The nerdy amounts of pandemic detail thread

[2hats]

(UWash) A study of the electrostatic structure of omicron/B.1.1.529 when interacting with a key monoclonal antibody (sotrovimab family) and human ACE2 provides an explanation for the apparent behaviour of this variant. CryoEM and X-ray diffraction analysis were performed in order to understand the spike structure and electrostatic interactions at the molecular level.

This work reveals that the N-terminal domain has substantially changed structural arrangement, explaining the loss of binding and neutralisation by a wide range of monoclonal antibodies which target epitopes in this region. Additionally, key mutations in the S2 subunit (part of the fusion machinery) have increased electrostatic binding to the S1 subunit. This has three effects: (1) reduction in cleavage reducing fusogenicity, (2) increase in spike stability and binding sites (and thus viral infectivity, as seen in earlier studies) and (3) limiting S1 shedding which (other studies in animal models have suggested) may increase antibody Fc effector functions (ie pathways to cellular immune response). Finally, they find that K417N, S477N, Q493R, Q498R and N501Y collectively enhance ACE2 binding through the electrostatic changes that they bring about.

Like others, they also note the efficiency with which omicron RBD binds to murine ACE2.
DOI: 10.1101/2021.12.28.474380.

 

[elbows]

A study into T cell protection via other coronaviruses (common cold ones). Not a very large study but still interesting.

T cells from common colds cross-protect against infection with SARS-CoV-2 | Imperial News | Imperial College London

People with higher levels of T cells from common cold coronaviruses are less likely to become infected with SARS-CoV-2.

www.imperial.ac.uk

 

[2hats]

(Rutgers) A new PCR test ("sloppy molecular beacon Alpha/Beta/Gamma RT-PCR melting temperature signature-based assay") that can identify VOCs and so also be used to quickly determine the most suitable treatment path as regards monoclonal antibody therapy.

DOI: 10.1101/2022.01.18.22269424.

 

[elbows]

I am running out of my own words today due to making many other posts, but want to stick this here after mentioning it in the worldwide thread ( #10,631 )

Pandemic preparedness and COVID-19: an exploratory analysis of infection and fatality rates, and contextual factors associated with preparedness in 177 countries, from Jan 1, 2020, to Sept 30, 2021

Efforts to improve pandemic preparedness and response for the next pandemic might benefit from greater investment in risk communication and community engagement strategies to boost the confidence that individuals have in public health guidance. Our results suggest that increasing health...

www.thelancet.com

Findings​

The factors that explained the most variation in cumulative rates of SARS-CoV-2 infection between Jan 1, 2020, and Sept 30, 2021, included the proportion of the population living below 100 m (5·4% [4·0–7·9] of variation), GDP per capita (4·2% [1·8–6·6] of variation), and the proportion of infections attributable to seasonality (2·1% [95% uncertainty interval 1·7–2·7] of variation). Most cross-country variation in cumulative infection rates could not be explained. The factors that explained the most variation in COVID-19 IFR over the same period were the age profile of the country (46·7% [18·4–67·6] of variation), GDP per capita (3·1% [0·3–8·6] of variation), and national mean BMI (1·1% [0·2–2·6] of variation). 44·4% (29·2–61·7) of cross-national variation in IFR could not be explained. Pandemic-preparedness indices, which aim to measure health security capacity, were not meaningfully associated with standardised infection rates or IFRs. Measures of trust in the government and interpersonal trust, as well as less government corruption, had larger, statistically significant associations with lower standardised infection rates. High levels of government and interpersonal trust, as well as less government corruption, were also associated with higher COVID-19 vaccine coverage among middle-income and high-income countries where vaccine availability was more widespread, and lower corruption was associated with greater reductions in mobility. If these modelled associations were to be causal, an increase in trust of governments such that all countries had societies that attained at least the amount of trust in government or interpersonal trust measured in Denmark, which is in the 75th percentile across these spectrums, might have reduced global infections by 12·9% (5·7–17·8) for government trust and 40·3% (24·3–51·4) for interpersonal trust. Similarly, if all countries had a national BMI equal to or less than that of the 25th percentile, our analysis suggests global standardised IFR would be reduced by 11·1%.

Interpretation​

Efforts to improve pandemic preparedness and response for the next pandemic might benefit from greater investment in risk communication and community engagement strategies to boost the confidence that individuals have in public health guidance. Our results suggest that increasing health promotion for key modifiable risks is associated with a reduction of fatalities in such a scenario.

 

[elbows]

(Rutgers) A new PCR test ("sloppy molecular beacon Alpha/Beta/Gamma RT-PCR melting temperature signature-based assay") that can identify VOCs and so also be used to quickly determine the most suitable treatment path as regards monoclonal antibody therapy.

I think sloppy molecular beacon may have instantly become one of my favourite pieces of jargon in this pandemic.

 

[wemakeyousoundb]

Human challenge study preprint
from Imperial college london run at the royal free hospital.
as I originally read about here

 

[2hats]

Human challenge study preprint
from Imperial college london run at the royal free hospital.
as I originally read about here

A presentation on the research given by one of the PIs at a conference a couple of months ago.

 

[2hats]

(MGH/MIT/Harvard) A small T-cell study indicating that perhaps around one-fifth of people (irrespective of antigenic exposure history) might be more susceptible to degrees of disease progression following infection by omicron (or, perhaps, could be after initial post-vax circulating antibody levels naturally contract), though not to that arising from infection with delta: "we identify a subset of individuals (∼21%) with a >50% reduction in T-cell reactivity to the Omicron spike" (over 12% had a >70% reduction in the same). Those individuals exhibited a significant difference in CD8+ T-cell proliferation in response to omicron compared to earlier types.

"Booster [third] doses enhanced the magnitude of responses to wildtype and Omicron spike, although did not completely mitigate the comparatively reduced T-cell reactivity to Omicron in individual participants"; even after a booster vaccination some ~9% of participants still exhibited >50% reduced reactivity to omicron spike compared to earlier wildtype.

In summary:

• T-cell responses to Omicron are preserved in most infected and vaccinated individuals
• T-cell reactivity to Omicron spike is reduced by >50% in ∼20% of individuals
• Most Omicron epitopes have conserved sequence and retain binding to HLA-I
• T-cell reactivity to Omicron is enhanced shortly after booster vaccination

These data [...] raise the prospect that future SARS-CoV-2 variants may variably escape from antibody or T-cell responses. These findings thereby support continued evaluation of second-generation vaccine approaches that induce robust T-cell responses that target both variant spike and non-spike antigens in order to overcome current and future SARS-CoV-2 evolution.

DOI: 10.1016/j.cell.2022.01.029.

Note: This is a small study of some 76 donors (ages 36-61 years, median age 47, "consenting ambulatory adults") conducted in the first ~7 months after primary vaccination series (original EUA timing intervals) and shortly after any third dose boosters (typically <2 weeks). Another limitation is use of IFN-γ ELISPOT and proliferation assays. Additional T cell assays, and longitudinal sampling, are likely necessary to construct a clearer picture.

This is another small part of the puzzle relating to the potential role of human leukocyte antigen and how genetic variation may influence different COVID-19 outcomes for different individuals. This has been noted in a separate study (QIMR/La Trobe) which highlights the ablation of the immunodominant CD8+ T-cell response to omicron in a sub-population of individuals (convalescent or vaccinated).
DOI: 10.21203/rs.3.rs-1289622/v1.

 

[2hats]

This is another small part of the puzzle relating to the potential role of human leukocyte antigen and how genetic variation may influence different COVID-19 outcomes for different individuals. This has been noted in a separate study (QIMR/La Trobe) which highlights the ablation of the immunodominant CD8+ T-cell response to omicron in a sub-population of individuals (convalescent or vaccinated).
DOI: 10.21203/rs.3.rs-1289622/v1.

Again, regarding this, a small study (Imperial and others) of HLA‐DR polymorphism in SARS‐CoV‐2 infection and susceptibility to symptomatic COVID‐19 which suggests that the risk of developing symptoms and heterogeneity in T cell immunoresponse to vaccination might vary with associated genetics.

SARS-CoV-2 infection results in different outcomes ranging from asymptomatic infection, to mild or severe disease and death. Reasons for this diversity of outcome include differences in challenge dose, age, gender, comorbidity and host genomic variation. Human leukocyte antigen (HLA) polymorphisms may influence immune response and disease outcome. We investigated the association of HLAII alleles with case definition symptomatic COVID-19, virus-specific antibody and T cell immunity. 1,364 UK healthcare workers (HCW) were recruited during the first U.K. SARS-CoV-2 wave and analyzed longitudinally, encompassing regular PCR screening for infection, symptom reporting, imputation of HLAII genotype and analysis for antibody and T cell responses to nucleoprotein (N) and spike (S). Of 272 (20%) HCW who seroconverted, the presence of HLA-DRB1*13:02 was associated with a 6.7-fold increased risk of case definition symptomatic COVID-19. In terms of immune responsiveness, HLA-DRB1*15:02 was associated with lower nucleocapsid T cell responses. There was no association between DRB1 alleles and anti-spike antibody titres after two COVID vaccine doses. However, HLA DRB1*15:01 was associated with increased spike T cell responses following both first and second dose vaccination.

DO: 10.1111/imm.13450.

 

[2hats]

Some SARS-CoV-2 ORF sequences appear to comprise amyloid assemblies.

​

In conclusion, using a bioinformatics approach we identified two strongly amyloidogenic sub-sequences from the ORF6 and ORF10 sections of the SARS-COV-2 proteome. Nanoscale imaging, X-ray scattering, molecular modelling, spectroscopy and kinetic assays revealed that these self-assembled structures are amyloid in nature, and screening against neuronal cells revealed that they are highly toxic (approximately as toxic as the toxic amyloid assemblies in AD) to a cell line frequently used as a neurodegenerative diseases model. The neuroinvasive nature of SARS-COV-2 has been established previously; therefore, it is entirely plausible that amyloid assemblies either from these ORF proteins or other viral proteins could be present in the CNS of COVID-19 patients. The cytotoxicity and protease-resistant structure of these assemblies may result in their persistent presence in the CNS of patients post-infection that could partially explain the lasting neurological symptoms of COVID-19, especially those that are novel in relation to other post-viral syndromes such as that following the original SARS-CoV-1. The outlook in relation to triggering of progressive neurodegenerative disease remains uncertain. Given the typically slow progress of neurodegenerative disease if such a phenomenon exists, it will most probably take some time to become evident epidemiologically.

DOI: 10.1038/s41467-022-30932-1.

 

[elbows]

Oh, thats the topic that I've really struggled to go on about throughout this pandemic. I dont have a problem contemplating those possibilities myself, but I didnt feel good about drawing everyone elses attention to the subject all the time. It seems that despite the reputation I probably have for being gloomy and doomy, I have limits in terms of spreading such concerns and encouraging people to dwell on them. Plus if I did go on about such things then it would be as part of wanting to use that to underline my stance on how I think we should have dealt with this virus, ie suppressing levels of infection far more comprehensively than the authorities ever had any appetite for (AKA people wrote off zero covid prematurely). And its been bloody obvious for a very long time that I'd be fighting a losing battle on that front - there was a lengthy period where I could have relied on a fairly big chunk of the public to take things nearly that seriously, but that period came to an end in the last year. And my heart is only really in such things when there is some real chance of making it happen. So I've been reduced to retreating, with the prospect that should the worst case scenarios with brain degeneration be demonstrated to be true in the long term, I'll just end up spouting useless 'told you so' type sentiments. Maybe I won a few early battles but lost the war, bah. Short term wankers, fickle fuckers, with myself included to an admittedly lesser extent.

I suppose my decision not to dwell on such things was partly based on past experience with 'ticking time bomb' concerns in regards mad cow disease, and partly due to the long timescales required for sufficient evidence to emerge. I can see why coping strategies can involve wishful thinking, and the desire to only 'cross that bridge if we come to it'. But that robs us of the best opportunities to do something proactive about it when it really matters. But I suppose I have to balance that with more immediate mental health concerns and peoples ability to get on with living life without dwelling on all the future potential negatives in store. Stuff thats part of what makes the human condition a bit of a bad joke, with science and logic somewhat wasted on us because of our inherent contradictions and the sheer number of factors that get in the way of doing the right thing at the right time to the right extent.

A world where precautionary principals are our god would be more to my taste, but thats not the world I find myself in.

 

[2hats]

(Ragon/Brigham/MGH, Boston) A small (n=66) study characterising the viral decay kinetics of omicron/BA.1. It would appear to suggest that you still need to allow at least ~10 and perhaps up to ~14 days for shedding if you want to be totally sure transmission risk is close to zero.

The median time from symptom onset or the initial positive PCR assay, whichever was earlier, to culture conversion was [for delta] 6 days (interquartile range, 4 to 7) and [for omicron] 8 days (interquartile range, 5 to 10), respectively.

​

DOI:10.1056/NEJMc2202092.

 

[teuchter]

Does that bottom graph suggest that vaccination actually leads to people being infectious for slightly longer?

 

[2hats]

You might assume so on the face of it. However - some warnings:

1. These were nasal swabs so measuring URT infectious virus shedding only (the unvaccinated are far more likely to see the infection then progress to the LRT with shedding from there).
2. Small study numbers.
3. Viral-culture positivity may not wholly correlate with transmission (needs further study).

 

[HAL9000]

Brain fog after COVID-19 has similarities to ‘chemo brain,’ Stanford-led study finds

Researchers found that damage to the brain’s white matter after COVID-19 resembles that seen after cancer chemotherapy, raising hope for treatments to help both conditions.

med.stanford.edu

 

[2hats]

(Ragon/Brigham/MGH, Boston) A small (n=66) study characterising the viral decay kinetics of omicron/BA.1. It would appear to suggest that you still need to allow at least ~10 and perhaps up to ~14 days for shedding if you want to be totally sure transmission risk is close to zero.

More commentary on this - the latest scientific consensus suggests allowing at least 10 days after symptom onset/positive [LFT] test for isolation, and being aware of the need for longer where treating with anti-virals ("paxlovid rebound").
DOI:10.1038/d41586-022-02026-x.

 

[HAL9000]

Measuring of how many virus particles are breathed out



one person infected with Omicron breathed out a 1000x more particles.

paper..

Evolution of SARS-CoV-2 Shedding in Exhaled Breath Aerosols

Aerosol inhalation is increasingly well recognized as a major if not primary mode of transmission of SARS-CoV-2[1][1],[2][2]. Over the course of the COVID-19 pandemic, three highly transmissible lineages evolved and became globally dominant[3][3]. One hypothesis to explain increased...

www.medrxiv.org

highest viral EBA shedder in our study was a person with an Omicron infection whose fine EBA sample contained 1.8×107 RNA copies

(don't know if this was the machine they used)

 

[2hats]

Measuring of how many virus particles are breathed out



one person infected with Omicron breathed out a 1000x more particles.

paper..

Evolution of SARS-CoV-2 Shedding in Exhaled Breath Aerosols

Aerosol inhalation is increasingly well recognized as a major if not primary mode of transmission of SARS-CoV-2[1][1],[2][2]. Over the course of the COVID-19 pandemic, three highly transmissible lineages evolved and became globally dominant[3][3]. One hypothesis to explain increased...

www.medrxiv.org

Interesting to note that the (suspected prior) hybrid immunes shed zero (or the lowest) levels of detectable virus and, importantly, none of that that was detectable was culturable.

Five participants with Omicron infections (one with BA.1, one with BA.1.1, and three with BA.2) were positive for anti-nucleocapsid (anti-N) protein IgG in sera at the time of enrolment, one to six days post symptom onset. Four of the five had received a booster >8 days prior to onset of symptoms. Two reported prior infection(s); two denied prior infection and one did not respond to questions about prior infection. We detected viral RNA in MTS samples from all five. Their MTS, however, contained significantly lower RNA copy numbers than Omicron infections in the absence of anti-N IgG (p=0.00045). These five are the only Omicron infections that yielded culture negative MTS samples. We detected viral RNA in saliva from only one of the five, the non-boosted case, and that sample was not culturable. None of the five shed detectable levels of SARS-CoV-2 RNA in EBA (limit of detection = 75 copies).

Shame they didn't have more definitive prior infection histories for all participants though.

 

[8ball]

Measuring of how many virus particles are breathed out



one person infected with Omicron breathed out a 1000x more particles.

paper..

Evolution of SARS-CoV-2 Shedding in Exhaled Breath Aerosols

Aerosol inhalation is increasingly well recognized as a major if not primary mode of transmission of SARS-CoV-2[1][1],[2][2]. Over the course of the COVID-19 pandemic, three highly transmissible lineages evolved and became globally dominant[3][3]. One hypothesis to explain increased...

www.medrxiv.org

View attachment 336219
(don't know if this was the machine they used)

That’s something I’d expect to see on the audiophile thread.

 

[elbows]

A US study of children and adolescents between March 2020 and January 2022:

Post–COVID-19 Symptoms and Conditions Among Children and...

This report describes the potential of post-COVID symptoms and conditions among children and adolescents.

www.cdc.gov

Compared with patients aged 0–17 years without previous COVID-19, those with previous COVID-19 had higher rates of acute pulmonary embolism (adjusted hazard ratio = 2.01), myocarditis and cardiomyopathy (1.99), venous thromboembolic event (1.87), acute and unspecified renal failure (1.32), and type 1 diabetes (1.23), all of which were rare or uncommon in this study population.

 

[2hats]

Interesting to note that the (suspected prior) hybrid immunes shed zero (or the lowest) levels of detectable virus and, importantly, none of that that was detectable was culturable.

(UCSF) Transmission in hybrid immunes appears to be significantly curbed compared to vaxed only who are in turn unsurprisingly less likely to transmit than convalescent non-vaxed.
DOI:10.1101/2022.08.08.22278547.

 

[elbows]

COVID-19 survivors had a 69% higher risk of a new diagnosis of Alzheimer's disease within 1 year of infection than their uninfected peers (hazard ratio, 1.69; 95% confidence interval [CI], 1.53 to 1.72). Participants aged 85 years and older and women were at particularly high risk (HRs, 1.89 [95% CI, 1.73 to 2.07] and 1.82 [95% CI, 1.69 to 1.97], respectively).

"Our findings call for research to understand the underlying mechanisms and for continuous surveillance of long-term impacts of COVID-19 on Alzheimer’s disease," the authors wrote.

The team said it's not clear whether COVID-19 triggers or accelerates development of Alzheimer's disease, noting that SARS-CoV-2 has been associated with inflammation and central nervous system disorders.

"The factors that play into the development of Alzheimer’s disease have been poorly understood, but two pieces considered important are prior infections, especially viral infections, and inflammation," coauthor Pamela Davis, MD, PhD, said in a Case Western press release.

---

Possible 69% higher risk of Alzheimer's for older COVID survivors

www.cidrap.umn.edu

 

[elbows]

Quite early on in the pandemic we heard of some early signs that BCG vaccines might have an impact. It seems that there have been subsequent studies looking at this, such as this one I just stumbled across which is in the context of type 1 diabetes sufferers:

Multiple shots of the BCG vaccine protect type 1 diabetics from COVID-19, study finds

Researchers are hoping the results of a new study will spur a larger scale study of the effects of the BCG vaccine in patients with type 1 diabetes, considered among the most vulnerable groups to COVID-19.

www.sciencedaily.com

 

[elbows]

Another study based on analysing US veterans medical records:

Long-term neurologic outcomes of COVID-19 - Nature Medicine

Individuals with COVID-19 are at an increased risk for an array of neurologic disorders at 12 months, even in those who were not hospitalized during the acute phase of the infection.

www.nature.com

Here we use the national healthcare databases of the US Department of Veterans Affairs to build a cohort of 154,068 individuals with COVID-19, 5,638,795 contemporary controls and 5,859,621 historical controls; we use inverse probability weighting to balance the cohorts, and estimate risks and burdens of incident neurologic disorders at 12 months following acute SARS-CoV-2 infection.

Our results show that in the postacute phase of COVID-19, there was increased risk of an array of incident neurologic sequelae including ischemic and hemorrhagic stroke, cognition and memory disorders, peripheral nervous system disorders, episodic disorders (for example, migraine and seizures), extrapyramidal and movement disorders, mental health disorders, musculoskeletal disorders, sensory disorders, Guillain–Barré syndrome, and encephalitis or encephalopathy. We estimated that the hazard ratio of any neurologic sequela was 1.42 (95% confidence intervals 1.38, 1.47) and burden 70.69 (95% confidence intervals 63.54, 78.01) per 1,000 persons at 12 months. The risks and burdens were elevated even in people who did not require hospitalization during acute COVID-19. Limitations include a cohort comprising mostly White males. Taken together, our results provide evidence of increased risk of long-term neurologic disorders in people who had COVID-19.

 

[elbows]

A review of papers relating to myocarditis showed the risk of this from infection to be more than 7 times higher than from vaccination:

Myocarditis in SARS-CoV-2 infection vs. COVID-19 vaccination: A systematic review and meta-analysis

BackgroundThis study aimed to compare the incidence of myocarditis in COVID-19 vaccines and in severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection groups.MethodsElectronic databases (MEDLINE, Scopus, Cochrane Central Register of Controlled Trials, Cochrane Database of...

www.frontiersin.org

We identified 22 eligible studies consisting of 55.5 million vaccinated cohorts and 2.5 million in the infection cohort. The median age was 49 years (interquartile range (IQR): 38–56), and 49% (IQR: 43 to 52%) were men. Of patients diagnosed with myocarditis (in both vaccination and COVID-19 cohort) 1.07% were hospitalized and 0.015% died. The relative risk (RR) for myocarditis was more than seven times higher in the infection group than in the vaccination group [RR: 15 (95% CI: 11.09–19.81, infection group] and RR: 2 (95% CI: 1.44-2.65, vaccine group). Of patients who developed myocarditis after receiving the vaccine or having the infection, 61% (IQR: 39–87%) were men. Meta-regression analysis indicated that men and younger populations had a higher risk of myocarditis. A slow decline in the rates of myocarditis was observed as a function of time from vaccination. The risk of bias was low.

 

[elbows]

Better hope this is flawed:

Outcomes of SARS-CoV-2 Reinfection

First infection with SARS-CoV-2 is associated with increased risk of acute and post-acute death and sequelae in the pulmonary and extrapulmonary organ systems. However, whether reinfection adds to the risk incurred after the first infection is not clear. Here we use the national health care da...

www.researchsquare.com

We examined whether the risk of sequelae of SARS-CoV-2 reinfection was present in the acute and post-acute phase of the reinfection. We conducted analyses examining risk and burden starting from time of reinfection up to 180 days later in 30-day increments. Compared to those with first infection, those with reinfection exhibited increased risk and excess burden of all-cause mortality, hospitalization, and at least one sequela in the acute phase and the post-acute phase of the reinfection. The risks and excess burdens of all-cause mortality, hospitalization, and at least on sequela during the post-acute phase gradually attenuated over time but remained evident even six months after reinfection (Fig. 3, Supplementary Table 5). Examination of sequelae by organ system suggested an increased risk and excess burden in all organ systems during the acute phase (Fig. 4, Supplementary Table 5); the risks and burdens persisted in the post-acute phase of reinfection, and most were still evident at 6 months after reinfection.

There was a graded association in that the risks of adverse health outcomes increased as the number of infections increased. Compared to the non-infected control group, those who only had one infection had an increased risk of at least one sequela (HR 1.35 (1.4, 1.36); burden 84.13 (82.03, 86.24)); the risk was higher in those who had two infections (HR 2.11 (2.07, 2.15); burden 234.58 (227.08, 241.92)), and highest in those with three or more infections (HR 3.00 (2.71, 3.31); burden 362.82 (326.37, 398.08)). In pairwise comparison of those with two infections vs first infection, those with two infections had an increased risk of at least one sequela (HR 1.57 (1.53, 1.60); burden 150.36 (142.95, 157.79)); in pairwise comparison of those with three or more infections vs those with only two infections, those with three or more infections had a higher risk of at least one sequela (HR 1.42 (1.28, 1.57); burden 128.33 (91.88, 164.31)). Results were consistent in examination of all-cause mortality, hospitalization, and sequelae by organ system (Fig. 5, Supplementary Tables 8-13).

 

[8ball]

Acute death I understand.

Post-acute death = zombification?

 

[2hats]

Post-acute death = zombification?

Deaths occurring in the post-acute phase, ie many weeks to months (to years) after infection.

Wouldn't be surprising. Tallies with a lot of other recent research indicating increased risks for cardiovascular/neurodegenerative diseases (and combinations thereof) for many months (likely years) following any pattern of SARS-CoV-2 infection, even with adequate vaccine-acquired immunity (though the population-level risks are lower than for those for convalescent-only-acquired immunoresponses). SARS-CoV-2 infection does not only precipitate short-term respiratory disease (as was pointed out some time ago and should be readily apparent by now).

 

[8ball]

Deaths occurring in the post-acute phase, ie many weeks to months (to years) after infection.

Wouldn't be surprising. Tallies with a lot of other recent research indicating increased risks for cardiovascular/neurodegenerative diseases (and combinations thereof) for many months (likely years) following any pattern of SARS-CoV-2 infection, even with adequate vaccine-acquired immunity (though the population-level risks are lower than for those for convalescent-only-acquired immunoresponses). SARS-CoV-2 infection does not only precipitate short-term respiratory disease (as was pointed out some time ago and should be readily apparent by now).

So no zombie apocalypse just yet.

Phew!

 

[2hats]

So no zombie apocalypse just yet.

Phew!

One day.