enable molecular biologists identify and characterize key genetic determinants to facilitate the investigation of various biological processes.

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Genome editing via clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated (Cas) is considered as an innovative technique in programmable and high-throughput functional genomics. CRISPR-Cas system consists of pattern of repetitive sequences in the DNA of certain bacteria, who used it as an adaptive immune system to find a protection mechanism against invading foreign DNA.

In less than a decade, a host of novel targeted techniques and genomic engineering tools have been developed that facilitates precise and diverse genomic modifications in a variety of organisms and tissues. The recent tool having enormous potential in biomedical researches is the clustered regularly interspaced short palindromic repeats associated Cas9/sgRNA system, also called Cas9/sgRNA. Cas9 protein is an RNA guided endonuclease. Along with its variants it has generated considerable excitement versatile genomic engineering tool in the development of genetically edited (GE) crops. Primary areas research for this include examining gene function, understanding the regulatory signaling networks, and rewiring sgRNA for advance loss-of-function screening. This will help in combating biotic and abiotic stresses, thereby leading to the development of climate resilient crops and sustainable agriculture practices in the coming years.

Global CRISPR and CRISPR-Associated (Cas) Genes Market: Overview

In the past few years research and development of CRISPR or clustered regularly interspaced short palindromic repeats has allowed molecular biologists to designs solutions for repairing cells by genome editing. This method allows a change to a specific genome by the introduction of a new function or by correction of a mutation. The exceptional fidelity, simplicity of construction, and low cost has triggered a monumental demand for the several solutions offered by the global CRISPR and CRISPR-associated (Cas) genes market. The market is riding a wave of success as these factors have augmented the uptake of this method in several molecular biology laboratories.

The well-documented research report presents a fair case study of the global CRISPR and CRISPR-associated (Cas) genes market. The report includes a SWOT analysis and Porters five forces analysis, which help in understanding several facets of the global market in greater depth. Furthermore, analysts have used primary and secondary research methodologies, which ensure the authenticity of the facts. This information in the report has also been seconded by market experts with comments and recommendations about the subject matter. The comprehensive research report is aimed at guiding each of its readers to make well-informed business decisions.

Global CRISPR and CRISPR-Associated (Cas) Genes Market: Trends and Drivers

The products available in the global CRISPR and CRISPR-associated (Cas) genes market are DNA-free Cas and vector-based Cas. The widening applications of these are expected offer several lucrative opportunities to the global market. Out of various applications, genome engineering is expected to be a key contributor to the soaring revenue of the overall market in the near future. This trend will be attributable to eh increasing uptake of genome editing method for the therapeutic development and germline modifications. The report indicates that advancements in plant genome engineering will result in positive impact on the global market.

Analysts predict that CRISPR could be the next biotechnology treatment that has the ability to gradually replace the present single-antibody drugs. Genome engineering is anticipated to pick up a phenomenal pace in the coming years as it is being developed to build an immune response for targeting cancer. The widening application of these methods in the field of oncology is likely to change the game for the global market in the coming years.

Global CRISPR and CRISPR-Associated (Cas) Genes Market: Regional Outlook

In terms of geography, the global market is segmented into North America, Asia Pacific, Latin America, the Middle East and Africa, and Europe. North America is estimated to lead the global CRISPR and CRISPR-associated (Cas) genes market as the U.S. has shown a keen interest in developing effective therapeutics. Asia Pacific is also expected to offer several growth opportunities to the overall market as the region is facing a challenge of mounting unmet medical needs.

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Key Players Mentioned in the Report are:

The report has identified the following as the key operating players in the globalCRISPR and CRISPR-associated (Cas) genes market: Thermo Fisher Scientific, Inc., Caribou Biosciences, Inc., CRISPR THERAPEUTICS, Addgene, Mirus Bio LLC, Merck KGaA, Editas Medicine, GE Healthcare Dharmacon Inc., Takara Bio USA, Horizon Discovery Group plc, and Intellia Therapeutics, Inc.Analysts predict that these companies will focus on making strategic collaborations to ahead of the competition present in the overall market.

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TMR Research is a premier provider of customized market research and consulting services to business entities keen on succeeding in todays supercharged economic climate. Armed with an experienced, dedicated, and dynamic team of analysts, we are redefining the way our clients conduct business by providing them with authoritative and trusted research studies in tune with the latest methodologies and market trends.

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CRISPR and CRISPR-Associated (Cas) Genes Market Analysis Growth Opportunities and Trends by Forecast To 2025 - Scientect

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The Worst Animal in the World – The Atlantic

Posted: August 20, 2020 at 10:53 am

For about a week this past September, I adopted a wellness routine thatat the timefelt like neurotic overkill. I didnt bother with masks or hand sanitizer; back then, the virus we now know as SARS-CoV-2 was still presumably nestled in the warm body of an unknown animal. Instead, each morning, I spritzed my arms and legs with picaridin, a chemical repellent meant to ward off parasitic bugs. Then I covered myself with one of several increasingly crusty sets of khaki pants and long-sleeved shirts that I had infused with the insecticide permethrin. Only then, force field up, would I venture outside.

I had come to Dakar, Senegal, to get closebut not too closeto Aedes aegypti, a globally invasive mosquito that is arguably the worst animal in the world. The species carries yellow fever and dengue, both of which can cause more severe disease in young adults than SARS-CoV-2; Zika virus, which can lead to birth defects; and chikungunya virus, which can leave victims with debilitating joint pain.

Unlike viruses that travel person-to-person, most of these pathogens can spread only in places where mosquitoes live. Then again, aegyptis range is immense. All told, her bitesand only females bitecause an estimated 400 million infections each year, which means that several dozen people have been infected in the time it took you to read this sentence. In 2019, when the World Health Organization compiled a list of threats to global health, dengue got a whole slot to itself. Zika showed up in another slot, sharing billing with Ebola, SARS, and disease X, the prospect of some then-unknown pathogen with epidemic potential.

In Senegal, my own illusion of invulnerability lasted until I met Mawlouth Diallo, a medical entomologist from the Pasteur Institute in Dakar. Wearing a matching blue kaftan set, he sat with me in my hotel lobby for more than an hour, earnestly explaining his teams mosquito research in smooth, French-accented English. Finally, I had to ask a nagging, basic question.

Sitting here, right here, I said, gesturing to the air-conditioned lobby, where is the nearest Aedes aegypti?

Diallo seemed confused at the question. Where?

Like, could we go find some of them outside right now?

No, it is inside, he said, then laughed out loud at the expression on my face. For sure, aegypti is inside the hotel. When dengue broke out in Dakar in 2009, the citys Lebanese population was hit the hardest. One reason, Diallo said, was that mosquitoes and wealthy foreigners are both drawn to luxury indoor environments. In this lobby, he said, the best place to find Aedes aegypti would be the flowerpots.

I laughed with him, albeit less easily. Of the 3,000-plus mosquito species alive, most are fairly harmless. Only a handful are a concern for public-health officials. But Aedes aegypti is different. Whether in Rio de Janeiro, New Delhi, or Miami-Dade County, it will breed in clean water supplies, it will come indoors, it will make a beeline toward human odor, and it will bite when the sun is up, circumventing bed nets that protect at night. Masks to prevent the spread of COVID-19 wont make a difference. Neither will staying at home, unless you live in a closed, air-conditioned house. No other mosquito is so perfectly suited to live with, and on, human beings.

The problem will get worse. Beyond the tropics and subtropics, the species has strongholds in Florida, Texas, California, and Arizona, and at least one population has managed to survive multiple winters in Washington, D.C. One recent study projected that by 2050, thanks to the climate crisis, the North American range of Aedes aegypti will extend to Chicago; in China, its range will go as far north as Shanghai.

In response, the world is readying an arsenal of shiny new biological tools. But as scientists and policy makers plan to subvert the species evolutionary future, its especially important to grapple with its origins, the kind of processes that begin long before once-obscure pathogens emerge from clear-cut rainforests or animal markets. In tropical Africa, especially Senegal, researchers are uncovering the shared history of aegypti and its favorite host, learning how environmental change, slavery, and colonialism turned a local mosquito into a global menace.

After chatting in the hotel lobby, Diallo agreed to find me some mosquitoes. Outdoors, we walked half a block and poked around a construction site, looking for standing water in buckets and concrete blocks before fending off a nervous manager. Then Diallo saw a tire leaning against a wall. Reaching inside with a discarded coffee cup, he scooped out a little waterin which he pointed out at least a dozen larvae.

Read: A new way to keep mosquitoes from biting

Cup in hand, Diallo hailed us a cab and negotiated a fare to the Pasteur Institute. In his lab, he led me into a room full of mesh cages of aegypti from all over the country. The mosquitoes looked, in my paranoid imagination, very eager to get out.

That afternoon, when I returned to my hotel, I walked over to the pool. I waited until nobody was watching, then bent to look into the wet, shaded basin under one of the large flowerpots. The shadows wriggled, and I recoiled. The next morning, despite all my defenses, I noticed the first bites on my arm.

Aedes aegypti, whatever else you want to say about it, is a good-looking animal. Entomologists have described it to me as elegant, quite attractive, and even beautiful. Photographs often show it perched delicately on pink skin, displaying long limbs with black-and-white jailbird stripes. That pretty pattern belies an ugly disposition; the name of its scientific genus is derived from the Greek for unpleasant.

Fair enough. But aegypti wasnt always unpleasant. Within the past few thousand years, somewhere in Senegal or farther down the continent in modern-day Angola, biologists suspect that aegypti took its first step toward world domination.

Early hints of this story surfaced in the 1960s, when medical entomologists in the Rabai region of Kenya saw the species breeding in earthenware pots of water and feasting on their human hosts. Every house theyd go into would just be teeming with these mosquitoes, says the Princeton evolutionary biologist Lindy McBride, who has revisited the same sites.

No surprise so far. This was the familiar, human-obsessed aegypti. But outside the Rabai houses, researchers spotted another form of aegypti. This variant laid its eggs in holes in the trunks of trees, not pots of water; it preferred to bite animals, not people. Yet it wasnt a new species. It was a trace of the ancestral aegypti, a relic of a more innocent time.

Scientists have since found undomesticated populations of the species across tropical Africa. They hope to understand not just how the domesticated form picked up its particularly nightmarish set of skills, but how other species might be bending the same way under the same forces. If we can understand where [aegypti] comes from and how it works, the hope is, we can figure out how to stop it, says Noah Rose, a postdoc in McBrides lab at Princeton.

Senegal, especially, might be the key. Starting in 2017, Rose went on a series of road trips across sub-Saharan African countries. In Senegal, Rose teamed up with the ecologist Massamba Sylla, who had already discovered something unique about the countrys mosquitoes.

After an hour-and-a-half-long cab ride inland from Dakar, during which I watched the scenery change from very dusty to extremely dusty, I met Sylla in a caf in the city of This. Over croissants and caf au lait, we flipped through photos from his expeditions on his laptop as he described his lifelong, wife-vexing passion for field entomology. Once it catches you, you put all your time into doing it, he said.

During his travels, Sylla discovered a pattern. Senegals climate ranges from desert in the northwest to tropical rainforest in the southeast; as these habitats blend into one another, so do the parasites. In dry cities on the coast such as Saint Louis and Dakar, Sylla and collaborators found only domesticated mosquitoes. But in towns in the far southeast, they collected almost exclusively undomesticated mosquitoes, breeding in tree holes or in the husks of fallen fruit. Between the two extremes, Sylla found a continuum of domesticated and undomesticated aegypti.

Read: No one knows exactly what would happen if mosquitoes were to disappear

When Rose came to the country in August of 2018, he and Sylla drove along the same gradient, from dry Dakar in the south to where the countryside flushes green and rivers block the roads. The trip was not without risk: A decade earlier, another American researcher working in the southeast with Sylla flew back home before developing flu-like symptomsZika, it turned out, which he then transmitted to his wife through sex.

This time, though, no one got sick, and the collection process they followed was alarmingly easy. They collected the eggs in oviposition traps lined with filter paper, upon which the eggs can survive dormant for months. Once back in New Jersey, Rose submerged the eggs in water; most hatched overnight. Youve suddenly just transferred a whole population of mosquitoes between continents, he told me, with almost no effort expended.

Rose tested mosquitoes from across the Senegal transect and other countries, imprisoning them in plexiglass cages and presenting them with two olfactory options. They could fly down a tube that led to his own arm, or down another that led to a hapless guinea pig. Screens shielded both Rose and the guinea pig from actual bites.

These tests, recently summarized in the study, show that places in northern Senegal near Dakar with severe dry seasons but crawling with people, who come with their own water supply host the most human-craving mosquitoes Rose harvested anywhere in Africa. But the country also contains the widest range of aegypti behaviors, from almost exclusive animal-biting in the southeast to exclusive human-biting in the northwest. This diversity suggests that Senegal could be where the transformation happened.

Scientists still dont know the specific reasons for the change. But heres one plausible scenario of aegypti evolution, described to me by the biologist Jeffrey Powell at Yale University. Imagine a city near or encroaching on the forest. The climate slides into a drought, and animals are scarce. But human communities still offer warm-blooded bodies to drink from and cisterns of clean water to lay eggs in, enough to support aegypti until the rains return. Now imagine aegypti, over several generations, adapting to this new, more reliable lifestyle.

Some 500 years ago, after our domesticated aegypti had evolved in dry coastal cities in Senegal, Angola, and elsewhere on the African continent, European ships arrived on the Atlantic coast and began to carry away human beings. As the global tragedy of slavery unfolded, aegypti unleashed itself on the wider world.

Dakar, a French- and Wolof-speaking city clogged with determined street vendors, honking cabs, and clomping horse-drawn carts, was once the administrative center of French West Africa. Now its Senegals capital. The larger metropolitan area, home to some 3 million people, is still trying to cram itself onto the Cape Verde peninsula, which curls out into the Atlantic from the westernmost point of Africa like an arm bent at the elbow.

When the Portuguese sailed into the peninsulas enclosed harbor in 1444, the city of Dakar did not exist. For societies living between the Senegal and Gambia Rivers, the Atlantic was a dead end. Trade came instead from the Muslim world to the east. But after Europeans arrived, the slave-trading outposts they built along the African coast began to exert their own gravity.

To meet the European demand for enslaved people, some societies launched massive manhunts against neighbors. Normal economies collapsed. Famines struck, leaving victims so hungry that they offered themselves up to enslavers. This predatory business, which reduced the producer to an export commodity, pushed Senegambian societies into a state of regression, writes the West African historian Boubacar Barry. Violence became the dominant motive force of their history.

At staging grounds such as Goree Island, enslavers conducted invasive physical examinations to screen out unhealthy people. After loading their captives on boats, though, they locked many inside the hold in rank, appalling conditions rather than risk having them revolt or jump overboard. Disease and death were rampant. For the crew and a profitable percentage of the captives to survive the two-to-four-month journey across the ocean, the ships also needed to carry dozens of water barrels. The concentrated humanity combined with the abundant standing water offered domesticated aegypti everything it needed to stow along.

Meanwhile, the same bottomless avarice that brought enslaved people and aegypti to the Caribbean had terraformed their destination. After uprooting indigenous populations, enslavers cleared large areas for sugarcane, then razed even more forest for the fuel they needed to reduce cane juice to crystals. Clearing the dense, moist stands, they assumed, would also eliminate the noxious miasmas that they believed to be the ultimate source of disease.

They were wrong. With forests gone, invasive species replaced insect-eating birds. Erosion caused flash floods. Loose sediments collected into marshland, creating new breeding grounds for mosquitoes. Native Anopheles mosquitoes ingested the malaria parasite from the blood of incoming West Africans and spread malaria throughout the islands. As for the arriving aegypti, it found the Caribbeans ports and sugar plantations teeming with human victims, standing water, and pure cane juicewhich the species will also drink in a pinch. By the 1640s, aegypti had made itself at home in the islands, and was quietly setting the stage for something worse.

Around this time, the yellow-fever virus must have also made the trip over from Africa, likely volleying between mosquitoes and infected enslaved people or sailors during the long voyage. Yellow fever wreaks special havoc on adult immune systems that have never encountered it before. First victims get flu-like fever and aches for a few days, then appear to recover. Typically this recovery sticks. Otherwise, they get sick again, this time with jaundicehence the yellowand start vomiting up blood, hence the diseases Spanish name, vomito negro.

An early outbreak hit Barbados in 1647, leaving 6,000 people dead before rippling through the rest of the Caribbean. Yellow fever then sloshed from port to port for centuries, borne on silent wings. Ships, ports, and cities formed an invisible circulatory system. In summertime, the yellow-fever virus could materialize far outside its normal rangeas in 1793, when one of Americas foundational disease outbreaks killed one in 10 Philadelphians and abated only once fall brought frost.

Read: Two ways of making malaria-proof mosquitoes

Here aegypti, itself shaped by history, began to shape history back. Once established in the Americas, as the historian J. R. McNeill argues in his 2010 book, Mosquito Empires, endemic malaria and especially yellow fever gave local populations an advantage against foreign powers, whose soldiers would show up to fight with less seasoned immune systems. All locals had to do was survive outright confrontationand wait. Yellow fever helped Spain defend its holdings against European competitors; malaria weakened British forces during the American Revolution. When Toussaint LOuverture fought to liberate Haiti, yellow fever may have been his staunchest ally.

The domesticated aegypti had established itself quickly across the Atlantic, altering the history of the Americas in the process. In 2018, Powell at Yale published a landmark study showing that mosquito genomes and epidemiological records reflected the historical timeline. The histories of the slave trade, the mosquito populations, and the disease outbreaks are all telling the same story, he said.

And then aegypti kept going. After ships crossed from Africa to the Americas, they headed back to Europe laden with goods such as sugar. Soon, a few mosquitoes likely hitched a ride on this leg of the trip too. In 1801, Spains queen consort, Maria Luisa de Parma, suffered from a disease she called dengue. Around then, aegypti was making itself comfortable in the Mediterranean, and would go on to cause outbreaks of yellow fever and dengue there for decades. When the Suez Canal opened in 1869, it offered the species a back way out of the Mediterranean into the Pacific. Before that centurys end, the first clear outbreaks of chikungunya and dengue had appeared in Asia.

Meanwhile, yellow fever kept burning through the tropics. Nobody even knew what carried it until the 1880s, when a Cuban doctor named Carlos Finlay made a then-preposterous proposal: Maybe mosquitoes caused these outbreaks. The U.S. Army pathologist Walter Reed proved Finlays theory in 1900, finally giving humans a chance to slow the spread of the disease by putting up screens and getting rid of standing water. Between then and now, though, the sun still hasnt set on aegyptis empire.

Yellow fever itself has been mostly brought to heel. The breakthrough came in 1928, when competing American, French, and English research teams across Africa convened in Dakar to discuss the tragic case of one Adrian Stokes.

After France had abolished slavery in Senegal, in 1848, the colonial government conquered inland states and set up peanut farms, devising new systems to profit from African labor that soon expanded into other colonies. Senegal was a laboratory for the European powers, says Mor Ndao, a historian of tropical medicine at Dakars Cheikh Anta Diop University.

Disease stood in their way. Yellow fever was an obstacle for the exploitation of the African continent, Ndao told me. Senegals coastal cities had long been gripped by their own yellow-fever outbreaks, which public officials and even scientists invoked to justify race- and class-based sanitary segregation long after the mosquito hypothesis had proved what really carried the disease. But the death of Stokes, an Irish pathologist, offered a new way forward.

Read: How the rise of cities helped mosquitoes thrive

The year before, in 1927, Stokes had contracted yellow fever while helping isolate the virus from the blood of a Ghanaian man named Asibi. The pathologist demanded that his colleagues draw his blood and let mosquitoes bite him. Injections of that blood and bites from those mosquitoes both caused fatal yellow-fever cases in monkeys, proving that the team really had captured the infectious substance itself. Stokes died four days after contracting the virus, and was buried in Lagos. He was the first author on the pivotal scientific paper.

Upon hearing of this success, the French team at the Pasteur Institute isolated their own strain from a local patient named Francois Mayali. After sharing their findings in the Dakar meeting, multiple groups of scientists started working on vaccines. Mass vaccination campaigns began in the following decades, pushing yellow fever and its bloodsucking vector out of mind and making the tropics less scary for Ndaos would-be exploiters. Today, virtually every yellow-fever vaccine, including the one I got before visiting Dakar, bears a hint of these colonial beginnings: They still use a watered-down version of the strain taken from Asibi.

With the worlds attention diverted, this win soured. During the past century, similar viruses emerged from forests in Africa and Asia. Reaching urban areas, they all found aegypti ready to ferry them from person to person. First came dengue, which leaked out into a bigger global problem as southeast Asia urbanized after World War II. Then in 2006, more than a million people in India may have caught chikungunya. This past decade, Zika emerged on a similar scale in the Americas. Even yellow feverstill the only aegypti-carried disease with a safe, publicly available vaccinehas staged a comeback: two African outbreaks in 2016.

All this, remember, wrought by what were once inoffensive forest insects.

Roses study projects that Africas milder, wilder populations of aegypti may crank up their own appetite for humans by 2050, as dense cities spring up across the continent. In response to that alarming forecast, a new collaboration of scientists from across the Sahel, the semiarid region south of the Sahara, is collecting more local eggsbut that research has gotten off to a slow start thanks to COVID-19 and extremist groups in the region, Rose says.

Perhaps a deeper worry is that thousands of other mosquito species out there have their own capacity to change. During the Second World War, when Londoners hid in the citys Underground tunnels to escape bombing during the Blitz, they were swarmed by a form of the mosquito Culex pipiens that had already adapted to the worlds oldest subway system. That same pest now haunts subterranean Manhattan. And just in the past four decades, Aedes albopictus, an aegypti cousin from Southeast Asia that carries many of the same diseases, has exploded its range through Europe, Africa, and the Americas.

Not to mention unknown others. We could be missing the tip of the iceberg here, says Scott Weaver, who directs the Institute for Human Infections and Immunity at the University of Texas. I think understanding aegypti, as a first step, will be very important.

As we approached the island, a crumbling stone fort with grass growing on top came into view, then a few buildings painted in fading pastels. Then a dock next to a small beach. The ferry engine kicked into reverse, sending a deep rumble through the deck.

This is Goree Island. Within sight of Dakar, its the kind of place where aegypti likely hitched a ride across the Atlantic. A UNESCO World Heritage Site, the island is already steeped in the global memory of slavery. First established as a coastal base by the Portuguese, Goree was controlled by the Dutch, the British, and the French until Senegal achieved independence in 1960.

After disembarking and buying admission to Goree, I headed southeast, passing a massive baobab tree and a few lounging stray kittens on my way to a museum called the House of Slaves. Since the 1990s, historians have argued that Goree was a relatively minor location in the overall slave tradethat perhaps only 33,000 captive human beings came through the islandand that the role of this specific house might have been mostly symbolic.

But memory, once established, doesnt work that way. The three U.S. presidents before the current one came here, and when Nelson Mandela visited, the story is that he sat by himself for five minutes in a cramped chamber marked for recalcitrant captivesand then came out shaken, his eyes red.

After the entrance, visitors pass through a pink courtyard. The ground floor under the house is divided by stone walls into various dim holding chambers, each room labeled by the museum with a sign in French: women, children, the sick. Running your hand along the wall, you can feel the occasional seashell embedded in the stone.

Read: The quest to make a better mosquito repellent

Behind the house, visitors paused for selfies in the Door of No Return, an empty frame backlit by the sky and ocean. I waited my own turn. The conceit here is that anyone kept under this house and then led through that door never came back. Their world was forever altered. The wider world was also altered, both by the tragedy of slavery and by its still-unfolding consequences, among them 400 million annual infections.

For this insect problem, at least, fixes are in the works. By asking questions about where aegypti came from, scientists such as Diallo and Sylla in Senegal and their overseas colleagues hope to save lives too. Understanding aegyptis evolution on its home turf might also help us anticipate and counter copycat trends in other mosquitoes or disease-vector species. And unravelling why aegypti and its viruses are so good at parasitizing us could also help us fight them.

For example, if McBride can pinpoint the genes and neurological systems that control the domesticated aegyptis fixation on people, hijacking that system to find new chemical repellents could be easier. So would crafting new kinds of bait, which would manipulate aegypti to avoid populated areas and head elsewhere. We might be able to design a super-stimulus that would be more attractive than humans, that would pull them into traps, she says.

But the limiting factors in 2020 are focus and funding, especially with another virus falling on the world like an anvil. Im optimistic that people are finally understanding we cant continue this boom and bust funding cycle, Weaver says, where a new outbreak occurs and we put a lot of resources into that viruswhether it be chikungunya, or Zika, now SARS-CoV-2and we do that by taking away resources from other diseases.

For now, though, public-health systems across the Global South have also been diverted to coronavirus work, scientists say, leaving papers unpublished and mosquitoes uncollected. And whereas vaccines for Zika and chikungunya have been in development for many years, the fact that the outbreaks of those diseases are unpredictable and their victims clustered in poorer countriesunlike those of the more widespread COVID-19means that the vaccines are difficult to test and less lucrative for the pharmaceutical industry, and thus still havent made it to market.

As for engineering options to target the mosquitoes themselves, new technologies are already out in the world, aiming to reshape this little critter at the nexus of so much suffering.

One option is a bacterium called Wolbachia, bred into laboratory aegypti and then into wild populations. A greedy pathogen itself, the bacteria competes with the viruses that want to piggyback on the mosquitos life cycle. Tested in Indonesia, Malaysia, and even in Fresno, California, it reduces the mosquitos ability to spread disease.

An even more formidable option might be the gene drive, a type of genetic modification that would spread altered genes from a few sterile or disease-free mosquitoes throughout entire wild populations. The method is undergoing preliminary testing in Burkina Faso and elsewhere, and aegypti is high on the list of potential targets.

Meanwhile, less fancy kinds of genetically altered aegypti are already out in the wild. From 2013 to 2015, for example, one mosquito-control program released millions of modified male mosquitoes designed by a British company called Oxitec in the city of Jacobina, Brazil. The idea was that when they mated with wild females, the resulting offspring would die in infancy, causing populations to plummetwhich they did.

Apparently, though, not all those doomed offspring actually died. Some found a way to live and breed, passing on little bits of themselves. As Powell and other researchers pointed out in an eyebrow-raising study this past September, the wild aegypti population near Jacobina now contains a sprinkling of mosquito genes from Mexico and Cuba, where the Oxitec mosquitoes ancestors were harvested.

This crossbreeding might have actually strengthened the Jacobina aegypti, the study suggestedsparking a media firestorm, a fierce response from Oxitec, and concern from several of Powells Brazilian co-authors. I thought I was pretty conservative, Powell said, but it seems like that got blown out of hand. This summer, both the U.S. Environmental Protection Agency and the state of Florida granted Oxitec permits to begin releasing a version of the same technology in the Florida Keys, although there are still regulatory hurdles to clear.

As we continue to influence its evolution, aegypti, as it always does, is beginning to respond. Standing on Goree Island, though, I didnt think much about the wizardry of all these fixes in the works, or the engineering required, or the consideration of known and unknown consequences. Instead, I took a moment to dwell on what has already happened.

And maybe with this past in mind, or maybe because of a simpler superstition, I didnt walk through the threshold of the Door of No Return when I got to it. I just stood there, blinking in the light, looking out at the turquoise waves.

Ousmane Balde contributed reporting.

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The Worst Animal in the World - The Atlantic

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