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Seroconversion was observed in 13 of the 14 patients either by anti-viral IgG (FIA) or by antigen capturing anti-N protein assay by 14 days after the onset of the symptoms. In contrast, anti-viral IgM was detectable only in 10 patients by14 days, and in 13 patients by 30 days after the onset of the symptoms. By comparison, anti-viral IgG and anti-N protein antibodies were detected in all the patients from 30 to 210 days after the onset of the symptoms. Antiviral IgM was shown to be negative in 4, 8, 12 and all 14 patients by day 60,120,180 and 210 days post disease onset, respectively. These results may indicate that antiviral IgG may correlate better with viral neutralization. Also, the recombinant nucleocaspid protein based antigen-capturing ELISA was at least as sensitive as the anti-viral IgG(IFA) assay.

Anti-viral IgG and anti-Nucleocaspid antibodies were detectable earlier than anti-viral IgM antibodies, and the highest antibody titer was reached at 120 days (anti-viral IgG) and 180 days (anti-N protein) after the onset of the symptoms. The titer decreased slowly after that time point, and high titers of antibodies were observed in all patients 210 days after the onset of symptoms. Geometric mean values of the antibodies were shown in Fig. 1. In contrast, a significantly lower titer of anti-viral IgM antibody was found with a peak titer at 30 days. Moreover, anti-viral IgM could not be detected in any of the 14 patients 210 days after the onset of the symptoms.

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Total IgGAM antibody is the antibody detectable earliest (mean, 14.2 days; range, 9 to 19 days) in patients with SARS. Of the subclass-specific assays, IgM antibodies were the earliest antibody to be detectable (mean, 16.6 days; range, 13 to 22 days). Although IgM antibody titers declined significantly during the first 7 months after infection, we demonstrated that SARS CoV IgM remains detectable in 63.6% (7/11) of patients for at least 7 months. It was previously reported that IgM antibody detected by ELISA became undetectable by 11 weeks after onset of illness (15). These differences in results may be related to differences to the sensitivity of the methods used for the serology tests.

In contrast, neutralizing antibody titers and IF IgGAM and IgG levels seem stable over the first 7 months postinfection. In addition, there was no significant difference in the kinetics of the appearance of the antibody responses between patients who survive or die.

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Ranger222 said:

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Quick literature search on SARS gives two different answers -

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Seroconversion was observed in 13 of the 14 patients either by anti-viral IgG (FIA) or by antigen capturing anti-N protein assay by 14 days after the onset of the symptoms. In contrast, anti-viral IgM was detectable only in 10 patients by14 days, and in 13 patients by 30 days after the onset of the symptoms. By comparison, anti-viral IgG and anti-N protein antibodies were detected in all the patients from 30 to 210 days after the onset of the symptoms. Antiviral IgM was shown to be negative in 4, 8, 12 and all 14 patients by day 60,120,180 and 210 days post disease onset, respectively. These results may indicate that antiviral IgG may correlate better with viral neutralization. Also, the recombinant nucleocaspid protein based antigen-capturing ELISA was at least as sensitive as the anti-viral IgG(IFA) assay.

Anti-viral IgG and anti-Nucleocaspid antibodies were detectable earlier than anti-viral IgM antibodies, and the highest antibody titer was reached at 120 days (anti-viral IgG) and 180 days (anti-N protein) after the onset of the symptoms. The titer decreased slowly after that time point, and high titers of antibodies were observed in all patients 210 days after the onset of symptoms. Geometric mean values of the antibodies were shown in Fig. 1. In contrast, a significantly lower titer of anti-viral IgM antibody was found with a peak titer at 30 days. Moreover, anti-viral IgM could not be detected in any of the 14 patients 210 days after the onset of the symptoms.

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Source 1

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Total IgGAM antibody is the antibody detectable earliest (mean, 14.2 days; range, 9 to 19 days) in patients with SARS. Of the subclass-specific assays, IgM antibodies were the earliest antibody to be detectable (mean, 16.6 days; range, 13 to 22 days). Although IgM antibody titers declined significantly during the first 7 months after infection, we demonstrated that SARS CoV IgM remains detectable in 63.6% (7/11) of patients for at least 7 months. It was previously reported that IgM antibody detected by ELISA became undetectable by 11 weeks after onset of illness (15). These differences in results may be related to differences to the sensitivity of the methods used for the serology tests.

In contrast, neutralizing antibody titers and IF IgGAM and IgG levels seem stable over the first 7 months postinfection. In addition, there was no significant difference in the kinetics of the appearance of the antibody responses between patients who survive or die.

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Source 2


In summary IgG seems detectable months after infection, some disagreement on whether IgM remains detectable but the trend is that is does decrease over time

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plain_o_llama said:

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Here is the podcast, Ranger222 refers to:

http://www.microbe.tv/twiv/twiv-591/


Speculation on how coronavirus population immunity might develop in humans (47:20)
Why children are not showing symptoms (43:50)

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Safe at Home said:

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On the doctor reville thread this morning, he said that some researchers believe that children's high level of melatonin might contribute to their immunity. Do you have thoughts on that? Do you think that taking melatonin supplements could be helpful in preventing the disease?

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Tmoneyag99 said:

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So what you're saying is that if we don't find a vaccine we all have to remain in shelter not producing anything, the world economy is going to collapse and the only people that will be living are people in Asia who eat raw bat and have a developed immunity.

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slacker00 said:

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Tmoneyag99 said:

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So what you're saying is that if we don't find a vaccine we all have to remain in shelter not producing anything, the world economy is going to collapse and the only people that will be living are people in Asia who eat raw bat and have a developed immunity.

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I'm not sure if all vaccines work the same way, but wouldn't that mean the vaccine wouldn't be long lasting either? My low level of understanding is vaccines cause OUR immune system to produce antibodies in the same manner as if we had the infection...........

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Thomas Ford 91 said:

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Let's assume for moment that infection leads to long-term immunity. Does the mostly benign nature of C19 mean a lower percentage threshold for herd immunity?

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KidDoc said:

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Oops I already need to redact my co-infection statement. From this source:

https://www.ebmedicine.net/topics/infectious-disease/COVID-19?utm_source=engagement&utm_medium=email&utm_campaign=COVID19&__s=qikxdqvyescq3xta6dgm&fbclid=IwAR2-JDjSBIcDXXNHgObBEy_ffTaJ0nV8qdwx8QAM8dB08CStx7K85hOvBN0

After an exhaustive search of the literature, interviews with several infectious disease physicians, consultation of several national and international forums dedicated to both emergency medicine and COVID-19, we were able to find only a single non-peer reviewed Chinese study of 8274 specimens collected and analyzed for SARS-CoV-2 and other viral species. (Note that the publisher states, "This article is a preprint and has not been peer reviewed. It reports medical research that has yet to be evaluated and so should not be used to guide clinical practice.") In this study, they found that 5.8% of COVID-19 patients had co-infections with other viruses, and that 18.4% of other (non-SARS-CoV-2) infections had other co-infectants.52 The authors acknowledged the unreliability of their tests for both SARS-CoV-2 and other viruses, which may underreport the actual co-infection rate. Furthermore, in some preliminary data reported by Stanford Medicine Data scientists, and immediately available to the public online at the behest of the California Department of Public Health, researchers found that in the 49 positive SARS-CoV-2 results, 11 (22.4%) also had co-infection with another virus.53 We anticipate that a large, validated study will help to shed further light on the rate of co-infection with SARS-CoV-2. In the meantime, we must recommend that clinicians maintain a high index of suspicion for SARS-CoV-2, regardless of the presence of other viruses.

Given this information, emergency clinicians should re-emphasize to the lay public what we already know of viral respiratory infections: that seeking treatment in a hospital setting for mild symptoms, fever, mild diarrhea, or cough alone likely carries with it more risk than benefit, both to themselves and to vulnerable patients around them. Patients experiencing severe symptoms such as difficulty breathing, high fever (>39C), and an inability to tolerate oral hydration should seek emergency evaluation. For those who are concerned about their symptoms or concerned about spreading the infection to vulnerable family members, care should be taken to practice social distancing, self-quarantining, and utilization of telehealth and drive-through screening clinics to receive medical evaluation and testing (if warranted) while minimizing risk of infectious spread. Though beyond the scope of this review, further discussions regarding institutional and departmental policies that weigh the need to protect the health of medical staff and care for patients versus the need to minimize nosocomial spread from asymptomatic healthcare workers who may infect patients, will need to continue.

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