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Plasma samples from the first SARS-CoV-2 wave (D614G-infected) were obtained from a previously described cohort across various sites in South Africa prior to September 2020 (3). Second wave samples (Beta-infected) were obtained from a cohort of patients admitted to Groote Schuur Hospital, Cape Town in December 2020 - January 2021 (18). Third wave samples (Delta-infected) were obtained from the Steve Biko Academic Hospital, Tshwane from patients admitted in July 2021.
In all waves, samples were collected when more than 90% of SARS-CoV-2 cases in South Africa were caused by the respective variants. Sequence confirmation was only available for a subset of samples but all the samples that were sequenced corresponded to the appropriate variant for that wave.

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D614G-elicited plasma triggered robust neutralization of the matched D614G spike (autologous neutralization), but showed very low levels of cross-reactivity, with a 12-15-fold decrease in neutralization towards all SARS-CoV-2 VOCs tested and to SARS-CoV-1 (Figure 1A). In contrast, as we previously reported, plasma from Beta infections was highly cross-reactive against the D614G variant (2.9 fold reduction) (18) but showed less cross-reactivity against other VOCs, with reductions against Delta, Omicron and SARS-CoV-1 of 11.3-fold, 9.4-fold and 9.3-fold, respectively (Figure 1A). We also tested plasma from Delta-infected individuals and found that although autologous titers against the matched spike were very high, there was a 15-41-fold drop in neutralization potency across VOC/VOIs and SARS-CoV-1. The higher level of cross-reactivity for the D614G variant (15-fold drop in potency, compared to Beta (35-fold drop) in Delta-elicited plasma is consistent with what others have reported (19, 21).

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Thrombosis in COVID-19
American Journal of Hematology Volume 95........Issue 12, December 2020, Pages 1578-1589

Pulmonary embolism (PE) and deep vein thrombosis are the most frequently noted thrombotic events in COVID-19, with initial reports noting an incidence of 20% to 30% in critically ill patients (Figure 1).13 In a Dutch cohort of 184 subjects with COVID-19 in the intensive care unit (ICU), the cumulative incidence of large-vessel thrombotic events was 49%, the majority of which were pulmonary emboli seen on computed tomography in segmental and subsegmental pulmonary arteries.8 This occurred in spite of universal thromboprophylaxis with nadroparin at 2800 or 5700?IU once or twice daily, and the risk of all-cause death in that cohort was 5-fold higher among patients with a thrombotic event (HR 5.4; 95% CI 2.4 to 12). An Italian cohort of 388 patients observed a smaller but nevertheless sizable cumulative incidence of thromboembolic events at a rate of 21% (27.6% in the ICU, 6.6% on the general ward), half of which were diagnosed within 24?hours of hospital admission.14 A French cohort observed a similar cumulative incidence of thrombotic events and compared these to event rates from two different historical control populations: (a) ICU patients without COVID-19 admitted to the ICU in the Winter of 2019, and (b) patients with influenza admitted to the same ICU in 2019.15 Among COVID-19 ICU patients, 20.6% exhibited evidence of pulmonary embolism (diagnosed a median of 6?days from ICU admission), which was >2-fold higher compared to either historical control group. Therefore, it appears that COVID-19 may be uniquely prothrombotic compared to other severe viral respiratory pneumonias.

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Abstract:
Background: The rapid worldwide spread of the mildly pathogenic SARS-CoV-2 Omicron variant has led to the suggestion that it will induce levels of collective immunity that will help putting an end to the COVID19 pandemics.

Methods: Convalescent serums from non-hospitalized individuals previously infected with Alpha, Delta or Omicron BA.1 SARS-CoV-2 or subjected to a full mRNA vaccine regimen were evaluated for their ability to neutralize a broad panel of SARS-CoV-2 variants.

Findings: Prior vaccination or infection with the Alpha or to a lesser extent Delta strains conferred robust neutralizing titers against most variants, albeit more weakly against Beta and even more Omicron. In contrast, Omicron convalescent serums only displayed low level
of neutralization activity against the cognate virus and were unable to neutralize other SARS-CoV-2 variants.

Interpretation: Moderately symptomatic Omicron infection is only poorly immunogenic and does not represent a substitute for vaccination.

dturm wrote:

I suspect many of these reactions are due to the immune response induced by either the vaccine or the disease. The reason the reactions might be more severe in the disease could be due to greater number and types of immune complexes created by the disease. After all, COVID can affect many different systems in the body while the vaccine produces a more focused immune response.

The typical vaccine reaction we see in practice is usually due to vaccine components that the individual is allergic to. Aside from the active ingredient most typical vaccine might include adjuvants, preservatives, stabilizers and residual particles from manufacturing.

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In this pilot study we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 + patients’ thrombi. In addition, in all the three COVID-19 + thrombi analyzed for molecular biology, no SARS-CoV-2 RNA could be detected by real time-polymerase chain reaction. These data confirm the hypothesis that free SP besides the whole virus, may be the trigger of platelet activation and clot formation in COVID-19.