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Vaccines (Basel) ; 10(1)2021 Dec 25.
Article in English | MEDLINE | ID: covidwho-1580357


The high transmissibility, mortality, and morbidity rate of the SARS-CoV-2 Delta (B.1.617.2) variant have raised concerns regarding vaccine effectiveness (VE). To address this issue, all publications relevant to the effectiveness of vaccines against the Delta variant were searched in the Web of Science, Scopus, EMBASE, and Medline (via PubMed) databases up to 15 October 2021. A total of 15 studies (36 datasets) were included in the meta-analysis. After the first dose, the VE against the Delta variant for each vaccine was 0.567 (95% CI 0.520-0.613) for Pfizer-BioNTech, 0.72 (95% CI 0.589-0.822) for Moderna, 0.44 (95% CI 0.301-0.588) for AstraZeneca, and 0.138 (95% CI 0.076-0.237) for CoronaVac. Meta-analysis of 2,375,957 vaccinated cases showed that the Pfizer-BioNTech vaccine had the highest VE against the infection after the second dose, at 0.837 (95% CI 0.672-0.928), and third dose, at 0.972 (95% CI 0.96-0.978), as well as the highest VE for the prevention of severe infection or death, at 0.985 (95% CI 0.95-0.99), amongst all COVID-19 vaccines. The short-term effectiveness of vaccines, especially mRNA-based vaccines, for the prevention of the Delta variant infection, hospitalization, severe infection, and death is supported by this study. Limitations include a lack of long-term efficacy data, and under-reporting of COVID-19 infection cases in observational studies, which has the potential to falsely skew VE rates. Overall, this study supports the decisions by public health decision makers to promote the population vaccination rate to control the Delta variant infection and the emergence of further variants.

Stroke ; 52(5): e117-e130, 2021 05.
Article in English | MEDLINE | ID: covidwho-1195876
Front Cardiovasc Med ; 8: 649922, 2021.
Article in English | MEDLINE | ID: covidwho-1186796


Since the early days of the pandemic, there have been several reports of cerebrovascular complications during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Numerous studies proposed a role for SARS-CoV-2 in igniting stroke. In this review, we focused on the pathoetiology of stroke among the infected patients. We pictured the results of the SARS-CoV-2 invasion to the central nervous system (CNS) via neuronal and hematogenous routes, in addition to viral infection in peripheral tissues with extensive crosstalk with the CNS. SARS-CoV-2 infection results in pro-inflammatory cytokine and chemokine release and activation of the immune system, COVID-19-associated coagulopathy, endotheliitis and vasculitis, hypoxia, imbalance in the renin-angiotensin system, and cardiovascular complications that all may lead to the incidence of stroke. Critically ill patients, those with pre-existing comorbidities and patients taking certain medications, such as drugs with elevated risk for arrhythmia or thrombophilia, are more susceptible to a stroke after SARS-CoV-2 infection. By providing a pictorial narrative review, we illustrated these associations in detail to broaden the scope of our understanding of stroke in SARS-CoV-2-infected patients. We also discussed the role of antiplatelets and anticoagulants for stroke prevention and the need for a personalized approach among patients with SARS-CoV-2 infection.