Summary of research and medical reports about the pandemic. Part of a series of occasional updates

Mike Davis Sat, Mar 21, 2020 at 11:50 PM

Does infection lead to immunity ?  

Viral immunologist Michael Diamond: “We don’t know that much about immunity to this virus.” 

If does produce immunity, how long does that last?  According to coronavirologist Stanley Perlman,  “Immunity is short-lived for the coronaviruses that cause common colds: even people who have high levels of antibodies can still become infected.” 

What percentage of positive cases are asymptomatic?

SARS in 2003 killed 10 per cent of people affected.  It was contained largely because carriers became contagious when they were symptomatic (feverish, coughing, etc,) and were thus easy to identify.  Also despite initial errors, contact tracing was implemented aggressively.

It is now clear that people are spreading the infection without obvious symptoms, but their ratio is unknown.  A study of the cases aboard one cruise ship indicated that only half of those who tested positive displayed recognizable symptoms.   But it’s unclear what to make of this finding since it conflated truly asymptomatic cases – those who never develop symptoms over the course of the infection – with those who were are simply in the early stages.  

The best guess at the moment from the CDC is that the 12 per cent of positive cases lack fevers, contrasted to only 1 per cent amongst SARS positives.  But if the rate is actually this high, it may be case that the viral load of asymptomatic cases is lower and less transmissible – but this could be  merely wishful thinking.

As community spreading increases will the transmission rate accelerate?  Or will the virus become less transmissible after passage through several humans? Will pathogenicity start to decrease?

As Chinese researchers recently writing in Cell & Bioscience emphasize “the answers to the above questions hold the key to the outcome of the outbreak.  There are different estimates of SARS-CoV-2’s attack rate or basic reproduction number.  One estimate is that R0 seems to be

2.68 which leads to a doubling time of 6.4 days.  But “other estimates of R0  could go up to 4, higher than that of SARS-CoV (2003) which lower than 2. 

What do we know about comorbidity, the interaction of infection with underlying health conditions?

Not nearly enough.  SARS showed a similar affinity for the aged while MERS (the camel virus) is deadly in duets with diabetes.  All exploit poor sanitation.  Thus…

Could fecal-oral transmission increase?

Before SARS emerged in 2003 highly pathogenic coronavirus epidemics were confined to domestic animals, above all pigs.  Researchers soon recognized  two different routes of infection: fecal-oral which attacked stomach and intestinal tissue and respiratory which attacked lungs.  In the first case there was usually very high mortality while the second generally resulted in milder cases.  A small percentage of current positives, especially the cruise ship cases, report diarrhea and vomiting, and “the possibility of SARS-CoV-2 transmission via sewage, waste, contaminated water, air conditioning systems and aerosols cannot be underestimated.’

The pandemic has now reached the slums of Africa and South Asia where fecal contamination is everywhere: in the water, in home grown vegetables and as windblown dust.  (Yes, shit storms are real.)  Will this favor the enteric route?  Will, as in the case of animals, this lead to more pathogenic infections? 

If the switch is turned on to higher rates of gastrointestinal infection, it will probably diminish the chance that warmer weather will mitigate the outbreak.  Spring does reduce respiratory inflammation and thus vulnerability to flu and colds, but it will have no effect on fecal-oral transmission.

Will other coronaviruses continue to make the journey from bats to mammals to human bodies?

Almost certainly.   The viral reservoir is surprisingly large.  Researchers investigating coronavirus in bats recently identified some 400 different subtypes or strains, each of which has some possibility of making the leap.  Moreover deforestation and the increasing use of bushmeat in human diets is ever expanding the sphere of interaction between wild viruses, domestic animals, and humans.  We need to recognize that we’re under simultaneous attack from emergent viruses and anti-biotic-resistant bacteria, plagues new and old, at a time when our defenses are crumbling  –  mainly because Big Pharma refuses to develop the next generation of antivirals and antibiotics.  Talk about existential issues.

Until a vaccine is available, will remdesivir – an anti-Ebola drug – reduce mortality?

Right now drug development is a crap shoot and there are dozens of candidates being tested.  In laboratory work remdesivir has shown an impressive ability to prevent the replication of MERS-Cov (the corona virus that recently jumped to humans from camels).  The bookies would probably rate it favorite in the race.  Steroids, promptly administered, were used widely during the SARS outbreak in cases of viral pneumonia to stop  deadly autoimmunity reactions (cytokine storm) and again in Wuhan, but research has not yet drawn clear conclusions about their current potential.  

Given the collapse of early detection and testing, will we soon move to rationing and triage?

For those who test positive it’s obviously crucial to immediately identify all of the individuals they have had recent contact with as well as their contacts’ contacts.  South Korea has done this with impressive success; indeed contact tracing has been one of the pillars of their suppression strategy.   In contrast public health authorities in Seattle failed to question exposed workers at the Life Care Center in Seattle, many of whom work at other facilities, and as a result the infection quickly spread to ten other nursing homes. 

When early efforts at contact tracing fail, original exposures soon become epidemic.  To deal with community transmission, the textbook response is widespread testing followed by isolation of infected individuals and the quarantining of their families or workmates.  The failure or inability to test is the first stage of catastrophe, aggravated by the lack of airport screening.  (The passengers arriving at LAX from South Korea, for instance, have been mostly waved through without even the ritual of taking their temperature).

As a result of this sequence of failures, we now have to rely on locking down vast populations while rationing testing on the basis of physicians’ subjective impression of whether or not the individual will require hospitalization.  This is the threshold of life-and-death triage, when faced with shortages of ICU beds, respirators and vital supplies, hospitals and ICU physicians will have to decide who lives and who dies.  China avoided this, but reports suggest it has been occurring in Italy.

Has our health system identified the mostly likely concentrations of critical illness and focused resources to protect them?

This is a no brainer – sickly confined people are the easiest targets for the SARS-CoV-2 swarms.

They’re in nursing homes and sanitariums; jails and prisons; migrant detention facilities; refugee camps and homeless shelters; and, of course, in hospitals.  Has Washington unrolled an emergency response for these, most vulnerable groups and institutions.  Of course, not.  Although the massacre behind the bars has not yet happening, nursing homes are going ablaze across the country without federal intervention of any kind.

Meanwhile the incomparably more deadly second phase of the pandemic is beginning.  Cases will explode over the next ten days in Africa and South Asia, and as I argued in a previous piece, slum ecology may shape, as did famine in India with the Spanish flu, a far more lethal outbreak with different, emergent properties (such as a switch to enteric infections discussed above).

I’ll continue to summarize and occasionally synthesize research in future reports.

MUST VISIT:  https://www.quora.com/q/coronavirus?source=email

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