College Students' Belonging and Loneliness in the Context of Remote Online Classes during the COVID-19 Pandemic

The COVID-19 pandemic has drastically affected how higher education operates, but relatively little is known about its effects on students enrolled in remote online classes. Across two data collection timepoints, we sought to examine college students' experiences, focusing particularly on their sense of belonging/loneliness, their course formats, and their experiences in the pandemic. Though some findings differed between data collected in fall 2020 and in spring 2021, we generally found that students' belonging/loneliness was linked with their class format, aspects of their virtual classes, social contact, and experiences in the pandemic. This research demonstrates the importance both of understanding students' experiences in general and of continuing to study students' experiences as we progress from one stage of the pandemic to the next. © 2022, The Online Learning Consortium. All rights reserved.

Heterologous vaccination of BNT162b2 in Ad26. COV2.S-vaccinated healthcare workers elicits long-term humoral immune response

Background. To date, there are no immunological data for the SARS-CoV-2 heterologous vaccination schedule in the South African (SA) population. Objectives. To assess and compare the immunogenicity and reactogenicity of the Jansen Ad26.COV2.S vaccine with the Pfizer/BioNTechBNT162b2 booster following prime Ad26.COV2.S in 65 SA healthcare workers. Methods. In a prospective, quantitative, cross-sectional trial on individuals >18 years of age vaccinated with a single Ad26.COV2.S dose or single Ad26.COV2.S and a BNT162b2 single-dose/both doses booster, participants filled in a questionnaire on their demographics, type of vaccination, breakthrough infection/s (BTI/s), vaccine reactogenicity, prior SARS-CoV-2 infection and dates of vaccination. Qualitative analysis for presence/absence of anti-S (spike) immunoglobulin G (IgG) was performed using the Euroimmun anti-IgG enzyme-linked immunoassay kit, and anti-S IgG titres were quantitatively assessed using the Abbott IgG Quant II kit. Results. Between 28 October 2021 and 30 November 2021, 65 individuals were enrolled and assigned as either prime Ad26.COV2.S (n=18) or Ad26.COV2.S with a BNT162b2 supplement (n=47) at Charlotte Maxeke Johannesburg Academic Hospital, SA (mean age 45 years (95% confidence interval (CI) 29.5 - 58), 42 women (64.6%) and 23 men (35.4%)). The median IgG titre for the primed Ad26.COV2.S group was 4 272.55 (95% CI 68.40 - 10 351.40) and that for the BNT162b2 supplement group was 7 360.80 (95% CI 4 207.40 - 15 372.60). In the univariate model, the BNT162b2 supplement group showed a significant 1.99 times higher antibody titre factor (95% CI 0.045 - 5.553;p<0.005) than the Ad26.COV2.S group. In both univariate and multivariate models, age, time since prime vaccination, BTI and prior infection failed to show any statistically significant association (p>0.05) with antibody titres in both groups. However, sex (-55.381 (95% CI -76.984 - -13.498;p=0.018) in a multivariate model was found to have a statistically significant association with anti-S IgG titres observed in both groups. Participants who received their first dose of BNT162b2 9 - 10 months after their prime Ad26.COV2.S (n=44) had a higher degree of antibody response than those who received it earlier. Reactogenicity was observed to be manageable, with mild/moderate adverse effects in the study population. Conclusion. A BNT162b2 supplement given in single or two doses as booster in individuals primed with Ad26.COV2.S induced immunological response, with acceptable and manageable reactogenicity. This study provides novel evidence of the highest degree of antibody response in individuals who received a BNT162b2 first dose 9 - 10 months after prime Ad26.COV2.S, implying that a longer time gap between the two vaccines stimulates higher antibody response than a shorter gap, and that this antibody response can persist for as long as 6 months after the last BNT162b2 dose. Copyright © 2022 South African Medical Association. All rights reserved.

Change in platelet indices in patients with coronavirus infection disease (COVID-19): A reflection of platelet activation and contribution to immunothrombosis?

Background : Activation of the coagulation system, as reflected by raised D-dimers, is prevalent in patients with COVID-19 resulting in coagulopathies as well as venous and arterial macro-and microthromboses. Laboratory tests in patients admitted with COVID-19 should include prothrombin time (PT) and D-dimers. The role of platelets in COVID-19 related immunothrombosis has not been extensively documented. Aims : Investigate platelet indices in patients with COVID-19 with raised D-dimer levels and compare the results to COVID-19 infected patients with normal D-dimer levels as well as to COVID-19 uninfected patients with raised D-dimers. Methods : This retrospective observational study was approved by the Human Research Ethics Committee of the University of the Witwatersrand (M201010). The laboratory results of patients admitted to a quaternary referral centre in Johannesburg, South Africa from June to December 2020 were reviewed. Platelet indices including platelet large cell ratio (P-LCR), mean platelet volume (MPV) and platelet distribution width (PDW) were recorded and analysed in the following 3 cohorts: 281 COVID-19 patients with raised D-dimers, 72 COVID-19 patients without raised D-dimers and 51 COVID-19 negative patients with raised D-dimers and disseminated intravascular coagulation (DIC). Results : The platelet indices P-LCR, MPV and PDW in COVID-19 positive patients were statistically different from patients without COVID-19 ( P < 0.001) (Table 1). No statistically significant difference in the platelet indices was however observed between COVID-19 patients with and without raised D-dimers. COVID-19, Corona virus disease-19;n , number of patients;SD, standard deviation;P-LCR, platelet large cell ratio;MPV, mean platelet volume;PDW, platelet distribution width. Conclusions : Platelet laboratory indices are statistically different between COVID-19 positive and COVID-19 negative patients but were not predictive of the presence of an underlying coagulopathy in COVID-19 as reflected by elevated D-dimer levels. The alterations in platelet indices in COVID-19 patients probably reflect activation of platelets and contribution to immunothrombosis.

Heparin-induced thrombocytopenia: An update for the COVID-19 era.

The increased use of heparin during the current COVID-19 pandemic has highlighted the risk of a rare but potentially serious complication of heparin therapy, viz. heparin-induced thrombocytopenia (HIT). This is a short review on the pharmacology of heparin and its derivatives, and the pathophysiology of HIT. Guidance on laboratory testing for and clinical management of HIT is presented in accordance with international guidelines. There are important similarities and differences between HIT and the new entity of vaccine-induced immune thrombotic thrombocytopenia, also known as thrombosis with thrombocytopenia syndrome, which clinicians need to be aware of.

Recommendations for the diagnosis and management of vaccine-induced immune thrombotic thrombocytopenia

There have recently been safety concerns regarding an increased risk of vaccine-induced immune thrombotic thrombocytopenia (VITT) following administration of SARS-CoV-2 adenoviral vector vaccines. The Southern African Society of Thrombosis and Haemostasis reviewed the emerging literature on this idiosyncratic complication. A draft document was produced and revised by consensus agreement by a panel of professionals from various specialties. The recommendations were adjudicated by independent international experts to avoid local bias. We present concise, practical guidelines for the clinical management of VITT.

The Novel Coronavirus and Haemostatic Abnormalities: Pathophysiology, Clinical Manifestations, and Treatment Recommendations.

The COVID-19 pandemic, caused by the SARS-C0V-2 virus, was initially considered and managed in a similar manner to the previous SARS epidemic as they are both caused by coronaviruses. What has now become apparent is that a major cause of morbidity and mortality in COVID-19 is abnormal thrombosis. This thrombosis occurs on a macro- and microvascular level and is unique to this disease. The virus has been demonstrated in the endothelium of the pulmonary alveoli and as such is thought to contribute to the devastating respiratory complications encountered. D-dimer concentrations are frequently raised in COVID to levels not frequently seen previously. The optimal anticoagulation treatment in COVID remains to be determined, and the myriad of pathophysiologic effects caused by this virus in the human host have also yet to be fully elucidated.