29 January 2021 ~ 26 Comentarios

Colombia in danger

Por Carlos Alberto Montaner

It appeared in Semana. They published a secret dossier, written by the intelligence bodies for President Iván Duque. This happened after the entry in the publication of the “Gilinski Group.” The sensational content reveals Cuban manipulation and interference in internal political affairs. Semana is a very important Colombian magazine directed by journalist Vicky Dávila.

Colombia is in the sights of “the Cubans.” Naturally, the president of Cuba himself, Miguel Díaz-Canel, has denied it, but the mark is very clear. Why is Havana dedicated to conquering Colombia? For at least three reasons. Because they already rule in Venezuela and the country has been thoroughly looted and destroyed. Cuba needs to replace the sources of oil supply and economic funds. The Island has an absolutely parasitic and unproductive system at the service of the military and doesn’t want to change it.

Second, because it counts on old apparatchiks like Gustavo Petro and Iván Cepeda. It’s no longer necessary to knock down the old structures of the Republic with cannon fire. It’s enough to participate in the elections and win. The Quislings are inside the country, as happened with Chávez and Maduro. And third, because Cuba has always done it and has done it “well.” Fighting bulls charge because they charge. It’s not necessary to find the guilty ones or play psychoanalysis. It’s in their nature.

Iván Duque will have to decide what to do with the Havana regime. He already knows that Cuban ambassador José Luis Ponce Caraballo is a smiling and skilled intelligence officer trained to penetrate and win friends, as former Cuban intelligence officer Enrique García, exiled in Miami, told me. And besides, he knows that Colombia is a desired target because of its oil production (although it has diminished substantially), and its ability to produce food for the hungry Cuban people.

If he breaks relations with Cuba, “the Cubans” assure sotto voce, they will release their internal pack of dogs, including the ELN, created by them half a century ago. But if he doesn’t, Cuban political operators will find a way for Petro to win the election. “Chávez had less than 5% when we started to operate in 1998. At the end we defeated Henrique Salas Römer by a wide margin,” they say with pride.

If Cuba conquered Venezuela when Fidel was alive and there was some hope that it would improve the quality of life of the Cuban people, today there is almost no one on the island who thinks the same regarding Colombia. All have watched with fear the gradual destruction of the country. The plummeting drop in oil production. Caracas’ inability to produce food or to meet its financial obligations. The blackouts. The sudden exile of almost six million Venezuelans. In short, they have seen in Venezuela what happens when the Cuban model is copied.

What’s the purpose of subjecting the people of Colombia to Venezuelan or Cuban horror? Why should they take the same path if Cubans are rehearsing or studying how to eliminate the Soviet model copied from the USSR in the sixties, when the USSR existed, and when Fidel, Raúl, Che Guevara and a dozen “revolutionaries” more believed the tale of Marxism and imposed an implacable dictatorship? What will they do after destroying Colombia? Will they try the same in Brazil?

Joe Biden administration’s officials in charge of Latin American affairs should ask themselves these questions. Over many years, since Clinton and his successor George W. Bush administrations, they have invested billions of dollars in strengthening Colombia, an effective and sincere ally in the fight against drug trafficking and for the preservation of democracy. Will they allow all that effort to fade away? Will they allow the sacrifices and the deaths to be without a purpose?

One of the symptoms of Third-Worldism is to completely ignore the predecessor’s acts of government. Not everything Trump did was wrong. One of his last decrees was to include Cuba once again among the nations that sponsor terrorism. Presumably, President Obama hastened to eliminate the description of the Cuban state as “terrorist,” thinking that the good intentions of one of the two contenders were enough for the other to change its behavior. He hadn’t realized that fighting bulls are programmed to charge. It’s their nature.

26 Responses to “Colombia in danger”

  1. Manuel 30 January 2021 at 11:18 am Permalink

    “ In his first inaugural address, as the Union fractured, Lincoln appealed to “the better angels” of Americans’ nature. His pleas could not prevent the worst conflict in American history. There are echoes of other moments of crisis in this transition—the recession presidencies of Franklin Roosevelt and Mr Obama; the pandemic ignored by Woodrow Wilson; the racial strife under Dwight Eisenhower and Johnson. For a president to navigate any one of these crises would be gruelling. To navigate them all at once will be a formidable job. Yet that is Mr Biden’s charge.
    The Economist is keeping tabs on Joe Biden’s cabinet, progress and the latest polling at economist.com/tracking-joe-biden

    • Manuel 30 January 2021 at 11:26 am Permalink

      las 4 grandes crisis en las que cabalga
      El esplendor de este año

      • manuel 30 January 2021 at 1:38 pm Permalink


        error: los que crean que resolviendo la sanitaria se resolveran las demas, cada una con su provia dinamica interna alimentada por profundas causas que no encontraran soluciones en el actual gobierno con sus amenazas de seguir profundizando todas estas con sus torpes politicas y agendas en pleno desarrollo de las que vamos teniendo avances de terrar en apenas diez dias de haber tomado posesion

  2. Manuel 31 January 2021 at 3:30 pm Permalink

    On January 11th Mr Xi declared that China was entering a “new development stage”, having achieved a first centennial goal of building a “moderately prosperous society”. China’s new goal is to be a “great modern socialist country” by 2049, when the People’s Republic turns 100. In plainer language, China wants to be a superpower of unchallenged strength and influence.

    • Manuel 31 January 2021 at 3:37 pm Permalink

      On January 15th a senior security official, Chen Yixin, told colleagues that the great trend of the moment was “a rising East and a declining West”. China has much to gain, he declared, if it can manage a protracted struggle with America and public-security risks at home. Once again liberals will be losers, for there is no room in Mr Xi’s China for checks and balances on an all-powerful, all-controlling party and state.
      China’s smoothest envoys will spend 2021 assuring foreigners that these are slogans about long-term ambitions, and should not be taken literally. That is too glib. The world should take seriously Mr Xi’s talk of China “becoming strong”, after a period of “standing up” (a reference to nation-building under Mao), and decades of “getting rich” (a nod to market reforms unleashed by Deng Xiaoping). In China, leaders’ speeches are not mere words. They are political marching orders. A turbulent year looms. ■

    • Manuel 31 January 2021 at 7:35 pm Permalink

      ‘ The biggest obstacle to China’s rise is poorly educated rural children’

      • Manuel 31 January 2021 at 7:36 pm Permalink

        Invisible China. By Scott Rozelle and Natalie Hell. University of Chicago Press; 248 pages; $27.50 and £22
        THE CHINA that most foreigners see is modern and metropolitan. The skyscrapers glitter. The bullet trains are fast and comfortable. Anyone who visits only Beijing, Shanghai or Shenzhen would conclude that China was already a rich country.
        Yet there is another China: poor, rural and scarcely visible to outsiders, especially when covid-19 has made travel so hard. Toilets can be holes in the dirt, tricky to find in the dark. Women sometimes break river ice to wash clothes by hand. In many villages, most working-age adults have moved to the cities, where they lay bricks, deliver packages and only occasionally return to see their children. “It’s a hard life being away from your family so much,” one migrant in Hebei province told this reviewer.
        Granted, rural Chinese are far better off than they used to be. In the 1950s, when Mao Zedong forced them onto collective farms, tens of millions starved to death. Now they generally have enough to eat, and proudly insist that guests in their draughty homes have second helpings of oily noodles. But a crisis is brewing in these villages, argue Scott Rozelle of Stanford University and Natalie Hell, a Californian researcher, that could prevent China from attaining Xi Jinping’s dream of widespread prosperity. Two-thirds of Chinese children are rural, partly because rural parents have more babies than urban ones. And rural Chinese children—the workforce of the future—are doing terribly at school.
        China has invested huge amounts in physical infrastructure, but neglected its human capital. Do not be fooled by league tables, such as the OECD’s PISA rankings, that show Chinese high-school students outperforming those of nearly every other country. The Chinese figures are not for the whole country, but only for the better schools in the richer cities.
        The children of rural migrants are barred from such schools, thanks to China’s brutal hukou (household registration) system, which excludes people with rural origins from many public services in big cities. Migrant workers’ children must either pay to attend awful urban private schools or stay back in the countryside with grandma and go to a mediocre government school there. Such discrimination is keenly resented.
        Healthy bodies, healthy minds

        After decades of research, Mr Rozelle and Ms Hell present some startling data. Their team gave an IQ-like test to thousands of rural Chinese toddlers. They found that more than 50% were cognitively delayed and unlikely to reach an IQ of 90 (in a typical population, only 16% score so poorly). There were several reasons for this.
        Half of rural babies are undernourished. Caregivers (often illiterate grandmothers) cram them with rice, noodles and steamed buns, not realising that they also need micronutrients. Studies in 2016 and 2017 found that a quarter of rural children in central and western China suffer from anaemia (lack of iron), which makes it hard for them to concentrate in school. Two-fifths of rural children in parts of southern China have intestinal worms, which sap their energy. A third of rural 11- and 12-year-olds have poor vision but no glasses, so struggle to read their schoolbooks.
        Some of these problems would be laughably cheap to fix. A pair of glasses costs $30. Multivitamin pills are a few cents. De-worming tablets cost $2 per child each year. One reason the problems persist is that harmful myths abound. Many rural folk believe that—as a grandmother told this reviewer—glasses are bad for children’s eyesight. Some fret that de-worming pills reduce fertility in girls. A recent study found that 99% of Chinese farmers gave their pigs de-worming drugs, but hardly any did the same for their children.
        Rural children fall behind long before they are old enough to go to school. Whereas urban parents constantly talk to their babies, rural grandmothers often strap them to their backs while they work in the fields, keeping them safe but barely stimulating their minds. The segregation of rural children into second-class schools then widens the gulf between the two Chinas.
        Among the entire labour force in 2010, 44% of urban and 11% of rural Chinese had graduated from high school. Among the current crop of students, the figures are much better: 97% of urban students graduated from high school in 2015, and 80% of rural children went to a high school of some sort. But the rural “high schools” were often dreadful, opened rapidly to meet official targets and staffed by teachers with little interest in teaching. The authors tested thousands of children at “vocational” rural high schools, and found that 91% had learned practically nothing: they scored the same or worse on tests at the end of a year of schooling as at the beginning.
        Currently, 70% of the Chinese workforce is unskilled. Such labourers can do repetitive factory work, but as their wages rise, those jobs will move to poorer countries such as Vietnam. To escape from what economists call the “middle-income trap”, China needs rapidly to improve its people’s skills, so that they can handle more complex tasks. Yet its workers are far less educated than those in other middle-income countries, such as Mexico, Turkey and South Africa. They are also less educated than workers were in countries that recently grew rich, such as Taiwan and South Korea, when those places were no better off than China is today.
        Much of the blame for all this rests with Mao, whose Cultural Revolution was “perhaps the largest intentional destruction of human capital the world has ever seen”. But the authors also blame “an almost unbelievable oversight” on the part of China’s more recent leaders. Correcting that is arguably the most important challenge facing China’s current rulers. They have the resources to succeed. A country that invests a whopping 43% of GDP can surely afford to spend a bit less on bridges and a bit more on its people’s brains. The authors offer sound prescriptions: improve rural schools, end discrimination against rural children, teach rural parents to read to their babies (instead of policing how many they may have), and so on.
        If rural Chinese do not learn essential cognitive skills, the authors predict mass unemployment, social unrest and perhaps a crash that would “lead to huge economic shocks around the world”. China’s rulers should order crates of de-worming pills—and copies of this book. ■

  3. Manuel 1 February 2021 at 7:13 pm Permalink

    The rabies virus is suddenly gone. The polio virus is gone. The gruesomely lethal Ebola virus is gone. The measles virus, the mumps virus, and the various influenzas are gone. Vast reductions of human misery and death. HIV is gone, and so the AIDS catastrophe never happened. Nipah and Hendra and Machupo and Sin Nombre are gone—never mind their records of ugly mayhem. Dengue, gone. All the rotaviruses, gone, a great mercy to children in developing countries who die by the hundreds of thousands each year. Zika virus, gone. Yellow fever virus, gone. Herpes B, carried by some monkeys, often fatal when passed to humans, gone. Nobody suffers anymore from chicken pox, hepatitis, shingles, or even the common cold. Variola, the agent of smallpox? That virus was eradicated in the wild by 1977, but now it vanishes from the high-security freezers where the last spooky samples are stored. The SARS virus of 2003, the alarm that we now know signaled the modern pandemic era, gone. And of course the nefarious SARS-CoV-2 virus, cause of COVID-19 and so bewilderingly variable in its effects, so tricky, so dangerous, so very transmissible, is gone. Do you feel better?
    This scenario is more equivocal than you think. The fact is, we live in a world of viruses—viruses that are unfathomably diverse, immeasurably abundant. The oceans alone may contain more viral particles than stars in the observable universe. Mammals may carry at least 320,000 different species of viruses. When you add the viruses infecting nonmammalian animals, plants, terrestrial bacteria, and every other possible host, the total comes to … lots. And beyond the big numbers are big consequences: Many of those viruses bring adaptive benefits, not harms, to life on Earth, including human life.
    We couldn’t continue without them. We wouldn’t have arisen from the primordial muck without them. There are two lengths of DNA that originated from viruses and now reside in the genomes of humans and other primates, for instance, without which—an astonishing fact—pregnancy would be impossible. There’s viral DNA, nestled among the genes of terrestrial animals, that helps package and store memories—more astonishment—in tiny protein bubbles. Still other genes co-opted from viruses contribute to the growth of embryos, regulate immune systems, resist cancer—important effects only now beginning to be understood. Viruses, it turns out, have played crucial roles in triggering major evolutionary transitions. Eliminate all viruses, as in our thought experiment, and the immense biological diversity gracing our planet would collapse like a beautiful wooden house with every nail abruptly removed.
    Jason Shepherd, a neuroscientist at the University of Utah, holds an image of a three-dimensional reconstruction of a virus-like protein capsule that plays a critical role in cognition and memory. The ARC gene, which carries the code to create this spherical marvel, was acquired by terrestrial vertebrates from a viral-like ancestor about 400 million years ago. The capsule, which resembles the capsids that surround viral genomes, ferries genetic information between neurons in the human brain as well as in the brains of many other animals.
    A virus is a parasite, yes, but sometimes that parasitism is more like symbiosis, mutual dependence that profits both visitor and host. Like fire, viruses are a phenomenon that’s neither in all cases good nor in all cases bad; they can deliver advantage or destruction. Everything depends: depends on the virus, on the situation, on your point of reference. They are the dark angels of evolution, terrific and terrible. That’s what makes them so interesting.
    TO APPRECIATE the multifariousness of viruses, you need to start with the basics of what they are and what they are not. It’s easier to say what they are not. They are not living cells. A cell, of the sort assembled in great number to make up your body or mine or the body of an octopus or a primrose, contains elaborate machinery for building proteins, packaging energy, and performing other specialized functions—depending on whether that cell happens to be a muscle cell or a xylem cell or a neuron. A bacterium is also a cell, with similar attributes, though much simpler. A virus is none of this.
    Saying just what a virus is has been complicated enough that definitions have changed over the past 120-some years. Martinus Beijerinck, a Dutch botanist who studied tobacco mosaic virus, speculated in 1898 that it was an infectious liquid. For a time a virus was defined mainly by its size—a thing much smaller than a bacterium but that, like bacteria, could cause disease. Still later, a virus was thought to be a submicroscopic agent, bearing only a very small genome, that replicated inside living cells—but that was just a first step toward a better understanding.
    “I shall defend a paradoxical viewpoint,” wrote the French microbiologist André Lwoff in “The Concept of Virus,” an influential essay published in 1957, “namely that viruses are viruses.” Not a very helpful definition but fair warning—another way of saying “unique unto themselves.” He was just clearing his throat before beginning a complex disquisition.
    Lwoff knew that viruses are easier to describe than to define. Each viral particle consists of a stretch of genetic instructions (written either in DNA or that other information-bearing molecule, RNA) packaged inside a protein capsule (known as a capsid). The capsid, in some cases, is surrounded by a membranous envelope (like the caramel on a caramel apple), which protects it and helps it catch hold of a cell. A virus can copy itself only by entering a cell and commandeering the 3D-printing machinery that turns genetic information into proteins.
    If the host cell is unlucky, many new viral particles are manufactured, they come busting out, and the cell is left as wreckage. That sort of damage—such as what SARS-CoV-2 causes in the epithelial cells of the human airway—is partly how a virus becomes a pathogen.
    But if the host cell is lucky, maybe the virus simply settles into this cozy outpost—either going dormant or back-engineering its little genome into the host’s genome—and bides its time. This second possibility carries many implications for the mixing of genomes, for evolution, even for our sense of identity as humans, a topic to which I’ll return. One hint, for now: In a popular 1983 book the British biologist Peter Medawar and his wife, Jean, an editor, asserted, “No virus is known to do good: It has been well said that a virus is ‘a piece of bad news wrapped up in protein.’” They had it wrong. So did a lot of scientists at the time, and it remains a view still embraced, understandably, by anyone whose knowledge of viruses is limited to such bad news as the flu and COVID-19. But today some viruses are known to do good. What’s wrapped up in the protein is a genetic dispatch, and that might turn out to be good news or bad, depending.
    WHERE DID THE FIRST VIRUSES come from? This requires us to squint back almost four billion years, to the time when life on Earth was just emerging from an inchoate cookery of long molecules, simpler organic compounds, and energy.
    Let’s say some of the long molecules (probably RNA) started to replicate. Darwinian natural selection would have begun there, as those molecules—the first genomes—reproduced, mutated, and evolved. Groping for competitive edge, some may have found or created protection within membranes and walls, leading to the first cells. These cells gave rise to offspring by fission, splitting in two. They split in a broader sense too, diverging to become Bacteria and Archaea, two of the three domains of cellular life. The third, Eukarya, arose sometime later. It includes us and all other creatures (animals, plants, fungi, certain microbes) composed of cells with complex internal anatomy. Those are the three great limbs on the tree of life, as presently drawn.
    But where do viruses fit? Are they a fourth major limb? Or are they a sort of mistletoe, a parasite wafted in from elsewhere? Most versions of the tree omit viruses entirely.
    One school of thought asserts that viruses shouldn’t be included on the tree of life because they aren’t alive. That’s a lingering argument, hinging on how you define “alive.” More intriguing is to grant viruses inclusion within the big tent called Life, and then wonder about how they got in.
    There are three leading hypotheses to explain the evolutionary origins of viruses, known to scientists as viruses-first, escape, and reduction. Viruses-first is the notion that viruses came into existence before cells, somehow assembling themselves directly from that primeval cookery. The escape hypothesis posits that genes or stretches of genomes leaked out of cells, became encased within protein capsids, and went rogue, finding a new niche as parasites. The reduction hypothesis suggests that viruses originated when some cells downsized under competitive pressure (it being easier to replicate if you’re small and simple), shedding genes until they were reduced to such minimalism that only by parasitizing cells could they survive.
    There is also a fourth variant, known as the chimeric hypothesis, which takes inspiration from another category of genetic elements: transposons (sometimes called jumping genes). The geneticist Barbara McClintock deduced their existence in 1948, a discovery that earned her a Nobel Prize. These opportunistic elements achieve their Darwinian success simply by bouncing from one part of a genome to another, in rare cases from one cell to another, even one species to another, using cellular resources to get themselves copied, over and over. Self-copying protects them from accidental extinction. They accumulate outlandishly. They constitute, for instance, roughly half of the human genome. The earliest viruses, according to this idea, may have arisen from such elements by borrowing proteins from cells to wrap their nakedness inside protective capsids, a more complex strategy.
    Each of these hypotheses has merits. But in 2003 new evidence tipped expert opinion toward reduction: the giant virus.
    IT WAS FOUND within amoebas, which are single-celled eukaryotes. These amoebas had been collected in water taken from a cooling tower in Bradford, England. Inside some of them was this mysterious blob. It was big enough to be seen through a light microscope (viruses supposedly were too small for that, visible only by electron microscope), and it looked like a bacterium. Scientists tried to detect bacterial genes within it but found none.
    How to count viruses
    To count viruses in the Aquarium of the Pacific’s Tropical Reef Habitat and Soft Coral Garden, we enlisted Alexandra Rae Santora, a doctoral student working with Jed Fuhrman, a professor at the University of Southern California. She ran a sample through a 0.02-micron filter, which catches bacteria and viruses. She used a DNA-binding stain to make them visible under an epifluorescence microscope. The larger organisms are bacteria; the dots are viruses. With a counting grid, she determined the number of viruses in the field of view. Knowing the filter size and the volume of water allowed her to calculate the population per gallon.
    An image of a human embryo with just eight cells looms behind Joanna Wysocka, a professor of developmental biology at Stanford University. Wysocka and her colleagues discovered that a human endogenous retrovirus—a genetic sequence acquired from an ancient viral infection — turns on during this developmental stage and produces proteins. Wysocka believes the gene, known as HERV-K, could protect the embryo from viral infection and help control fetal development. By the time a human embryo has grown into a many-celled blastocyst, HERV-K, shown here stained green, is present throughout, but is concentrated in cells that will become a baby.
    As far back as 150 million years ago, viruses infected mammals and left genes that led to a dramatic evolutionary advance: the placenta, which allows nutrients and oxygen to reach the fetus and waste and carbon dioxide to pass out. Humans and other mammals with placentas can move around with their unborn young, making them less vulnerable to predators. In humans, two genes originating from viruses—syncytin-1 and syncytin-2—help form the placental membrane that attaches to the uterus. This membrane also may aid in preventing the mother’s immune system from attacking the fetus as a foreign object.
    Finally a team of researchers in Marseille, France, invited the thing to infect other amoebas, sequenced its genome, recognized what it was, and named it Mimivirus, because it mimicked bacteria, at least with regard to size. In diameter it was huge, bigger than the smallest bacteria. Its genome was also huge for a virus, almost 1.2 million letters long, compared to, say, 13,000 for an influenza virus, or even 194,000 for smallpox. (DNA, like RNA, is a long molecule built with four different molecular bases, which scientists abbreviate by their first letters.) It was an “impossible” virus: viral in nature but too big in scale, like a newly discovered Amazon butterfly with a four-foot wingspan.
    Jean-Michel Claverie was a senior member of that Marseille team. The discovery of Mimivirus, Claverie told me, “caused a lot of trouble.” Why? Because sequencing the genome revealed four very unexpected genes—genes for coding enzymes presumed to be uniquely cellular and never before seen in a virus. Those enzymes, Claverie explained, are among the components that translate the genetic code to assemble amino acids into proteins.
    “So the question was,” Claverie said, “what the hell has a virus the need” for those fancy enzymes, normally active in cells, “when he has the cell at his disposal, OK?”
    What need indeed? The logical inference is that Mimivirus has them as holdovers because its lineage originated by genomic reduction from a cell.
    Mimivirus was no fluke. Similar giant viruses were soon detected in the Sargasso Sea, and the early name became a genus, Mimivirus, containing several giants. Then the Marseille team discovered two more behemoths—again, both parasites of amoebas—one taken from shallow marine sediments off the coast of Chile, the other from a pond in Australia. Up to twice as big as a Mimivirus, even more anomalous, these were assigned to a separate genus, which Claverie and his colleagues named Pandoravirus, evoking Pandora’s box, as they explained in 2013, because of “the surprises expected from their further study.”
    Claverie’s senior co-author on that paper was Chantal Abergel, a virologist and structural biologist (and also his wife). Of the Pandoraviruses, Abergel told me, with a weary laugh: “They were highly challenging. They are my babies.” She explained how difficult it had been to tell what they were, these creatures—so different from cells, so different from classical viruses, carrying many genes that resembled nothing ever before seen. “All of that makes them fascinating but also mysterious.” For a while she called them NLF: new life-form. But from observing that they didn’t replicate by fission, she and her colleagues realized they were viruses—the largest and most perplexing ones found so far.
    These discoveries suggested to the Marseille group a bold variant of the reduction hypothesis. Maybe viruses did originate by reducing from ancient cells, but cells of a sort no longer present on Earth. This kind of “ancestral protocell” might have been different from—and in competition with—the universal common ancestor of all cells known today. Maybe these protocells lost that competition and were excluded from all the niches available for free-living things. They may have survived as parasites on other cells, downsized their genomes, and become what we call viruses. From that vanished cellular realm, maybe only viruses remain, like the giant stone heads on Easter Island.
    The preserved lungs of a two-year-old girl who died in 1912 at the Charité, a hospital in Berlin, offer evidence that the measles virus spilled over to humans from cattle in the fourth century B.C., more than a thousand years earlier than initially thought. Sébastien Calvignac-Spencer, an evolutionary biologist at the Robert Koch Institute, came across the specimen at Berlin’s Museum of Medical History. He sequenced the measles genome, the oldest known, and used it and other measles genomes to calculate when it diverged from the cattle virus. (MARKUS BACHMANN)
    DISCOVERY OF THE GIANT VIRUSES inspired other scientists, notably Patrick Forterre at the Pasteur Institute in Paris, to formulate novel ideas about what viruses are and what constructive roles they have played, and continue to play, in the evolution and functions of cellular life.
    Previous definitions of “virus” were inadequate, Forterre proposed, because scientists were confusing viral particles—the capsid-enclosed bits of genome, properly known as virions—with the totality of a virus. That, he argued, was as wrong as confusing seed with a plant, or a spore with a mushroom. The virion is just the dispersal mechanism, he argued. The real wholeness of the virus also includes its presence within a cell, once it has seized the cell’s machinery to replicate more virions, more seeds of itself. To see the two phases together is to see that the cell has effectively become part of the virus’s life history.
    Forterre bolstered that notion by inventing a new name for the combined entity: the virocell. This idea also cut through the alive-or-not-alive conundrum. A virus is alive when it’s a virocell, according to Forterre, never mind that its virions are inanimate.
    “The idea behind the virocell concept,” he told me by Skype from Paris, “was mainly to focus on this intracellular stage.” That’s the delicate stage when the infected cell, like a zombie, obeying the viral mandate, reading the viral genome and replicating it, but not always without skips, staggers, and mistakes. During that process, Forterre said, “new genes can originate in viral genome. And this is a major point for me.” Viruses bring innovation, but cells respond with their own defensive innovations, such as the cell wall or the nucleus, and so it’s an arms race toward greater complexity. Many scientists have assumed that viruses achieve their major evolutionary changes by the virus pickpocket” paradigm, snatching DNA from this infected organism and that one, and then putting the stolen pieces to use within the viral genome. Forterre argues that the pilfering might more often go the other way, cells taking genes from viruses.
    An even more sweeping view, held by Forterre and Claverie and some other scientists in the field, including Gustavo Caetano-Anollés at the University of Illinois at Urbana-Champaign, is that viruses are the preeminent font of genetic diversity. According to this thinking, viruses have enriched the evolutionary options of cellular creatures over the past several billion years by depositing new genetic material in their genomes. This bizarre process is one version of a phenomenon known as horizontal gene transfer—genes flowing sideways, across boundaries between different lineages. (Vertical gene transfer is the more familiar form of inheritance: from parents to offspring.) The flow of viral genes into cellular genomes has been “overwhelming,” Forterre and a co-author have argued, and may help explain some great evolutionary transitions, such as the origin of DNA, the origin of the cell nucleus in complex creatures, the origin of cell walls, and maybe even the divergence of those three great limbs on the tree of life.
    Scientists are still trying to track down where the coronavirus known as SARS-CoV-2 originated. The greater horseshoe bat and the Chinese pangolin have been considered as possible hosts. Viruses found in the two species are related to the pandemic virus. Maciej Boni, an associate professor of biology at Penn State University, and an international team traced the virus back about a hundred years, when coronaviruses in pangolins diverged from those in bats. SARSCoV-2 may have evolved from the most closely related known bat viruses between 40 and 70 years ago. “Very little is known about the diversity of these viruses,” Boni said, adding that tens of thousands of avian flu virus genomes have been identified, but fewer than a hundred are known for coronaviruses. “There could in principle be viruses circulating in bats that are closer to SARS-CoV-2 or very similar to SARSCoV-2, but we haven’t done enough studies in bats; we haven’t collected enough viruses in bats, and we just don’t know.” This bat (Rhinolophus ferrumequinum) was collected in the Tashkent Region of Uzbekistan in 1921; the pangolin (Manis pentadactyla) came from Guizhou Province in China in 1945.
    The flow of viral genes into cellular genomes has been “overwhelming,” scientists argue, and may help explain some great evolutionary transitions, such as the origin of DNA, the cell nucleus, and cell walls, and even the divergence of the three great domains of life.
    IN THE OLDEN DAYS, the days before COVID-19, engrossing discussions with scientists sometimes happened in person, not by Skype. Three years ago, I flew from Montana to Paris because I wanted to talk with a man about a virus and a gene. The man was Thierry Heidmann, and the gene was syncytin-2. He and his group had discovered it by screening the human genome—all 3.1 billion letters of code—to find stretches of DNA that looked like the kind of gene a virus would use to produce its envelope. They found about 20.
    “At least two proved to be very important,” Heidmann told me. They were important because they had the capacity to perform functions essential to human pregnancy. Those two were syncytin-1, which was first discovered by other scientists, and syncytin-2, which he and his group found. How these viral genes became part of the human genome, and to what purposes they have become adapted, are aspects of a remarkable story that begins with the concept of human endogenous retroviruses.
    A retrovirus is a virus with an RNA genome that operates backward from the usual direction (hence retro). Instead of using DNA to make RNA, which then serves as a messenger sent to the 3D printer to make proteins, these viruses use their RNA to make DNA and then integrate it into the genome of the infected cell. HIV, for instance, is a retrovirus that infects human immune cells, inserting its genome into the cell genome, where it may lie dormant. At some point, the viral DNA gets activated, becoming a template for production of many more HIV virions, which kill the cell as they come exploding out.
    Here’s the big twist: Some retroviruses infect reproductive cells—the cells that produce eggs or sperm—and in doing that, they insert their DNA into the heritable genome of the host. Those inserted stretches are “endogenous” (internalized) retroviruses, and when incorporated into human genomes, they are known as human endogenous retroviruses (HERVs). If you remember nothing else from this article, you might want to remember that 8 percent of the human genome consists of such viral DNA, patched into our lineage by retroviruses over the course of evolution. We are each one-twelfth HERV. The gene syncytin-2 is among the more consequential of those patches.
    For four hours I sat in Heidmann’s office while he explained to me, with a laptop at his elbow for bringing up graphs and charts, the origin and the functions of this particular gene. The essence is almost simple. A gene that originally helped a virus fuse with host cells found its way into ancient animal genomes. It was then repurposed to generate a similar protein that helps fuse cells to create a special structure around what became the placenta, opening a new possibility in some animals: internal pregnancy. That innovation was vastly consequential in evolutionary history, making it possible for a female to carry her developing offspring from place to place, inside her body, rather than leaving them vulnerable in one place, as eggs in a nest.
    The first gene of this sort from an endogenous retrovirus eventually was replaced by others that were similar but better suited for the role. Over time, the design of this new mode of reproduction improved and the placenta evolved. Among these acquired viral genes is syncytin-2, one of two syncytins in humans helping to fuse cells to form a placental layer next to the uterus. That unique structure, mediating between mother and fetus, allows nutrients and oxygen in, carries waste products and carbon dioxide out, and probably protects the fetus from being attacked by the mother’s immune system. It’s a near miracle efficient design, in which evolution shaped a viral component into a human component.
    Heidmann and I broke for lunch and then resumed for another two hours. Finally, my brain buzzing, my notebook full, I asked him: What does it all say about how evolution works? He laughed with delight, and I laughed too, from amazement and fatigue.
    “Our genes are not only our genes,” he said. “Our genes are also retroviral genes.”
    THE CONTRIBUTION of that retrovirus, giving us syncytin-2, is only one instance of a grand pattern. Another is the gene ARC, expressed in response to neuronal activity in mammals and flies. It closely resembles a retroviral gene that codes for a protein capsid. Recent research by several teams, including one led by Jason Shepherd at the University of Utah, suggests that ARC plays a key role in storing information within neural networks. Another word for that: memory. ARC seems to do it by packaging information derived from experience (embodied as RNA) into little protein sacs that carry it from one neuron to another.
    And at the Stanford University School of Medicine, Joanna Wysocka, along with a group of colleagues, has found evidence that viral fragments produced by another human endogenous retrovirus, known as HERV-K, are present within human embryos at the earliest stage and might play some positive role in protecting the embryo from viral infection, or in helping control fetal development, or both. Further, her group has focused on a particular transposon that seems to have entered the human genome as a sort of prologue section of HERV-K, then found ways of copying itself and bouncing to other parts of the genome, so that it’s now present in 697 scattered copies. Those copies seem to help turn on almost 300 human genes.
    “To me what is really mind-boggling,” Wysocka said, “is that HERVs are about 8 percent of the human genome,” a portion of our being that is essentially “the graveyard of previous retroviral infections.” It’s even more boggling to contemplate how, as Wysocka put it, “our history of past retroviral infections is continuing to shape our evolution as a species.”
    If 8 percent of your genome and mine is retroviral DNA, and half is transposons, then maybe the very notion of human individuality (let alone human supremacy) is not as solid as we like to believe.
    THE DOWNSIDE of such evolutionary agility, of course, is that viruses can sometimes switch hosts, tumbling from one kind of creature into another and succeeding as pathogens in the unfamiliar new host. That’s called spillover, and it’s how most new human infectious diseases arise—with viruses acquired from a nonhuman animal host.
    In the original host—known to science as a reservoir host—a virus may have abided quietly, at low abundance and low impact, for thousands of years. It may have reached an evolutionary accommodation with the reservoir host, accepting security in exchange for causing no trouble. But in a new host, such as a human, the old deal doesn’t necessarily hold. The virus may explode in abundance, causing discomfort or misery in that first victim. If the virus not only replicates but also manages to spread, human to human, among a few dozen other individuals, that’s an outbreak. If it sweeps through a community or a country, that’s an epidemic. If it encircles the world, it’s a pandemic. So now we’re back to SARS-CoV-2.
    Some types of viruses are more likely to cause pandemics than others. Near the top of the list of the most worrisome candidates are coronaviruses, because of the nature of their genomes, their capacity to change and evolve, and their history of causing serious human disease, such as SARS (severe acute respiratory syndrome) in 2003 and MERS (Middle East respiratory syndrome) in 2015. So when the phrase “novel coronavirus” began to be used to describe the new thing causing clusters of illness in Wuhan, China, those two words were enough to make disease scientists around the world shudder.
    The inner workings of a cryogenic transmission electron microscope showcase its technological complexity.
    The instrument, which can create images of viruses down to near atomic level in three dimensions, revealed the now familiar spiky structure of SARSCoV-2. A monitor used with the microscope displays a cross section of the virus and a three-dimensional computational model.
    A slice of a reconstruction of SARS-CoV-2 from cryo-electron tomographyshows that the spikes protrude at odd angles.
    These spikes have three joints—hip, knee, and ankle—that allow them to flop around, most likely to increase the odds of attaching to a cell. A molecular model at atomic resolution shows the proteins making up the spike, with identical chains indicated by red, orange, and yellow. They are shielded by chains of glycans — sugarlike molecules colored blue—that hide the spike from human antibodies that could destroy it. Understanding the spike’s structure is key to designing effective vaccines.
    Coronaviruses belong to an infamous category of viruses, the single-stranded RNA viruses, that includes influenzas, Ebola viruses, rabies, measles, Nipah, hantaviruses, and retroviruses. They are infamous partly because a single-stranded RNA genome is subject to frequent mutation as the virus replicates, and such mutation supplies a richness of random genetic variation upon which natural selection can work.
    Coronaviruses, though, evolve relatively slowly for RNA viruses. They carry fairly long genomes—the SARS-CoV-2 genome runs to about 30,000 letters—but their genomes change less quickly than some others because they have a proofreading enzyme to correct mutations. Yet they are also capable of a trick called recombination, in which two strains of coronavirus, infecting the same cell, swap sections of their genomes and give rise to a third, hybrid strain of coronavirus. That may be what happened to create the novel coronavirus, SARS-CoV-2.
    The ancestral virus probably resided in a bat, possibly a horseshoe bat, belonging to a genus of small, insectivorous creatures with horseshoe-shaped noses, which commonly carry coronaviruses. If recombination did occur, adding some crucial new elements from a different coronavirus, this could have happened in a bat or possibly in another animal. (Pangolins have been suggested; other species could also be candidates.) Scientists are exploring these possibilities and others by sequencing and comparing genomes of the viruses found in various potential hosts. All we know for now is that SARS-CoV-2 as it exists today in humans is a subtle virus capable of further evolution.
    SO VIRUSES GIVE and viruses take away. Maybe the reason they are difficult to place on the tree of life is that life’s history, after all, isn’t quite shaped like a tree. The arboreal analogy is just our traditional way of illustrating evolution, made canonical by Charles Darwin. But Darwin, great as he was, knew nothing about horizontal gene transfer. In fact, he knew nothing about genes. He knew nothing about viruses. Everything is very complicated, we realize now. Even viruses, which seem so simple at first glance, are very complicated. And if seeing them in all their complexity gives us humans a clearer vision of the tangled connectedness of the natural world, if reflecting upon our own viral contents takes away some of our sublime detachment, then I leave it to you to say whether those are benefits or harms.

  4. manuel 8 February 2021 at 1:55 pm Permalink


    • Julian Perez 8 February 2021 at 2:17 pm Permalink

      Creo que yo no llego a esas Grandes Ligaa. Me quedo en las menores. Se quienes son el tercer, cuarto y quinto hate (en cantidad, que es lo que tienen en comun, pues en calidad, para mi criterio muy personal, encuentro notables diferencias que no entrare a discutir porque no vale la pena hacerlo

      • manuel 8 February 2021 at 2:24 pm Permalink

        yo traigo cosas que me inquietan buscando la oponion de los que pasan por aca; y lanzo fuertes declaraciones mas para provocar que porque este seguro de la veracidad de lo que estoy publicando

        • manuel 8 February 2021 at 2:28 pm Permalink

          muy dificil hoy estar seguro 100% de algo mas alla de lo mas inmediato: por eso cdo mi padre me pregunto sobre que escribir, le dije que sobre lo que habia vivido, ergo tuvo que conformase con escribir NADA, pues al parecer pretendia escribir algo mas que loas a su vida y gobierno, todo su pensamiento que no ensalse a la dictadura esta censurado por el regimen fascista al cual el y todas sus vivencias no apologeticas del mismo pertenecen

          • manuel 8 February 2021 at 2:30 pm Permalink

            vivimos un silencio, un vacio, que quiza nunca pueda llenarlo nada ni nadie

          • manuel 8 February 2021 at 2:31 pm Permalink

            el terror de los corderos

          • Julian Perez 8 February 2021 at 2:42 pm Permalink

            Manuel, tu traes cosas que puede que no interesen a todos, y con las que no todos estaran de acuerdo, pero al menos son de un interes bastante general. En todo caso se podria objetar que los posts a menudo son demasiado largos, no su contenido.

          • manuel 8 February 2021 at 2:47 pm Permalink

            a veces las pongo por el puro interes de que me sea mas facil su lectura luego en la pantalla grande del escritorio, y quiza por miedo a que se piedan en el eter de la internet, como ha sucedido con muchas cosas buenas, con Parler por ejemplo

          • manuel 8 February 2021 at 2:49 pm Permalink

            a lo que CAM podria objetar “publicalas en tu blog”, pero es mucha mas facil hacerlo aca como comentario de una de esas publicaciones por las que no pasa nadie, como suele suceder con las que hace en ingles

          • Julian Perez 8 February 2021 at 4:10 pm Permalink

            Yo se que algunos aquí (y otros amigos míos) tienen blogs, pero nunca me ha motivado tener uno propio. No sé, parece que se me dan mejor los comentarios aquí y en el CaucusRoom (que relevó al Patriot Post, que los quitó) La prueba está en el trabajo que me da hilvanar un texto para el blog del amigo Ramiro, estoy quedando muy mal con él. No sé ni como escribi el libro. Quizás porque el blog implica cierta continuidad obligatoria que no me apetece y el libro y los posts no.

  5. Julian Perez 8 February 2021 at 2:58 pm Permalink

    De mis tiempos en Cuba recuerdo que los ultimos anios todas las conversaciones entre amigos, cualquiera fuera su inicio, el final era siempre el mismo: el aumento del desastre que nos envolvia. El monotema llegaba a resultar asfixiante. Tengo cierto temor de que aqui pueda pasar lo mismo. Antes se podia hablar de otros temas: de literatura, de cine, de nuestras vidas personales o de pelota. Creo que el punto de inflexion fue la rectificacion de errores y tendencias negativas, en coincidencia temporal con lo de la perestroika y la glasnost en bololandia

    • Julian Perez 8 February 2021 at 3:04 pm Permalink

      Se decia que la URSS tenia la perestroika y nosotros la espera historica.

      • Julian Perez 8 February 2021 at 3:18 pm Permalink

        Aquellos tiempos fueron importantes porque muchos creiamos que, aunque lo de Cuba y los experimentos anteriores habian sido un horror, la teoria era buena y existia el “otro comunismo”. El Gorba tuvo la virtud de demostrar de una vez por todas que aquello no tenia arreglo y que el mal era de raiz. Y si algo me quedo de la ilusion, pues hay ciertos paralelos entre la teoria y las ensenianzas de Cristo, el vivir la version light de la social democracia en gallegolandia me acabo de convencer.

        • Julian Perez 8 February 2021 at 3:28 pm Permalink

          Recuerdo lo popular que se hizo Novedades de Moscu, que antes nadie leia y de repente se agotaba en los estanquillos. Sputnik, el otro heraldo de la perestroika, siempre tuvo circulacion. Me parece recordar que el gobierno acabo porr dejarlas de distribuir.

  6. Julian Perez 8 February 2021 at 3:01 pm Permalink

    El post anterior salio mas repetido que las postalitas por ciertas dificultades tecnicas. O quizas subconscientemente quise clasificar cuantitativamente para las Grandes Ligas por la envidia de la que tanto habla el amigo Ramiro.

    • manuel 8 February 2021 at 3:03 pm Permalink

      siempre habia creido que ramiro exageraba el papel de la envidia. Ya no estoy tan seguro 😀

      • Julian Perez 8 February 2021 at 3:06 pm Permalink

        El amigo Ramiro lleva razon. Lo debatible seria el peso que le asigna a las pasiones.

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