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reinfection 4 months later, despite high antibodies after the first run

coronavirus

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#1 xEva

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Posted 13 July 2020 - 04:05 AM


These anecdotes about people getting sick again keep popping up.  Listen to this doc from "this week in virology" starting at 10:38.  And the rumor has it, the second time is worse! Bye-bye vaccine and herd immunity idea

 

https://youtu.be/LYo9oK-Giso?t=638

 

 


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#2 hotbit

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Posted 14 July 2020 - 10:04 AM

So they gossip some anecdotal incidents.
At 22:30:
- I don't know of any virus you get infected and just 3 months later you get infected again and have serious disease, do you know any?

- Em, uhm, umm....


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#3 Hip

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Posted 14 July 2020 - 04:22 PM

Interesting that for both doctors who suffered a second coronavirus infection 4 months after the first, the second coronavirus infection was worse (the second time was bad enough to require hospitalization). See timecode 13:05.

 

You might expect the residual antibodies remaining from the first infection to offer some protection, and thus expect that if anything, the second infection would be milder than the first.

 

Normally it takes the body around 3 days to figure out how to make the right antibodies to target a new infection, during which time the virus gets the upper hand. But once the body has learnt to make antibodies, it remembers how to make them for decades. So even if antibody levels are low, the body should be able to instantly start producing lots of coronavirus antibodies the second time the person is exposed to the virus (rather than the 3 day wait to make antibodies from scratch). So you would have thought a prior coronavirus infection would offer some protection, even with antibody levels being low, as antibody production should be at the ready.

 

Yet the infection was worse second time around in these two twice-infected doctors. 

 

Of course this is just two cases, so we cannot draw any hard conclusions from that. However, whistleblower doctors in China are also saying that coronavirus infection is worse the second time around (although they blame the medications for this: "the meds they use are damaging their heart tissue, and when they get it the second time, the antibody doesn’t help but makes it worse, and they die a sudden death from heart failure"). Whether it is the meds is an open question; but in any case, they are observing that infections are worse second time around.

 

Looks like coronavirus may be the diligent assassin which does not give up after a first failed attempt at killing you: this assassin may come back for you 4 months later when your antibodies have subsided, and on the second occasion, its homicidal skills may have become honed and deadlier. And should this assassin not kill you on the second try, there is always the third attempt, and the fourth attempt...

 

 

 

So it seems the only way out of this pandemic is the vaccine, which we hope will create long-lasting antibody protection.


Edited by Hip, 14 July 2020 - 04:24 PM.

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#4 rodentman

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Posted 14 July 2020 - 06:04 PM

 

So it seems the only way out of this pandemic is the vaccine, which we hope will create long-lasting antibody protection.

 

 

I've heard that 10% of people infected lose the anti-bodies over a 4 month period.  I have no idea if this is accurate, and if it means that eventually, the anti-bodies will disappear for a everyone, or if it just wears off for a small percentage of people.

 

If it just wears off for a small percentage,  we can still achieve herd immunity (hopefully with the help of a traditional vaccine to speed it up).

 

There are a few locations that are right at herd immunity levels now, including multiple areas in NY & Stockholm that are over 60% infected.  It they suddenly have an uptick, it will be a sign that the anti-bodies may be disappearing.


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#5 Hip

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Posted 14 July 2020 - 08:01 PM

I've heard that 10% of people infected lose the anti-bodies over a 4 month period.  

 

Just found this study which followed two groups of patients after they had (1) asymptomatic coronavirus infections, and (2) mild coronavirus infections. They found that after 4 months, 90% had a significant reduction in coronavirus-specific IgG antibodies, with 40% of the asymptomatic group having undetectable antibody levels, and 12% of the mild symptomatic group having undetectable antibody levels.



#6 Turnbuckle

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Posted 14 July 2020 - 08:30 PM

Just found this study which followed two groups of patients after they had (1) asymptomatic coronavirus infections, and (2) mild coronavirus infections. They found that after 4 months, 90% had a significant reduction in coronavirus-specific IgG antibodies, with 40% of the asymptomatic group having undetectable antibody levels, and 12% of the mild symptomatic group having undetectable antibody levels.

 

This is consistent with a retracted study that found covid19 attacks the immune system in a fashion similar to HIV. The retraction was due to methodology errors, but if correct after all, it suggests long term problems for those infected, even apart from the possibility of reinfection.

 

The original paper.


Edited by Turnbuckle, 14 July 2020 - 08:33 PM.


#7 gamesguru

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Posted 14 July 2020 - 08:45 PM

This is consistent with a retracted study that found covid19 attacks the immune system in a fashion similar to HIV. The retraction was due to methodology errors, but if correct after all, it suggests long term problems for those infected, even apart from the possibility of reinfection.

 

The original paper.

 

Bro, like stfu.  There are, like, Republicans on this forum and stuff.

 

Can't be suggesting anything contrary to "re-open now" lest ye earn ye thee label o thou "heretic" a pronto


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#8 rodentman

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Posted 14 July 2020 - 09:35 PM

Just found this study which followed two groups of patients after they had (1) asymptomatic coronavirus infections, and (2) mild coronavirus infections. They found that after 4 months, 90% had a significant reduction in coronavirus-specific IgG antibodies, with 40% of the asymptomatic group having undetectable antibody levels, and 12% of the mild symptomatic group having undetectable antibody levels.

 

No, I didn't see that study, just looked it up now.. that's a bit depressing. The study I read was the munich study, (44% of the patients showed lower neutralizing antibodies (IGG) , and 10% went to undetectable levels.   But I don't believe that included asymptomatic patients.
 
There's no question that Covid19 antibodies in general seem to fall quicker than with other viruses.  But the key unknowns are, it's still not known if the IgG antibodies would reach a steady state after the follow-up period or if it would continue to decline.  And also, we still don't have an estimation of the minimum antibody level we need to be safe from reinfection.
 
I think we will know the answer to those questions in the coming months.  But worse case scenario... we would have to have 60-70% of the population getting vaccinated every 4-5 months until it's wiped out.


#9 gamesguru

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Posted 14 July 2020 - 11:28 PM

IIRC a redditor estimated the immunity period between 0.8-4 years depending on age, genetics.  This was based on previous coronaviruses (not SARS) and spike protein assays.  Probably somewhere closer to 2 years. So not that long.

 

Interesting pre-print substantiating the HIV-like mechanism, based on suspicious and eerie gene expression changes involving the adaptive and innate immune systems.

 

I don't know about Turnbuckle's speculation this could turn into chronic deficiencies however.  I would interpret it so far as meaning it is a temporary thing it does to evade initial detection, not a dormancy mechanism invoked deep in the lympnodes or bone marrow to indefinitely avoid detection.  Certainly an alarming observation, but not a consistent or severe one at this stage we should have been hearing about immune-related complications in previously recovered patients, things such as Kaposi's sarcoma, secondary sepsis or tuberculousis, and other frightening resurgant oddities about which the liberals are so credulous and enthusiastic.

 

This article is a preprint
Preprints have not been peer reviewed.
Upper airway gene expression differentiates COVID-19 from other acute respiratory illnesses and reveals suppression of innate immune responses by SARS-CoV-2
 
Abstract

We studied the host transcriptional response to SARS-CoV-2 by performing metagenomic sequencing of upper airway samples in 238 patients with COVID-19, other viral or non-viral acute respiratory illnesses (ARIs). Compared to other viral ARIs, COVID-19 was characterized by a diminished innate immune response, with reduced expression of genes involved in toll-like receptor and interleukin signaling, chemokine binding, neutrophil degranulation and interactions with lymphoid cells. Patients with COVID-19 also exhibited significantly reduced proportions of neutrophils and macrophages, and increased proportions of goblet, dendritic and B-cells, compared to other viral ARIs. Using machine learning, we built 26-, 10- and 3-gene classifiers that differentiated COVID-19 from other acute respiratory illnesses with AUCs of 0.980, 0.950 and 0.871, respectively. Classifier performance was stable at low viral loads, suggesting utility in settings where direct detection of viral nucleic acid may be unsuccessful. Taken together, our results illuminate unique aspects of the host transcriptional response to SARS-CoV-2 in comparison to other respiratory viruses and demonstrate the feasibility of COVID-19 diagnostics based on patient gene expression.

 

 

At least with MERS, it is something seen early in the infection, to delay immune response, and so the virus can earn itself a head start.  No reports of Kaposi's sarcoma or the likes from recovered victims of SARS or MERS.  But there is some chronic fatigue and shortness of breath, but SARS -CoV-1 was thought to be more "severe". New reports did emerge of these same two symptoms in COVID recoveries, but it's not clear what percent of people experience this or to what extent.

 

Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment

The high mortality associated with the novel Middle East respiratory syndrome coronavirus (MERS-CoV) has raised questions about the possible role of a cytokine storm in its pathogenesis. Although recent studies showed that MERS-CoV infection is associated with an attenuated IFN response, no induction of inflammatory cytokines was demonstrated during the early phase of infection. To study both early and late cytokine responses associated with MERS-CoV infection, we measured the mRNA levels of eight cytokine genes [TNF-α, IL-1β, IL-6, IL-8, IFN-β, monocyte chemotactic protein-1, transforming growth factor-β and IFN-γ-induced protein (IP)-10] in cell lysates of polarized airway epithelial Calu-3 cells infected with MERS-CoV or severe acute respiratory syndrome (SARS)-CoV up to 30 h post-infection. Among the eight cytokine genes, IL-1β, IL-6 and IL-8 induced by MERS-CoV were markedly higher than those induced by SARS-CoV at 30 h, whilst TNF-α, IFN-β and IP-10 induced by SARS-CoV were markedly higher than those induced by MERS-CoV at 24 and 30 h in infected Calu-3 cells. The activation of IL-8 and attenuated IFN-β response by MERS-CoV were also confirmed by protein measurements in the culture supernatant when compared with SARS-CoV and Sendai virus. To further confirm the attenuated antiviral response, cytokine response was compared with human HCoV-229E in embryonal lung fibroblast HFL cells, which also revealed higher IFN-β and IP-10 levels induced by HCoV-229E than MERS-CoV at 24 and 30 h. Whilst our data supported recent findings that MERS-CoV elicits attenuated innate immunity, this represents the first report to demonstrate delayed proinflammatory cytokine induction by MERS-CoV. Our results provide insights into the pathogenesis and treatment of MERS-CoV infections.

 


Edited by gamesguru, 14 July 2020 - 11:39 PM.

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