--strange flu back in November 2019 was you-know-what--
i know a few other folks who had a strange flu back in nov. 2019.
cdc says don't get a test for antibodies:
"...Serologic testing does not replace virologic testing and should not be used to establish the presence or absence of acute SARS-CoV-2 infection..."
and goes on to discuss 'natural infection':
"...Nearly all immunocompetent persons develop an adaptive immune response following SARS-CoV-2 infection, including B and T cell-mediated immunity (1-3) due to antiviral humoral and cellular immune responses, respectively. Our understanding of the immune response to SARS-CoV-2 is incomplete but rapidly advancing. In humans, the humoral response includes antibodies directed against S and N proteins. The S protein contains two subunits, S1 and S2. The S1 subunit contains the RBD that mediates binding of virus to susceptible cells. RBD is the main target for neutralizing antibodies. Antibodies – including IgM, IgG, and IgA – against S and its subunits can be detected within 1-3 weeks after infection (4, 5). IgM and IgG antibodies can arise nearly simultaneously (4); however, IgM (and IgA) antibodies decay more rapidly than IgG (4, 6). The clinical significance of IgA in SARS-CoV-2 is not yet established.
How long anti-SARS-CoV-2 antibodies persist after infection remains unknown, although IgG antibodies, including IgG against the S and N proteins, persist for at least several months in most persons (7). Seroreversion has been reported among persons with mild disease (8). Persons with more severe disease appear to develop a more robust antibody response with IgM, IgG, and IgA all achieving higher titers and exhibiting longer persistence (8, 9). The observed persistence of antibodies can vary by assay (10), and some studies have found that approximately 5-10% do not develop detectable IgG antibodies following infection (11, 12). Although neutralizing antibodies may not be detected among patients with mild or asymptomatic disease (13), the humoral immune response appears to remain intact even with loss of specific antibodies over time (14). SARS-CoV-2 neutralizing antibodies that inhibit viral replication in vitro mainly target the RBD (2, 3). A need exists for standardized assays that can correlate antibody titers with neutralization (15).
SARS-CoV-2 reinfection has been documented (16, 17); however, studies indicate that persons with anti-SARS-CoV-2 antibodies are less likely to develop subsequent infection than persons without such antibodies. Outbreak investigations from a fishing vessel and a summer camp in the United States found that persons with pre-existing SARS-CoV-2 antibody were protected from subsequent infection (18, 19). In sequential outbreaks among staff and residents of two British nursing homes, persons who tested antibody-positive following the first outbreak were approximately 96% less likely to become infected during the second outbreak four months later (20). In a British prospective cohort study of persons with and without SARS-CoV-2 antibody, the adjusted incident rate ratio for subsequent infection was 0.11 among persons followed for a median of 200 days after a positive antibody test, compared to those who tested negative for anti-SARS-CoV-2 antibody (21). Another British cohort study found an 83% reduction in SARS-CoV-2 infection incidence over a five-month period among persons who had tested antibody positive for SARS-CoV-2 or had prior infection documented by revers transcription polymerase chain reaction (RT-PCR) (22). A large study in the United States of commercial laboratory results linked to medical claims data and electronic medical records found a 90% reduction in infection among persons with antibody compared to persons without (23), and another study of military recruits found that seropositive individuals had an 82% reduction in incidence of SARS-CoV-2 infection over a 6-week period (24). Additionally, antibody development following SARS-CoV-2 in humans infection correlates with a marked decrease in viral load in the respiratory tract, although a clinical correlation with viral load in the respiratory tract has not been definitively established (5). Experiments on non-human primates support the above observations in humans. Experimentally infected rhesus macaques that developed humoral and cellular immune responses were protected against reinfection when re-challenged 35 days later (25). Another study found that transfer of purified IgG from rhesus macaques infected with SARS-CoV-2 was effective in protecting naïve rhesus macaques from infection and the threshold titers for protection, based upon binding and neutralizing antibodies, were determined (26).
Taken together, the above findings in humans and non-human primates suggest SARS-CoV-2 infection and development of antibody can result in some level of protection against SARS-CoV-2 reinfection. The durability of this immunity has yet to be determined. While life-long immunity has not been observed with endemic seasonal coronaviruses (27), studies of persons infected with the novel SARS-CoV-1 and Middle East Respiratory Syndrome (MERS-CoV) coronaviruses demonstrated measurable antibody for 18 – 24 months following infection (28, 29), and neutralizing antibody was present for 34 months in a small study of MERS-infected patients (30). It is not known to what extent persons re-infected with SARS-CoV-2 might transmit infection to others or whether the clinical spectrum differs from that of primary infection..."
cdc.gov
it's not clear to me why cdc discourages antibody testing...
they seem to be more reliable than pcr tests:
"...The IgG antibody-positive rates for samples taken after 13 days of onset were 100.0%, 97.6%, and 97.6%, respectively..."
ncbi.nlm.nih.gov
per pcr tests, harvard says:
"...Unfortunately, it’s not clear exactly how accurate any of these (covid19 virus) tests are..."
health.harvard.edu
i am agnostic. |
