Convalescent plasma from Norwegian blood donors to treat COVID-19. / Rekonvalesensplasma mot covid-19 fremstilt fra norske blodgivere.

BACKGROUND: At the start of the pandemic, the Norwegian Directorate of Health and Norwegian blood banks initiated the production of COVID-19 convalescent plasma within the framework of clinical studies. In this article we describe the blood donors who participated. MATERIAL AND METHOD: Blood donors who had recovered from COVID-19 were recruited to donate single donor plasma for the purpose of patient treatment. Data on the course of infection, leukocyte antibodies and antibody level against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) per plasma unit were registered after informed consent was obtained. We calculated a disease score defined as the total number of self-reported symptoms/findings and hospitalisation where relevant (score 0-⁠11). RESULTS: A total of 1644 plasma units were collected from 266 plasma donors at 12 blood banks. Median disease score was 5 (interquartile range 3-⁠6), and 15 donors had recovered from pneumonia and/or been hospitalised. A total of 599/1644 plasma units from 106/266 donors met our requirement for SARS-CoV-2 antibody content (> 60 % inhibition of virus binding to angiotensin-converting enzyme 2 (ACE2)) or positive virus neutralisation test. The antibody level in donors waned over time following infection, and showed no clear correlation with disease score. INTERPRETATION: The number of symptoms and findings in blood donors could not predict antibody response at individual level, and antibody testing was crucial for the production of effective convalescent plasma.

Screening for antibodies to HLA class I in apheresis donors following Covid-19 or SARS-CoV-2 vaccination.

Transfusion of HLA-specific antibodies may play a role in induction of TRALI, the transfusion complication responsible for most transfusion-related deaths. In Oslo, we screen our apheresis donors and defer HLA-immunized donors from donation of plasma-rich blood components. During the second year of the Covid-19 pandemic and following the first months of SARS-CoV-2 vaccination, both the virus itself and the vaccines were suspected of inducing de novo production of antibodies to HLA class I in patients. For the blood center, the possibility of finding HLA-antibodies in an increased number of blood donors has serious implications. We therefore conducted a study to map the extent of de novo HLA-specific antibodies in representative donor groups. 106 apheresis donors were screened for antibodies to HLA class I/II following Covid-19 or vaccination with either mRNA or adenovirus-vector vaccines, and the findings were compared to pre-Covid blood samples from the same donors. In addition, we analyzed pre-Covid samples from 11 HLA-antibody-positive donors of Covid convalescence plasma. Only three established thrombapheresis donors were deferred due to vaccine-induced HLA-antibodies. In short, our findings did not support the hypothesis that SARS-CoV-2 virus or vaccination cause de novo HLA immunization in healthy blood donors. However, some donors with pre-existing antibodies showed increased antibody expression, confirming a general boost of the immune response following infection or vaccination.

HLA-B*27 typing using a triplex real time PCR in routine laboratory.

We have established an in-house HLA-B*27 multiplex typing assay by using a combination of previously published, newly designed and commercial primers and probes for use with real-time PCR instruments. Hence, facilitating quick and large-scale HLA-B*27 typing.

The novel HLA-A*01 variant, HLA-A*01:308N, detected by sequencing-based typing.

One nucleotide changes in position 740 of HLA-A*01:01 result in a novel null-allele, HLA-A*01:308N.

The novel HLA-A*03 variant, HLA-A*03:08:01:02, detected by sequencing-based typing.

One nucleotide change in position 2606 of HLA-A*03:08:01:01 results in the novel allele, HLA-A*03:08:01:02.

Presensitization revisited: pitfalls of vascular allografts in transplant candidates.

Vascular allografts in end-stage renal disease (ESRD) patients represent a particular immunological challenge. A broad HLA immunization led us to study in depth the history of two patients with vascular allografts. In Case 1 the allograft was added to a Gore-Tex graft used for haemodialysis access and no immunosuppression was administered. In Case 2 the allograft was used to prolong a renal artery from living donor and immunosuppression was suboptimal. In vascular surgery, immunosuppression is mainly used to improve graft patency. ESRD patients are potential organ recipients and immunosuppression should therefore be tailored to reduce HLA immunization.