Vi som är kritiska till Sveriges handhavande av pandemin
"Conclusions
Whether a virus infection results in severe, sometimes prolonged, lesions or is resolved with minimal bystander tissue damage depends on numerous factors. Some viruses (for example, HIV and HCV) have intrinsic properties that make immune control difficult, and attempts by the host immune system to achieve control results in notable tissue damage. Other infectious agents (for example, many herpesviruses) are successfully controlled in most individuals, but tissue damage occurs in those individuals that have predisposing genetic or acquired problems affecting one or more components of innate or adaptive immune system. Finally, some infections that are normally well controlled can cause extensive tissue damage under unusual circumstances. These might relate to the dose or route of exposure, the age of infection, host genetics and priming with cross-reacting viruses or co-infection with other agents."
"Persistent Cytokine Deregulation and Interferon Type I and III Responses in COVID-19 Patients We reasoned that the previously reported cytokine storm in COVID-19 may be responsible for some of the blood count abnormalities of these patients (Mehta et al., 2020). IL-6 and IL10, both involved in class switch recombination but also in T cell exhaustion, were significantly increased in the plasma of patients with active COVID-19, in line with previous data (Chen et al., 2020; Diao et al., 2020), while the recovered patients showed normal concentrations (Figure 3A). Also, plasma concentrations of B cell-activating factor (BAFF) were exclusively increased in active COVID-19 patients and exhibited a very unusual positive correlation with B cell counts, while a proliferation-inducing ligand (APRIL) was elevated only in the plasma of recovered patients (Figures 3A and S1). The antiviral cytokine pattern was compatible with an IFN type I and type III response, the latter persisting at increased levels during the recovery phase in COVID-19 (Figure 3B). COVID-19 had strong effects on the secretory variants of immune checkpoint molecules such as soluble Tim-3 (sTim-3), sLAG-3, sCD25, and sGalectin-9, which were normal in the recovered state, suggesting massive antiviral responses and counterregulation at the time point of active (and severe) disease (Figure 3C). All of the cytokines showing less profound alterations in COVID-19 are shown in Figure S2."