The biology of coronavirus COVID-19 - including research and treatments

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Characterizing Cognitive Impairment in Patients Recovered from COVID-19
Claire Wilcox, MD reviewing Zhou H et al. J Psychiatr Res 2020 Oct

Impairments in selective attention were found in recently recovered patients.

Viral infections (e.g., influenza A, severe acute respiratory syndrome, and Middle East respiratory syndrome) can impair neuropsychiatric function, and inflammation can adversely affect cognitive function. In a study examining the effects of COVID-19 on cognition, 29 otherwise healthy patients in China (age range, 30–64; 18 men) who had recently been hospitalized for COVID-19 and subsequently recovered and 29 age-, education-, and sex-matched healthy controls underwent neuropsychiatric testing (attention and memory, executive function, processing speed, and perceptual abilities).

Recovered COVID-19 patients were tested usually 2 to 3 weeks after admission and after they had two negative nucleic acid tests. During acute infection, COVID-19 patients had tests for various inflammatory markers (interleukins, tumor necrosis factor-α, interferon-γ, and C-reactive protein [CRP]) the morning after hospital admission.

Significant differences in test performance between COVID-19 patients and controls were found only on the Continuous Performance Test, which assesses selective and continuous memory in a measure with three levels of difficulty. COVID-19 patients showed more missed responses during the test's more challenging section and more missed responses and fewer correct responses during its most challenging section. Furthermore, reaction time, except during the most challenging section, correlated positively with CRP levels measured at hospital admission.
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https://www.jwatch.org/na51986/2020/07/20/characterizing-cognitive-impairment-patients-recovered
 
akrasia said:
Derya Unutmaz on the decline in antibodies post Covid-19:
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Everyone needs to understand that the decline of SARS-CoV-2 Abs after the peak of infection is normal. This is basic immunology. If our immune system did not contract after viral infections, we would all be walking around with gigantic lymph nodes. SARS-CoV-2 Abs look good!
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This seems so basic I have been wondering if I am missing something when everyone is worried about antibody levels dropping.
 
Mithriel said:
This seems so basic I have been wondering if I am missing something when everyone is worried about antibody levels dropping.
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I think there are two facets to this, one is people worrying that undetectable antibodies means no immunity, and that's a misperception -- there are other components to immune memory: memory B and memory T cells, that can quickly escalate an immune response, including regenerating antibodies, to a previously encountered antigen.

But the other facet, is that disappearing antibodies make the antibody tests much less useful for estimating prevalence rates, as it means they can only really provide a snapshot of infections over, say, the previous 6 week period with any degree of certainty. Perhaps this could mean that population exposure to Sars-Cov-2 is multiples greater than community samples suggest, depending on when the pandemic started and sample date.
 
Daily Mail again, sorry, but:

Protein drug 'reversed' deadly cytokine storm in COVID-19 patients

http://www.msn.com/en-gb/health/med...9-patients/ar-BB174xSi?li=BBoPWjQ&ocid=ASUDHP

A protein drug may help improve the conditions of severely ill coronavirus patients, a new small study suggests.

Interleukin 7 (IL-7) immunotherapy was found to restore counts of a specific white blood cell in those critically with COVID-19, the disease caused by the virus.

The international team, led by Université Catholique de Louvain in Brussels, Belgium, says the treatment also seemed to help quell and even 'reverse' dangerous inflammation in patients.
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Moved from the spread and control thread.

A new coronavirus mutation is taking over the world. Here's what that means.

https://www.livescience.com/new-coronavirus-mutation-explained.html

A mutation in the protein that allows SARS-CoV-2 to enter cells might make it easier for the virus to spread — or it might not make a difference at all.

That's the crux of a debate over a mutation known as D614G, which affects the spike protein on the virus' surface. The mutation is not new. It appears in low levels in samples taken from COVID-19 patients as far back as February. But this variation of the virus (nicknamed the "G" variation) seems to show up in more and more of the virus samples taken from people infected recently compared to early in the pandemic.
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It goes on to rather blind me with science a bit, but I guess quite a few people here will be able to make sense of it :)
 
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Mithriel said:
This seems so basic I have been wondering if I am missing something when everyone is worried about antibody levels dropping.
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The antibody levels aren't disappearing, they're merely dropping because the immune system has no ongoing need of high antibody levels once the infection has been dealt with. The people who are "worried" have not bothered to read or cite what happens after other infections or vaccinations. It is a case of overreacting due to ignorance. The only surprise might be that such sloppy thinking is not merely limited to certain fields.
 
I didn't know on which of the many threads to say this, but this is as good as any.

It may, or may not, be worth pointing out that whatever it was that caused the Dalston outbreak of ME in 1955, which was considered similar in many respects to the Royal Free, it apparently affected the sense of taste and smell in a similar, but perhaps not identical way to Covid.

Walis said:

Impaiment acuity of the sense of taste and smell was
present in most cases and abnormal perception of various tastes
and smells was also commonly found.

Is this common in viral illnesses?
 
@chrisb

What causes abnormal sense of taste and smell?
The most common causes of smell disorders are nasal and/or sinus disease, viral upper respiratory infections, and head trauma. The most common causes of taste disorders are upper respiratory tract infections and head injuries. Other infrequent causes of both include masses in the nasal or oral passageways, endocrine problems, side effects from medications, and degenerative processes of the brain.

https://my.clevelandclinic.org/health/diseases/16708-abnormal-sense-of-taste-and-smell
 
chrisb said:
Walis said:

Impaiment acuity of the sense of taste and smell was
present in most cases and abnormal perception of various tastes
and smells was also commonly found.

Is this common in viral illnesses?
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It is not common of all viral illnesses, and tends to be specific to 'neurotropic' viruses that infect the olfactory bulb. (of course herpesviruses and enteroviruses are on that list.)

Of course if you want to go down the speculative path of betacoronaviruses...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194943/
 
chrisb said:
I didn't know on which of the many threads to say this, but this is as good as any.

It may, or may not, be worth pointing out that whatever it was that caused the Dalston outbreak of ME in 1955, which was considered similar in many respects to the Royal Free, it apparently affected the sense of taste and smell in a similar, but perhaps not identical way to Covid.

Walis said:

Impaiment acuity of the sense of taste and smell was
present in most cases and abnormal perception of various tastes
and smells was also commonly found.

Is this common in viral illnesses?
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Well I've had reduced sense of taste since I had both glandular fever and then coxsackie B3 in 1980. Though weirdly a times, or rather I think it's more with just some substances, my sense of smell is SO acute and I can react to small amounts of perfume, smoke, paint etc, so it's odd but certainly my taste has never fully recovered since these viral infections.
 
The Maths of Contagion: Why Things Spread and Why They Stop

(The audio and video go out of sync, but it doesn't matter as the talking head is just a small box in the corner. Plenty of good clear graphs and graphics.)

 
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New antibody mix could form 'very potent' Covid-19 treatment, say scientists

Researchers have identified a potent cocktail of antibodies that may help doctors treat Covid-19 infections and protect people at risk from falling ill with the disease.

The antibodies were collected from patients hospitalised with severe Covid-19, and they could be manufactured at scale by pharmaceutical firms and transfused into the blood to fight the virus or prevent it from taking hold.
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“We specifically isolated very potent antibodies that can be mass produced and then administered,” Ho said. “We would assume that these could be used to prevent or treat Sars-Cov-2. We’d be looking to treat early in the course of infection, particularly those at risk of developing severe disease such as the elderly and those with underlying illness.”
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Does anyone know exactly how these monoclonal antibodies are manufactured? Do they contain mouse protein, and would it be a problem if they did?

Full Liu et al, 22 July 2020, paper here:
Potent neutralizing antibodies directed to multiple epitopes on SARS-CoV-2 spike
 
Here are some research paper links that may belong in another thread. I'm hoping an administrator will find the right place. I'm dealing with other concerns at the moment.

BGR has a description of the paper in Nature Communications which details the discovery of an RNA cap which disguises viral mRNA, defeating one defense. This led me to some more investigation about enzymes involved leading to this publication. This is a very sophisticated natural pathogen which overcomes several problems typical of single-stranded RNA viruses.

We already knew it had RNA repair mechanisms to lower the rate at which it mutates. The next problem was hijacking mRNA without setting off alarms. A DNA virus could make changes inside the nucleus, so that the cell's own machinery would produce viral RNA. Working outside the nucleus requires a different solution.

SARS-CoV-2 also infects dogs and cats, as well as several other known species, including mustelids, like minks and feliforms, like palm-civets. This is a strong indication the host species where the different sequences from bats and pangolins came together was a member of the carnivora taxonomic group. Bats and pangolins are both insectovores with substantial divergence from common ancestors with this group. Predation is a natural way for infection to pass to such species.

The sophistication we see points to a long period of adaptation to new hosts, not human manipulation. Nobody knew a great deal about these mechanisms prior to this epidemic. Genetic manipulation also leaves artifacts, which are absent.

Interfering with enzymes like nsp16, or the nsp10 it requires, opens a new path to stopping infection. A year from now we will know exactly what we needed to know last year.
 
hinterland said:
Does anyone know exactly how these monoclonal antibodies are manufactured? Do they contain mouse protein, and would it be a problem if they did?
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The monoclonal antibodies are typically manufactured using novel cell culture techniques. (though in-vivo in mice is also possible, though less desirable)
Engineered antibodies can also be produced in a recombinant manner in bacterial cell culture.

As far as the actual engineering goes:
https://en.wikipedia.org/wiki/Hybridoma_technology
https://en.wikipedia.org/wiki/Fusion_protein
https://en.wikipedia.org/wiki/Phage_display
https://en.wikipedia.org/wiki/Genetically_modified_mouse
https://en.wikipedia.org/wiki/Recombinant_antibodies

These days there is a huge range of monoclonal antibodies available, most are for laboratory use and not used for therapeutic purposes.

The specific mabs in that study were made using recombinant technology in Expi293 (human based) cell culture, based on screened B-cell receptor sequences:

Antibody Expression and Purification
For each antibody, variable genes were optimized for human cell expression and synthesized by GenScript. VH and VL were inserted separately into plasmids (gWiz or pcDNA3.4) that encode the constant region for H chain and L chain. Monoclonal antibodies were expressed in Expi293 (ThermoFisher, A14527) by co-transfection of H chain and L chain expressing plasmids using polyethylenimine and culture in 37 °C shaker at 125 RPM and 8% CO2. On day 3 post transfection, 400 μL of supernatant were collected for screening for binding to S trimer and RBD by ELISA, and for neutralization of SARS-CoV-2 pseudovirus and authentic virus. Supernatants were also collected on day 5 for antibody purification by rProtein A Sepharose (GE, 17-1279-01) affinity chromatography.
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