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hannah

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From: https://www.neodemos.info/articoli/covid-19-proviamo-a-prevedere-cosa-succedera/

 See original article for table and figures

We are experiencing terrible days, and still do not seem to see the end of the tunnel. In this regard, Mauro Maltagliati, after reflecting on the choice of the best variable to analyze in order to understand how the Coronavirus pandemic is evolving in Italy, follows its temporal evolution and dares to predict.

 

Mauro Maltagliati, Covid-19: Let's try to predict what will happen

All of Italy now follows the statistics on the Corona virus with almost spasmodic interest, with the understandable objective of understanding how the phenomenon will evolve and, above all, when the pandemic will end, at least in our country.


When you venture into forecasts, there are essentially two ways you can go. The first is perhaps logically a little more defensible: a "causal" model is used, that is to say, the evolution of the phenomenon of interest (the spread of the virus) is expected according to others, those that favor or slow it down, such as for example containment policies, weather (with the arrival of the hot season: will it be useful?), progress in medicine.


However, the relationship between these "causal" factors and the spread of the virus is unclear, and even less so is their evolution in the coming days and weeks. In short: a difficult road.


A time series approach
Let's try to follow a different track,  already undertaken by many, even on Neodemos

 

https://www.neodemos.info/articoli/la-curva-dei-contagiati-da-covid-19-la-ricerca-del-punto-di-svolta/

 

The evolution of the phenomenon in the recent past is observed (say 10-15 days), and it is assumed that the regularity already highlighted is maintained even afterwards and the values thus obtained are projected. It is a "black-box" approach: we do not investigate the causal mechanisms mentioned above, but we simply follow the phenomenon, and extrapolate it to the future. Obviously, this approach is defensible only until "shocks" of any nature occur, which in the specific case hopefully are better (we hesitate to say "positive"), such as an unexpected success of the confinement policy of the Italians, or the discovery of a cure.


So many numbers, so little clarity


However, we must choose a variable to analyze. In these days many are named (infected, positive, dead, mortality rate, lethality rate, ...), but few say what is commonly thought.

Let's take the number of infected, or infected, for example. We actually know the "positives", or the number of infected among those who have been subjected to the swab. However, only those who are strongly suspected of being infected are subjected to the test, and this distorts the vision, both of the level and of the tendency of the phenomenon. To really know the infected, or rather to estimate them correctly, you should swab a random sample of the population - an operation that is obviously not possible today (and, of course, I am not proposing it here).


Even the "healed" are hardly measurable, as they are actually a fraction of the "positive", and not of the infected. Paradoxically, the increase in the healed can even provide a misleading image: it is not necessarily good news, because, with the same success of the therapy, the healed increase as the number of patients increases.


As for the various rates, the measurement problems are even greater. For example, the mortality rate will only be known at the end of the epidemic (deaths from Covid-19 / residents). In the meantime, one could think of the lethality rate (deaths from Covid-19 / infected), which however is not easy to calculate correctly for two reasons:


1) as mentioned, we do not know the number of infected people, but only the positive ones, which more or less correspond to the full-blown infected people, and therefore more serious. If we used the correct denominator for the lethality rate (the infected, not the positive), the lethality would probably be very low.


2) there is a time lag between when you are infected and when you unfortunately die (if this happens), and to calculate the true lethality we should know "what will happen to the infected" - that is, if they die or instead recover. But since we do not know the evolution of the number of infected, nor the moment in which they became infected, nor the times (different from each other) in which each infected transform into a healed or a dead person, the picture is considerably complicated


Let's talk the dead


Once the other variables have been discarded, the sad, but necessary (and in this case also useful) count of the dead remains. A less uncertain figure than many others, but which also needs some clarification. Not in all countries, in fact, we refer, as happens in Italy, to the number of deaths with Covid-19 (as opposed to the deaths for Covid-19). Yet it is the most reliable definition, since it is not trivial to ascertain whether some individuals, perhaps with other serious pathologies, would have remained alive (and for how long) if they had not been infected with the Corona virus.

And in fact, from February 27 to March 10, that is, at the beginning of the epidemic in Italy, the number of deaths followed an exponential law almost perfectly (tab. 1):


The slope of the line estimated on the logarithmic transform tells us that in the period considered the number of deaths per day was approximately 31% of the (overall) value updated to the previous day. But this regular evolution (linear in the logarithm, and therefore explosive in natural numbers) must sooner or later turn into a logistic curve, and no longer exponential. And luckily, that's what's actually going on.

 


The estimate of the logistic curve and ... D-Day


If we add the data of the last few days we get figure 2. On this basis, statisticians like me can do their job and estimate the logistic curve of the accumulated deaths. If, as in this one, a good adaptation for the past is observed, a forecast on the future, and in particular on the exhaustion of the process (= end of the pandemic, at least in Italy) can also be hazarded.

Well, strictly speaking, to be honest, logistics never "ends": it tends to a horizontal asymptote (the total number of deaths), without ever reaching it. But let's say that we are satisfied with estimating a day that we can conventionally define as the "end of the pandemic": the one after which, in total, there will be less than 10 deaths with Corona virus. Well, this day should be near now: April 10, or so.

 


Caution!


Of course, this is only an estimate: I can be wrong, and in a few days you will know how much. In the meantime, we can say that if the estimate was perfect, today's afternoon data (March 19) should lead to a (cumulated) number of deaths equal to 3,300, that is about 330 more than yesterday (March 18).


We must not forget that, as new data arrive, the model adapts and estimates adjust. Furthermore, this forecasting exercise implies that we are all homogeneous, that is, all equally subject to mortality from this virus, while we know it is not: there are more or less resistant people.
There are factors that can show discontinuity, collapsing (healthcare?), Or instead giving positive impulses (the confinement policy, the effects of which on the dead, still, in practice, have not been seen, and the discovery of new treatments).


And there is the mystery of southern Italy, so far relatively spared from the epidemic: virgin land (and therefore subject to rapid deterioration) or protected land (by confinement measures)? The answer, now, in a few days.

 

 

 

hannah

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And the numbers are getting better!

LUNEDI’ 23 MARZO, AGGIORNAMENTO DELLE ORE 19 +++
Gallera: oggi possiamo dire che e’ una giornata positiva

“Ieri eravamo moderatamente ottimisti. Avevamo detto che il era trend in calo e oggi si conferma. Oggi forse e’ la prima giornata positiva di questo mese duro, durissimo. Non e’ ancora il momento di cantar vittoria e rilassarci, ma iniziamo a vedere una luce in fondo al tunnel”.

Lo ha detto l’assessore al Welfare della Regione Lombardia, Giulio Gallera, durante la consueta diretta Facebook sulla pagina di LombardiaNotizeOnline per fare il punto sull’emergenza coronavirus.

“Per la prima volta – ha aggiunto – oggi sono diminuiti i ricoveri: dai 9.439 di ieri siamo scesi a 9.266 e anche gli accessi ai pronto soccorso stanno leggermente diminuendo, anche se non ovunque. Stiamo vedendo i frutti degli sforzi, tuttavia non e’ sufficiente qualche giorno positivo per rilassarci, anzi bisogna intensificare lo sforzo”.

L’assessore ha anche risposto alle domande che arrivavano in diretta sui tamponi. “Noi vogliamo farli – ha spiegato – a tutti coloro che ne hanno bisogno. Ai medici di medicina generale e ai pediatri li facciamo, cosi’ come da oggi misuriamo la temperatura al nostro personale sanitario. Se e’ a 37.5, li mandiamo a fare i tamponi, perche’ noi ci teniamo. Il nostro lavoro non e’ fare i tamponi random fuori dal supermercato, facciamo un lavoro condiviso. Vi chiediamo di stare a casa, chi ha l’influenza, chi ha un raffreddore stia a casa, anche solo con un raffreddore rafforzato. Poi vi teniamo monitorati, e se peggiorate e’ il medico di medicina generale che vi manda a fare il tampone”.

Continua anche la grande collaborazione fra pubblico e privato. Le strutture private lombarde continueranno infatti a mettere a disposizione dei cittadini tutti i posti letto che posseggono.

“Al San Raffaele di Milano – ha continuato Gallera – stiamo allestendo i 10 posti letto di terapia intensiva nel campo da calcetto. Intanto sono gia’ arrivati i primi 4 pazienti. Questi posti, con i 16 del San Carlo, portano a 1.350 il numero dei letti di terapia intensiva. A Monza ne apriremo altri 16, e al Policlinico altri 15. Da mercoledi’, se troviamo il personale, ne apriremo altri 10 a Niguarda. E siamo pronti ad aprirne 20 alla Asst Rhodense e altre 9 alla Asst Nord Milano”.

 

I DATI – Ecco i dati dei contagi odierni e quelli dei giorni precedenti

– i casi positivi sono: 28.761 (+1.555)

ieri: 27.206 (+1.691)

l’altro ieri: 25.515 (+3.251)

e nei giorni precedenti: 22.264(+2.380)

hannah

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https://steps-centre.org/blog/postnormal-pandemics-why-covid-19-requires-a-new-approach-to-science/

"Known unknowns include the real prevalence of the virus in the population; the role of asymptomatic cases in the rapid spread of the virus; the degree to which humans develop immunity; the dominant exposure pathways; the disease’s seasonal behaviour; the time to deliver global availability of an effective vaccine or cure; and the nonlinear response of individuals and collectives to the social distancing interventions in the complex system of communities interconnected across multiple scales, with many tipping points, and hysteresis loops (implying that society may not be able to rebound to the state it was in before the coronavirus interventions took place). These deep uncertainties make quantitative predictions speculative and unreliable."
hannah

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Keeping the health care workers from infecting health-care workers

by Atul Gawande

The message is getting out: #StayHome. In this early phase of the coronavirus pandemic, with undetected cases accelerating transmission even as testing ramps up, that is critical. But there are many people whom the country needs to keep going into work—grocery cashiers, first responders, factory workers for critical businesses. Most obviously, we need health-care workers to care for the sick, even though their jobs carry the greatest risk of exposure. How do we keep them seeing patients rather than becoming patients?
In the index outbreak in Wuhan, thirteen hundred health-care workers became infected; their likelihood of infection was more than three times as high as the general population. When they went back home to their families, they became prime vectors of transmission. The city began to run out of doctors and nurses. Forty-two thousand more had to be brought in from elsewhere to treat the sick. Luckily, methods were found that protected all the new health-care workers: none—zero—were infected.

But those methods were Draconian. As the city was locked down and cut off from outside visitors, health-care workers seeing at-risk patients were housed away from their families. They wore full-body protective gear, including goggles, complete head coverings, N95 particle-filtering masks, and hazmat-style suits. Could we do that here? Not a chance. Health-care facilities don’t remotely have the supplies that would allow staff members to see every patient with all that gear on. In Massachusetts, where I practice surgery, the virus is circulating in at least eleven of our fourteen counties, and cases are climbing rapidly. So what happens if you are exposed to a coronavirus patient and you don’t have the ability to go full Wuhan? My hospital system, Partners HealthCare, has already sent more than a hundred staff members home for fourteen days of self-quarantine because they were exposed to the coronavirus without complete protection. If we had to quarantine every health-care worker who might have come into contact with a COVID-19 patient, we’d soon have no health-care workers left.
Yet there are lessons to be learned from two places that saw the new coronavirus before we did and that have had success in controlling its spread. Hong Kong and Singapore—both the size of my state—detected their first cases in late January, and the number of cases escalated rapidly. Officials banned large gatherings, directed people to work from home, and encouraged social distancing. Testing was ramped up as quickly as possible. But even these measures were never going to be enough if the virus kept propagating among health-care workers and facilities. Primary-care clinics and hospitals in the two countries, like in the U.S., didn’t have enough gowns and N95 masks, and, at first, tests weren’t widely available. After six weeks, though, they had a handle on the outbreak. Hospitals weren’t overrun with patients. By now, businesses and government offices have even begun reopening, and focus has shifted to controlling the cases coming into the country.


All health-care workers are expected to wear regular surgical masks for all patient interactions, to use gloves and proper hand hygiene, and to disinfect all surfaces in between patient consults. Patients with suspicious symptoms (a low-grade fever coupled with a cough, respiratory complaints, fatigue, or muscle aches) or exposures (travel to places with viral spread or contact with someone who tested positive) are separated from the rest of the patient population, and treated—wherever possible—in separate respiratory wards and clinics, in separate locations, with separate teams. Social distancing is practiced within clinics and hospitals: waiting-room chairs are placed six feet apart; direct interactions among staff members are conducted at a distance; doctors and patients stay six feet apart except during examinations.

What’s equally interesting is what they don’t do. The use of N95 masks, faceprotectors, goggles, and gowns are reserved for procedures where respiratory secretions can be aerosolized (for example, intubating a patient for anesthesia) and for known or suspected cases of COVID-19. Their quarantine policies are more nuanced, too. What happens when someone unexpectedly tests positive—say, a hospital co-worker or a patient in a primary-care office or an emergency room? In Hong Kong and Singapore, they don’t shut the place down or put everyone under home quarantine. They do their best to trace every contact and then quarantine only those who had close contact with the infected person. In Hong Kong, “close contact” means fifteen minutes at a distance of less than six feet and without the use of a surgical mask; in Singapore, thirty minutes. If the exposure is shorter than the prescribed limit but within six feet for more than two minutes, workers can stay on the job if they wear a surgical mask and have twice-daily temperature checks. People who have had brief, incidental contact are just asked to monitor themselves for symptoms.

The fact that these measures have succeeded in flattening the COVID-19 curve carries some hopeful implications. One is that this coronavirus, even though it appears to be more contagious than the flu, can still be managed by the standard public-health playbook: social distancing, basic hand hygiene and cleaning, targeted isolation and quarantine of the ill and those with high-risk exposure, a surge in health-care capacity (supplies, testing, personnel, wards), and coördinated, unified public communications with clear, transparent, up-to-date guidelines and data. Our government officials have been unforgivably slow to get these in place. We’ve been playing from behind. But we now seem to be moving in the right direction, and the experience in Asia suggests that extraordinary precautions don’t seem to be required to stop it. Those of us who must go out into the world and have contact with people don’t have to panic if we find out that someone with the coronavirus has been in the same room or stood closer than we wanted for a moment. Transmission seems to occur primarily through sustained exposure in the absence of basic protection or through the lack of hand hygiene after contact with secretions.

Consider a couple of data points. Singapore so far appears not to have had a single recorded health-care-related transmission of the coronavirus, despite the hundreds of cases that its medical system has had to deal with. That includes one case reported this week of a critically ill pneumonia patient who exposed forty-one health-care workers in the course of four days before being diagnosed with COVID-19. These were high-risk exposures, including exposures during intubation and hands-on intensive care. Eighty-five per cent of the workers used only surgical masks. Yet, owing to proper hand hygiene, none became infected.

Our early experiences in the U.S. have so far been similar. The Centers for Disease
Control and Prevention, in the face of limited information, recommended stricter precautions than have been employed in Asia, putting health-care workers on fourteen-day self-quarantine if they are exposed to an infected person for even a few minutes without protection, including a mask and goggles. That policy was implemented at U.C. Davis Medical Center, where the first case of community transmission was diagnosed, in late February. Eighty-nine health-care workers involved in the patient’s care were put under self-quarantine. None, it turned out, had been infected. Sacramento, Seattle, and San Francisco became coronavirus hot spots; as of this writing, however, significant occupational transmission has not been found.


Keeping the Coronavirus from Infecting Health-Care Workers

https://www.newyorker.com/news/news-desk/keeping-the-coronavirus-from-infecting-health-care-workers



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I am sending you the information that was published in the newspaper "Clarin" and that coincides with the executive initiative of Trump releasing this antimalarial. The web page:

https://www.clarin.com/society/-treatment-effective-immoral-usage-dice-infectologist-frances-affirma-defeated-coronavirus_0_SqHmKu99L.html

It seems to be serious and in your same tone.


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hannah

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Everybody knows that. Somebody already overdosed on one of those chemicals.

He is anti-science. 


"As a practical example, chloroquine/hydroxychloroquine, azithromycin, and lopinavir-ritonavir have a variety of adverse effects, including QT prolongation, torsades de pointes, hepatitis, acute pancreatitis, neutropenia, and anaphylaxis. Considering that most patients who have died from COVID-19 were elderly and had cardiovascular comorbidities and that affected patients frequently have cardiac arrhythmias,4,5 chloroquine/hydroxychloroquine, azithromycin, and lopinavir-ritonavir could potentially increase the risk of cardiac death. Additionally, hepatitis and neutropenia are clinical manifestations of COVID-19, and both hepatic and bone marrow dysfunction could be made worse by the off-label use of these drugs; thus, it would be impossible to differentiate the drug-related adverse effects from the disease manifestations in the absence of a control group."
hannah

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https://jamanetwork.com/journals/jama/fullarticle/2763802?guestAccessKey=fa0e4d56-190e-47e3-9e89-5c0d68b4a39a&utm_source=silverchair&utm_medium=email&utm_campaign=article_alert-jama&utm_content=olf&utm_term=032420
hannah

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The economy v our lives? It's a false choice – and a deeply stupid one



‘What economism misses includes complexity, historical contingency, and the profound, uncountable power of human emotion.’

Ancient Hebrew texts are peppered with references to and prohibitions against pre-Judaic practices associated with Moloch, a Canaanite god to whom children were sacrificed for the greater good.

Now, millennia later, there are prominent voices among us who propose sacrificing the old and weak among us at the altar of another false god – the global economy.

Suddenly, the ghosts of Thomas Malthus and Jeremy Bentham have become priests for the 21st-century Moloch, and have haunted American public conversation about coronavirus.

Republican officials, conservative economists, unqualified pundits, and even the 73-year-old president of the United States have suggested that the short-term economic pain we have just begun inflicting on ourselves to slow the spread of coronavirus might cost too much, just to save the lives of a few million of our most vulnerable neighbors.

The University of Chicago economist Casey Mulligan, who served on President Trump’s council of economic advisers, told the New York Times that shutting down economic activity to slow the virus would be more damaging than doing nothing at all. He prefers some sort of weighing of the costs and benefits of saving lives.

“It’s a little bit like, when you discover sex can be dangerous, you don’t come out and say: there should be no more sex,” Mulligan said. “You should give people guidance on how to have sex less dangerously.”

And on Tuesday Trump announced that he wanted all US business back to normal levels of function by Easter, 12 April. “This cure is worse than the problem,” Trump said.

This is beyond immoral. It’s profoundly stupid. But this mode of thought is all too common

This is beyond immoral. It’s profoundly stupid. But this mode of thought is all too common among those who can’t see beyond their economic textbooks or their stock portfolios. And it has troubling intellectual roots.

In the late 18th century, Malthus warned that the poor would breed at a rate that would outpace the resources necessary to sustain a growing population, resulting in famine and misery. His predictions failed but were still deployed for decades to limit public amelioration of poverty.

In the late 18th and early 19th centuries, Bentham promoted the idea that public moral decisions should be made to foster the greatest good for the greatest number, forging the calculus that has pushed policymakers and economists to invoke simplified “cost-benefit analyses” to decide if a measure is worthy of consideration.

Overall, this approach is a stark example of a troubling ideology that grips too many of those with power and influence in the world. Economism is a belief system that leads people to believe that everything can be simplified to models and curves, and that it’s possible to count and maximize utility in every circumstance. What economism misses includes complexity, historical contingency and the profound, uncountable power of human emotion.

No one would trade with anyone for years. Trade would grind to a halt because of mourning, fear of infection, society-wide trauma and social unrest. Let’s note that despite the late and insufficient responses by North American and European leaders, those leading Mexico and Brazil have yet to take the threat seriously at all. They keep denying the gravity of our situation.

India only this week took measures that it should have taken in January prohibiting most people from leaving home and grounding flights for a month. But millions of Indians have no door to close, no place to store food, and no way to distance themselves from those infected. Corpses will soon pile up, waiting for cremation or burial, reinfecting communities weakened by this disease. No one is ready for the social, spiritual and economic devastation that is sure to come by June.

Anywhere in the world, positing this problem as a tradeoff between the economic interests of the young and the lifespan of the old is a terrible error. As the US Centers for Disease Control explains, those vulnerable to serious or fatal cases of the infection include not just the elderly, but anyone who is obese, diabetic, has high blood pressure, is HIV-positive, has undergone cancer treatment, suffers from asthma or smokes. Those factors are more common among poorer Americans as well as older Americans. And poor Americans occupy all age ranges.

Economic depression will come, regardless of how many we let die. The question is how long and devastating it will be

Soon enough, as hospitals around the world overflow with coronavirus patients, exhausting doctors, nurses, orderlies, custodians, medical supplies, ventilators and hospital cash accounts, doctors will have to make moral choices about who lives or dies. We should not supersede their judgment based on a false choice. Economic depression will come, regardless of how many we let die. The question is how long and devastating it will be.

So this is not a matter of young v old, or even rich v poor (although that would be more accurate and a more classic story of political conflict in America). Even those with none of the most dangerous conditions, who are as young as 12, could succumb to this powerful virus. It’s all of us v all of us. Or, if we choose, all of us for all of us.

  • Siva Vaidhyanathan is a regular columnist for Guardian US and a professor of media studies at the University of Virginia. He is the author of Antisocial Media: How Facebook Disconnects us and Undermines Democracy

godsons7

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Ignác Fülöp Semmelweis (1818-1865). In the 1840s he worked at the Vienna General Hospice.
There, to his horror, he discovered that women inmates who gave birth had many more puerperal fevers.
than the ones that lit up in their houses.
He saw it and —one of his contributions— measured it: a 30% mortality within the walls; 15% out.

However, he made many mistakes, looking at things "with the pages of yesterday's newspaper."
Your solution to the problem it
 came almost by chance. A medical friend who performed autopsies on the corpses of women interned in the Semmelweis ward, it was cut with dirty instruments with remains of an autopsy. He died of septicemia. This induced Semmelweis to wash all instruments and THE HANDS of all personnel with a dilution of calcium hydroxide.

It was a time of miasms and of still ignoring the agents of 
Pasteur and Koch. Semmelweis passed into oblivion and Lister, a British surgeon, took the laurels by imposing the spray with disinfectant of operating rooms.

Semmelweis' story is very similar to what happens today.


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Ensayos. Cómo actúan las drogas que se están investigando contra el coronavirus

en La Nacion

En medio del temor, las inquietantes advertencias de la OMS, las imágenes de salas de terapia intensiva sobrepasadas y el huracán de publicaciones (que ya superan las 20.000 sobre la pandemia del nuevo coronavirus ), se alzan voces que prometen curas que van desde sustancias experimentales hasta cócteles de vitaminas. Están en marcha un centenar y medio de estudios clínicos para ensayar moléculas que mitiguen los casos graves de Covid-19 , pero ya hay algo seguro: ninguna de las drogas que se están probando será la panacea. Es más, aunque su uso compasivo esté justificado en un escenario de falta de recursos terapéuticos, los especialistas afirman que es fundamental no caer en la tentación de automedicarse para prevenir la infección porque el remedio puede ser peor que la enfermedad .

Entre los múltiples ensayos en todo el planeta, sobresale el que acaba de lanzar la Organización Mundial de la Salud y del que participará la Argentina: "Solidarity", un esfuerzo sin precedente para explorar si fármacos ya conocidos pueden servir para tratar la infección. El estudio incluirá a miles de pacientes en docenas de países, y explorará los efectos de un "combo" de antivirales utilizado contra el VIH (lopinavir+ritonavir, formulados en una sola pastilla), un antiguo tratamiento contra la malaria (cloroquina/hidroxicloroquina), y un nuevo antiviral que el año pasado se usó con resultados esperanzadores contra el Ébola (remdesivir).

"Ante un virus nuevo como éste, lo que se hace en general es recurrir a antivirales ya utilizados en otros casos hasta que se puedan desarrollar drogas más específicas -explica Diego Flichman, profesor adjunto de la cátedra de Virología de la Facultad de Farmacia y Bioquímica de la UBA-. Se están estudiando dos que se emplean contra el HIV, aunque se trata de virus que no tienen nada que ver entre sí. Pero como no son medicamentos específicos, se necesitan concentraciones muy altas para que tengan algún efecto. Sería como utilizar una llave que no entra exactamente en la cerradura. Algún efecto pueden tener, pero es subóptimo, y hay que recordar que todos los antivirales tienen toxicidad".

Según Lucía Cavallaro, titular de la misma cátedra y presidenta de la Sociedad de Virología, "la experiencia del VIH nos enseñó que con los virus nunca conviene hacer monoterapia, porque la población viral es heterogénea. La idea siempre es aplicar una terapia combinada, que permita dosis más reducidas de cada uno, y por lo tanto, menos toxicidad, y menos probabilidad de persistencia".

Ensayos controvertidos

Uno de los brazos del estudio analizará esta combinación con un interferón beta. "Ante cualquier infección, el organismo sintetiza moléculas inmunomoduladoras (citoquinas e interferones) -destaca Flichman-. Los interferones actúan contra todo lo que sea 'extraño', pero tienen el riesgo de generar una respuesta inmune exacerbada. Es como darle un plus al sistema inmunológico". Cabe mencionar que hace unos días se difundió ampliamente por las redes sociales la llegada de un avión a Italia con grandes cantidades de interferón enviado por Cuba, pero ningún reporte científico informó efectos benéficos comprobados.

La cloroquina y la hidroxicloroquina (más moderna y con menos efectos adversos) se usan desde hace mucho. Son inhibidoras de un mecanismo celular llamado "autofagia": es la forma que tienen las células de reciclar lo que ya no les sirve para obtener nuevos suministros. "Los virus muchas veces usufructuan de ese mecanismo en su beneficio -afirma Flichman-, y está descripto que este coronavirus induce la autofagia para favorecer su replicación. Entonces, si usamos un medicamento que la inhibe, indirectamente también impedimos su replicación".

En el sitio The Conversation , la bioquímica Katherine Seley-Radtke cuenta que ambas drogas se usan para prevenir la malaria. La cloroquina fue desarrollada originalmente en 1934 por Bayer y utilizada en la Segunda Guerra Mundial. Y, aunque no fueron aprobadas para ese uso, en la actualidad también se indican para tratar la artritis reumatoidea y el lupus. Después del brote de MERS en 2012 (también causado por un coronavirus), se analizaron miles de moléculas para identificar alguna que pudiera bloquear la infección. Varias mostraron indicios prometedores (entre ellas, la cloroquina), pero finalmente no mostró suficiente actividad.

"Estos compuestos inerrumpen el ingreso de los virus a la célula elevando el pH de la superficie celular, impidiendo de ese modo que puedan liberar el genoma en el interior y se repliqiuen", dice Cavallaro.

Un ensayo reciente realizado en Marsella probó la hidroxicloroquina en combinación con un antibiótico, la azitromicina. Lo condujo el virólogo francés Didier Raoult, asesor de Emmanuel Macron, que llegó a proclamar que era "inmoral" no usar esta fórmula. Pero además de que la publicación fue meteórica (se terminó el 16 de marzo, se subió a Internet el 17 y se publicó el 20), el diseño del estudio fue muy discutido por el pequeño número de pacientes que intervinieron y cómo se habían seleccionado, y por cómo se habían tratado los datos.

La tercera línea de investigación del studio de la OMS se hará con el remdesivir, desarrollado por el laboratorio Gilead, que pareciera ser efectivo en la prevención de infecciones virales. Este mes, la compañía lanzó ensayos de fase III con esta droga en centros médicos de Asia.

Diferentes enfoques

Una estrategia diferente están encarando los hospitales neoyorquinos: utilizar la sangre de personas recuperadas de Covid-19 como un posible antídoto contra la enfermedad. "Los investigadores esperan que ese enfoque centenario de infundir la sangre con altos niveles de anticuerpos de los que sobrevivieron a la infección podría ayudar a evitar la situación que se dio en Italia", escribe Deborah Blum, en Nature .

¿Que estas drogas estén en estudio significa que pueden tomarse preventivamente? Los especialistas son terminantes: absolutamente, no. Todavía no fueron bien evaluadas y además pueden tener efectos adversos muy serios. En los Estados Unidos, un hombre murió y su esposa se encuentra en estado crítico después de haber ingerido fosfato de cloroquina, que también se emplea para limpiar peceras.

En un reciente editorial del Journal of the American Medical Association (JAMA) sobre los tratamientos compasivos, André Kalil, de la División de Enfermedades Infecciosas del Centro Médico de la Universidad de Nebraska, Estados Unidos, hace notar que durante el brote de Ébola de 2014, cerca de 3000 individuos desarrollaron la enfermedad y se probaron muchas terapias (incluyendo la cloroquina y la hidroxicloroquina) con el objetivo de determinar cuál de ellas protegía a las peronas. Al final, ninguna fue efectiva ni segura.

"Hay que ser más cuidadosos con el optimismo exagerado y esperar que haya estudios rigurosos. Incluso si se encontrara una fórmula útil, requerirá una aplicación muy personalizada", afirma Cavallaro.

Aunque necesitará tiempo para concretarse, tal vez la noticia más alentadora sea la que llega desde la investigación básica. Científicos chinos y alemanes acaban de publicar en Science que lograron cristalizar la principal proteasa (una enzima que rompe los enlaces de las proteínas) del nuevo coronavirus, lo que permitirá diseñar fármacos específicos con más probabilidades de éxito.

"Obtuvieron la estructura cristalina de una enzima del coronavirus que hidroliza una proteína más grande y la desarma en varios pedazos -explica Alberto Iglesias, investigador del Conicet en el Instituto de Agrobiotecnología del Litoral-. Derivadas de esa hidrólisis, hay dos enzimas que replican la información genética del virus. O sea que determinan la replicación viral".

Y más adelante agrega. "Esta determinación cristalográfica es importante porque esta proteasa actúa en una secuencia de aminoácidos (ladrillos de las proteínas) que es bastante específica de estos virus y no se encuentra en las células humanas. Es un blanco perfecto y ya se están desarrollando inhibidores específicos para bloquearlo".

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