Objective Cases of thrombosis have been reported after administration of SARS-CoV-2 vaccines, with controversial results relating to Oxford-AstraZeneca’s ChAdOx1-S. Despite such cases being rare, they still raised concerns for their involvement in coagulopathies. Anti-cardiolipin (aCL) IgG antibodies have been linked to venous and arterial thrombosis. The aim was to evaluate the concentration of aCL IgG antibodies in vaccinated and COVID-19 positive individuals using indirect ELISA and commercial sourced calibrators. Results The concentration of aCL IgG antibodies was measured in the serum of COVID-19 positive (n = 37), ChAdOx1-S vaccinated (n = 37) and BioNTech Pfizer BNT162b2 vaccinated (n = 42) individuals. Samples from COVID-19 negative, unvaccinated individuals (n = 41) served as controls. The highest percentage of positivity was in the COVID-19 positive group (18.9%). Concerning vaccination, BNT162b2 had the highest percentage of positivity (11.9%) (p = 0.0037). Additionally, aCL concentrations were evaluated at different time points in both vaccinated groups (before, 3 weeks after and 3 months after the second dose). A significant difference in the levels of aCL IgG antibodies over time (p = 0.0391) was observed only in ChAdOx1-S individuals. Our study concluded that levels of aCL, after vaccination with either of the vaccines or following SARS-CoV-2 infection, were not clinically pathogenic for the risk of thrombosis.

No abstract

No abstract

Background: Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) where both environmental and genetic risk factors play a role. Among the environmental risk factors, EBV and HSV infections have been suggested as strong candidates contributing to MS pathology/progression. Viral recognition and control is largely tasked to the NK cells via TLR recognition and various cytotoxic and immunoregulatory functions. The present work aimed to characterize NK cells isolated from MS patients for genetic polymorphisms in the gene encoding for TLR3, as TLR3 in NK cells is important in herpesvirus recognition. Methods: Highly purified NK cells isolated from peripheral blood of MS patients (n = 27) and healthy controls (n = 30) were used to sequence all five exons of the TLR3 gene using sanger sequencing. Alignment of the obtained sequences with the wild-type TLR3 sequence was used to identify genetic polymorphisms within the TLR3 gene. Results: The alignment identified multiple substitution mutations across the five exons of the TLR3 gene (rs116729895, rs3775296, rs377529, rs3775290, rs3775291, rs376735334 and rs73873710). A significant difference was observed in the allele distribution of rs3775291 (Leu412Phe) between MS patients and HC, whereby the minor allele was detected in 38.9% of MS patients versus 11% of HC (Fisher's exact test, p = 0.021). Conclusion: There appears to be a possible association between the TLR3 missense mutation rs3775291 and multiple sclerosis, which might be attributed to changes in the TLR3 functional properties.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has hit its second year and continues to damage lives and livelihoods across the globe. There continues to be a global effort to present serological data on SARS-CoV-2 antibodies in different individuals. As such, this study aimed to characterize the seroprevalence of SARS-CoV-2 antibodies in the Cypriot population for the first time since the pandemic started. Our results show that a majority of people infected with SARS-CoV-2 developed IgG antibodies against the virus, whether anti-NP, anti-S1RBD, or both, at least 20 days after their infection. Additionally, the percentage of people with at least one antibody against SARS-CoV-2 in the group of volunteers deemed SARS-CoV-2 negative via RT-PCR or who remain untested/undetermined (14.43%) is comparable to other reported percentages worldwide, ranging anywhere from 0.2% to 24%. We postulate that these percentages reflect the underreporting of true infections in the population, and also show the steady increase of herd immunity. Additionally, we showed a significantly marked decrease in anti-NP IgG antibodies in contrast to relatively stable levels of anti-S1RBD IgG antibodies in previously infected individuals across time.

There is an ongoing effort to report data on SARS-CoV-2 antibodies in different individuals. Ninety-seven healthcare workers were enrolled in this study (Pfizer’s BNT162b2, n = 52; and AstraZeneca’s ChAdOx1-S, n = 45) and S1RBD-specific IgG antibodies were analyzed over time. Both vaccines induced S1RBD-specific antibodies after the second dose. A significant increase in S1RBD-specific IgG median levels 3 weeks following the second dose was detected (BNT162b2, 118.0 BAU/mL to 2018.0 BAU/mL; ChAdOx1-S, 38.1 BAU/mL to 182.1 BAU/mL). At 3 months post the second dose, a significant decrease in S1RBD-specific IgG median levels was also evident (BNT162b2, 415.6 BAU/mL, ChAdOx1-S, 84.7 BAU/mL). The elimination rate of these antibodies was faster in BNT162b2- rather than ChAdOx1-S- vaccinated individuals. A booster dose induced a significant increase in the S1RBD-specific IgG median levels (BNT162b2, 1823.0 BAU/mL; ChAdOx1-S, 656.8 BAU/mL). This study is the first of its kind to characterize S1RBD-specific IgG antibody responses in vaccinated healthcare workers in Cyprus. While the positivity for S1RBD-specific antibodies was maintained 3 months after the second vaccine dose, the level of these antibodies waned over the same period, indicating the importance of a booster vaccination. The results herein could complement the public health policies regarding the immunization schedule for COVID-19.

No abstract

No abstract