Publication date: Available online 30 May 2023 Source: Infectious Disease Modelling Author(s): Sheng-Tao Wang, Yong-Ping Wu, Li Li, Yong Li, Gui-Quan Sun …

Publication date: Available online 28 May 2023 Source: Infectious Disease Modelling Author(s): Sittisede Polwiang …

Publication date: Available online 16 May 2023 Source: Infectious Disease Modelling Author(s): Jeffery Demers, William F. Fagan, Sriya Potluri, Justin M. Calabrese …

SARS‐CoV‐2 infection during pregnancy is associated with adverse maternal and neonatal outcomes, but no systematic synthesis of evidence on COVID‐19 vaccination during pregnancy against these outcomes has been undertaken. Thus, we aimed to assess the collective evidence on the effects of COVID‐19 vaccination during pregnancy on maternal and neonatal outcomes. PubMed/MEDLINE, CENTRAL, and EMBASE were systematically searched for articles published up to 1 November 2022. A systematic review and meta‐analysis were performed to calculate pooled effects size and 95% confidence interval (CI). We evaluated 30 studies involving 862,272 individuals (308,428 vaccinated and 553,844 unvaccinated). Overall pooled analyses in pregnant women during pregnancy showed reduced risks of SARS‐CoV‐2 infection by 60% (41%–73%), COVID‐19 hospitalisation during pregnancy by 53% (31%–69%), and COVID‐19 intensive care unit (ICU) admission by 82% (12%–99%). Neonates of vaccinated women were 1.78 folds more likely to acquire SARS‐CoV‐2 infection during the first 2, 4 and 6 months of life during the Omicron period. The risk of stillbirth was reduced by 45% (17%–63%) in association with vaccination (vs. no vaccination) in pregnancy. A decrease of 15% (3%–25%), 33% (14%–48%), and 33% (17%–46%) in the odds of preterm births before 37, 32 and 28 weeks\' gestation were associated with vaccination (vs. no vaccination) in pregnancy, respectively. The risk of neonatal ICU admission was significantly lower by 20% following COVID‐19 vaccination in pregnancy (16%–24%). There was no evidence of a higher risk of adverse outcomes including miscarriage, gestational diabetes, gestational hypertension, cardiac problems, oligohydramnios, polyhydramnios, unassisted vaginal delivery, cesarean delivery, postpartum haemorrhage, gestational age at delivery, placental abruption, Apgar score at 5 min below 7, low birthweight (…

There is a scarcity of scientific evidence addressing the outcomes of COVID‐19 in celiac disease (CD) patients. This systematic review and meta‐analysis aimed to evaluate the correlation between pre‐existing CD and COVID‐19. A rigorous literature search was conducted using multiple databases. All eligible observational studies were included from around the globe. The random effect model calculated the pooled prevalence and associated 95% confidence intervals (CI). Mantel‐Haenszel odds ratios were produced to report the overall effect size using random effect models for severity and mortality outcomes. Funnel plots, Egger regression tests, and Begg‐Mazumdar\'s rank correlation test were used to appraise publication bias. Data from 11 articles consisting of 44,378 CD patients were obtained. Overall pooled random‐effects estimate of SARS‐CoV‐2 infection in CD patients was 4.25% (95% CI,  = 98%). Our findings also indicated that pre‐existing CD was not associated with an increased risk of hospitalisation with COVID‐19 illness (OR = 1.04, 95% CI 0.87–1.24,  = 0%) and mortality due to illness (OR = 0.92, 95% CI 0.56–1.5,  = 45%) compared with patients without pre‐existing CD. No significant publication bias was evident in the meta‐analysis. The preliminary data from our analysis suggest that SARS‐CoV‐2 infection in patients with pre‐existing CD is not associated with an increased risk of hospitalisation or mortality. Additional studies are required to overcome the restrictions of the limited data available at present.

COVID‐19 was announced as a global pandemic in 2020. Several types of COVID‐19 vaccines are available such as mRNA vaccines, adenovirus vector vaccines, and protein subunit or inactivated virus vaccines. Vaccines are often administered in patients with chronic diseases who are likely to be treated with several drugs. A growing number of clinical observations indicated the possibility of interactions between COVID‐19 vaccines and drugs. A hyperinflammatory state may spark significant imbalances in drug metabolism that may result in the alteration of drug pharmacokinetics and therapeutic response. Furthermore, interactions may result in additive or antagonistic or synergistic vaccine immune response. Information about COVID‐19 vaccine–drug interactions is needed by physicians and pharmacists to make rational drug‐use decisions. In this review, several individual and categorical evidence‐based potential COVID‐19 vaccine–drug interactions of clinical importance are described. Vigilance is needed to detect previously unreported COVID‐19 drug interactions and to further assess known interactions. The clinical significance of which is not fully determined. Evidence suggests that adverse events to some drugs are rare after COVID‐19 vaccination and their possibility should not affect vaccination of patients at risk. Clinicians prescribing medications should be aware of the likely risk of interaction with COVID‐19 vaccines and may benefit from taking into account present recommendations of the best measures to avoid consequences of such interactions to preserve vaccine efficacy and patient safety.

We conducted this systematic review and meta‐analysis to evaluate the existing evidence and to quantitatively synthesise evidence on the impact of therapeutic plasma exchange (TPE) on severe COVID‐19 patients. This systematic review and meta‐analysis protocol was prospectively registered on PROSPERO (CRD42022316331). We systemically searched six electronic databases (PubMed, Scopus, Web of Science, ScienceDirect, , and Cochrane Central Register of Controlled Trials) from inception until 1 June 2022. We included studies comparing patients who received TPE versus those who received the standard treatment. For risk of bias assessment, we used the Cochrane risk of bias assessment tool, the ROBINS1 tool, and the Newcastle Ottawa scale for RCTs, non‐RCTs, and observational studies, respectively. Continuous data were pooled as standardized mean difference (SMD), and dichotomous data were pooled as risk ratio in the random effect model with the corresponding 95% confidence intervals (CI). Thirteen studies (one randomized controlled trials (RCT) and 12 non‐RCTs) were included in the meta‐analysis, with a total of 829 patients. There is a moderate‐quality evidence from one RCT that TPE reduces the lactic dehydrogenase (LDH) levels (SMD −1.09, 95% CI [−1.59 to −0.60]), D‐dimer (SMD −0.86, 95% CI [−1.34 to −0.37]), and ferritin (SMD −0.70, 95% CI [−1.18 to −0.23]), and increases the absolute lymphocyte count (SMD 0.54, 95% CI [0.07–1.01]), There is low‐quality evidence from mixed‐design studies that TPE was associated with lower mortality (relative risk 0.51, 95% CI [0.35–0.74]), lower IL‐6 (SMD −0.91, 95% CI [−1.19 to −0.63]), and lower ferritin (SMD −0.51, 95% CI [−0.80 to −0.22]) compared to the standard control. Among severely affected COVID‐19 patients, TPE might provide benefits such as decreasing the mortality rate, LDH, D‐dimer, IL‐6, and ferritin, in addition to increasing the higher absolute lymphocyte count. Further well‐designed RCTs are needed.

To provide a comprehensive systematic review and meta‐analysis regarding the cumulative incidence (incidence proportion) of human herpesvirus (HHV) reactivation among patients with coronavirus disease 2019 (COVID‐19), we searched PubMed/MEDLINE, Web of Science, and EMBASE up to 25 September 2022, with no language restrictions. All interventional and observational studies enrolling patients with confirmed COVID‐19 and providing data regarding HHV reactivation were included. The random‐effects model was used in the meta‐analyses. We included information from 32 studies. HHV reactivation was considered a positive polymerase chain reaction result taken at the time of COVID‐19 infection. Most of the included patients were severe COVID‐19 cases. The pooled cumulative incidence estimate was 38% (95% Confidence Intervals [CI], 28%–50%,  = 86%) for herpes simplex virus (HSV), 19% (95% CI, 13%–28%,  = 87%) for cytomegalovirus (CMV), 45% (95% CI, 28%–63%,  = 96%) for Epstein‐Barr virus (EBV), 18% (95% CI, 8%–35%) for human herpesvirus 6 (HHV‐6), 44% (95% CI, 32%–56%) for human herpesvirus 7 (HHV‐7), and 19% (95% CI, 14%–26%) for human herpesvirus 8 (HHV‐8). There was no evidence of funnel plot asymmetry based on visual inspection and Egger\'s regression test for the results of HSV ( = 0.84), CMV ( = 0.82), and EBV ( = 0.27) reactivation. In conclusion, the identification of HHV reactivation in severe COVID‐19 patients is helpful in the management of patients as well as the prevention of complications. Further research is required to elucidate the interaction between HHVs and COVID‐19. Systematic review registration: PROSPERO CRD42022321973.

The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) Delta variant (B.1.617.2) was the predominant variant behind the surges of COVID‐19 in the United States, Europe, and India in the second half of 2021. The information available regarding the defining mutations and their effects on the structure, transmission, and vaccine efficacy of SARS‐CoV‐2 is constantly evolving. With waning vaccine immunity and relaxation of social distancing policies across the globe driving the increased spread of the Delta variant, there is a great need for a resource aggregating the most recent information for clinicians and researchers concerning the Delta variant. Accordingly, this narrative review comprehensively reviews the genetics, structure, epidemiology, clinical course, and vaccine efficacy of the Delta variant. Comparison with the omicron variant is also discussed. The Delta variant is defined by 15 mutations in the Spike protein, most of which increase affinity for the ACE‐2 receptor or enhance immune escape. The Delta variant causes similar symptoms to prototypical COVID‐19, but it is more likely to be severe, with a greater inflammatory phenotype and viral load. The reproduction number is estimated to be approximately twice the prototypical strains present during the early pandemic, and numerous breakthrough infections have been reported. Despite studies demonstrating breakthrough infection and reduced antibody neutralisation, full vaccination effectively reduces the likelihood of severe illness and hospitalisation.

The coronavirus disease 2019 (COVID‐19) pandemic is transmitted by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and has affected millions of people all around the world, leading to more than 6.5 million deaths. The nucleocapsid (N) phosphoprotein plays important roles in modulating viral replication and transcription, virus‐infected cell cycle progression, apoptosis, and regulation of host innate immunity. As an immunodominant protein, N protein induces strong humoral and cellular immune responses in COVID‐19 patients, making it a key marker for studying N‐specific B cell and T cell responses and the development of diagnostic serological assays and efficient vaccines. In this review, we focus on the structural and functional features and the kinetic and epitope mapping of B cell and T cell responses against SARS‐CoV‐2 N protein to extend our understanding on the development of sensitive and specific diagnostic immunological tests and effective vaccines.

Severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2) is the causative agent of coronavirus disease 2019 (COVID‐19). In less than three years, an estimated 600 million infections with SARS‐CoV‐2 occurred worldwide, resulting in a pandemic with tremendous impact especially on economic and health sectors. Initially considered a respiratory disease, COVID‐19, along with its long‐term sequelae (long‐COVID) rather is a systemic disease. Neurological symptoms like dementia or encephalopathy were reported early during the pandemic as concomitants of the acute phase and as characteristics of long‐COVID. An excessive inflammatory immune response is hypothesized to play a major role in this context. However, direct infection of neural cells may also contribute to the neurological aspects of (long)‐COVID‐19. To mainly explore such direct effects of SARS‐CoV‐2 on the central nervous system, human brain organoids provide a useful platform. Infecting these three‐dimensional tissue cultures allows the study of viral neurotropism as well as of virus‐induced effects on single cells or even the complex cellular network within the organoid. In this review, we summarize the experimental studies that used SARS‐CoV‐2‐infected human brain organoids to unravel the complex nature of (long)‐COVID‐19‐related neurological manifestations.

Severe acute respiratory syndrome coronavirus 2 may inflict a post‐viral condition known as post‐COVID‐19 syndrome (PCS) or long‐COVID. Studies measuring levels of inflammatory and vascular biomarkers in blood, serum, or plasma of COVID‐19 survivors with PCS versus non‐PCS controls have produced mixed findings. Our review sought to meta‐analyse those studies. A systematic literature search was performed across five databases until 25 June 2022, with an updated search on 1 November 2022. Data analyses were performed with Review Manager and R Studio statistical software. Twenty‐four biomarkers from 23 studies were meta‐analysed. Higher levels of C‐reactive protein (Standardized mean difference (SMD) = 0.20; 95% CI: 0.02–0.39), D‐dimer (SMD = 0.27; 95% CI: 0.09–0.46), lactate dehydrogenase (SMD = 0.30; 95% CI: 0.05–0.54), and leukocytes (SMD = 0.34; 95% CI: 0.02–0.66) were found in COVID‐19 survivors with PCS than in those without PCS. After sensitivity analyses, lymphocytes (SMD = 0.30; 95% CI: 0.12–0.48) and interleukin‐6 (SMD = 0.30; 95% CI: 0.12–0.49) were also significantly higher in PCS than non‐PCS cases. No significant differences were noted in the remaining biomarkers investigated (e.g., ferritin, platelets, troponin, and fibrinogen). Subgroup analyses suggested the biomarker changes were mainly driven by PCS cases diagnosed via manifestation of organ abnormalities rather than symptomatic persistence, as well as PCS cases with duration of…

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.

The susceptibility, risk factors, and prognosis of COVID‐19 in patients with inflammatory bowel disease (IBD) remain unknown. Thus, our study aims to assess the prevalence and clinical outcomes of COVID‐19 in IBD. We searched PubMed, EMBASE, and medRxiv from 2019 to 1 June 2022 for cohort and case‐control studies comparing the prevalence and clinical outcomes of COVID‐19 in patients with IBD and in the general population. We also compared the outcomes of patients receiving and not receiving 5‐aminosalicylates (ASA), tumour necrosis factor antagonists, biologics, systemic corticosteroids, or immunomodulators for IBD. Thirty five studies were eligible for our analysis. Pooled odds ratio of COVID‐19‐related hospitalisation, intensive care unit (ICU) admission, or death in IBD compared to in non‐IBD were 0.58 (95% confidence interval (CI) = 0.28–1.18), 1.09 (95% CI = 0.27–4.47), and 0.67 (95% CI = 0.32–1.42), respectively. Inflammatory bowel disease was not associated with increased hospitalisation, ICU admission, or death. Susceptibility to COVID‐19 did not increase with any drugs for IBD. Hospitalisation, ICU admission, and death were more likely with 5‐ASA and corticosteroid use. COVID‐19‐related hospitalisation (Odds Ratio (OR): 0.53; 95% CI = 0.38–0.74) and death (OR: 0.13; 95% CI = 0.13–0.70) were less likely with Crohn\'s disease than ulcerative colitis (UC). In conclusion, IBD does not increase the mortality and morbidity of COVID‐19. However, physicians should be aware that additional monitoring is needed in UC patients or in patients taking 5‐ASA or systemic corticosteroids.

The Omicron variant of concern has a high level of mutations in different genes that has raised awareness about the performance of immunological products such as vaccines and antigen detection kits. In this systematic review and meta‐analysis, we investigated whether Omicron had a significant influence on rapid antigen test (RAT) performance in comparison to PCR. We registered this systematic review and meta‐analysis in PROSPERO with the registration number CRD42022355510. We searched PubMed, Scopus, Embase, and Web of Science databases systematically to 1 August 2022. After article screening, we assessed the quality of the included studies based on the JBI checklist. Following data extraction, we performed a meta‐analysis using R software. We included 18 qualified articles presenting sufficient data about RATs performance in comparison to RT‐PCR in Omicron infections. The pooled specificity and sensitivity of RATs were 1.000 (0.997–1.000) and 0.671 (0.595–0.721), respectively. The FDA‐approved kits showed a better performance than WHO‐approved ones with a sensitivity of 0.728 (0.620–0.815). The use of RATs with nasal swabs showed a higher sensitivity compared with nasopharyngeal swabs. The sensitivity for samples with a CT‐value >25 was 0.108 (0.048–0.227). Rapid antigen tests show impaired performance for COVID‐19 diagnosis when the Omicron variant is circulating, particularly in samples with low viral loads.

SARS‐CoV‐2 causes multiorgan damage to vital organs and tissue that are known to be due to a combination of tissue tropisms and cytokine‐mediated damage that it can incite in COVID‐19. The effects of SARS‐Co‐2 on the lymphocytes and therefore on the immune response have attracted attention recently in COVID‐19 to understand its effects in causing a chronic state of ongoing infection with Long‐COVID. The associated lymphopaenia and autoimmune disease state, which is an apparent paradox, needs to be researched to dissect possible mechanisms underlying this state. This paper attempts to unravel the aforesaid immune paradox effects of SARS‐CoV‐2 on the lymphocytes and discusses appropriate treatment modalities with antiviral drugs and nutraceuticals which could prove virucidal in SARS‐CoV‐2 seeding monocytes and lymphocytes in patients with COVID‐19 and Long‐COVID. Importantly it proposes a new in vitro treatment modality of immune regulating cells that can help patients fight the lymphopaenia associated with COVID‐19 and Long‐COVID.

Currently approved therapies for COVID‐19 are mostly limited by their low availability, high costs or the requirement of parenteral administration by trained medical personnel in an in‐hospital setting. Quercetin is a cheap and easily accessible therapeutic option for COVID‐19 patients. However, it has not been evaluated in a systematic review until now. We aimed to conduct a meta‐analysis to assess the effect of quercetin on clinical outcomes in COVID‐19 patients. Various databases including PubMed, the Cochrane Library and Embase were searched from inception until 5 October 2022 and results from six randomized controlled trials (RCTs) were pooled using a random‐effects model. All analyses were conducted using RevMan 5.4 with odds ratio (OR) as the effect measure. Quercetin decreased the risk of intensive care unit admission (OR = 0.31; 95% confidence interval (CI) 0.10–0.99) and the incidence of hospitalisation (OR = 0.25; 95% CI 0.10–0.62) but did not decrease the risk of all‐cause mortality and the rate of no recovery. Quercetin may be of benefit in COVID‐19 patients, especially if administered in its phytosome formulation which greatly enhances its bioavailability but large‐scale RCTs are needed to confirm these findings.

Some proportions of populations, such as immunocompromised patients and organ transplant recipients might have inadequate immune responses to the vaccine for coronavirus disease 2019 (COVID‐19). For these groups of populations, administering monoclonal antibodies might offer some additional protection. This review sought to analyze the effectiveness and safety of tixagevimab‐cilgavimab (Evusheld) as pre‐exposure prophylaxis against COVID‐19. We used specific keywords to comprehensively search for potential studies on PubMed, Scopus, Europe PMC, and sources until 3 September 2022. We collected all published articles that analyzed tixagevimab‐cilgavimab on the course of COVID‐19. Review Manager 5.4 was utilized for statistical analysis. Six studies were included. Our pooled analysis revealed that tixagevimab‐cilgavimab prophylaxis may decrease the rate of SARS‐CoV‐2 infection (OR: 0.24; 95% CI: 0.15–0.40,  …

The Coronavirus disease‐2019 (COVID‐19) pandemic continues, and the death toll continues to surge. This meta‐analysis aimed to determine the efficacy of anakinra on mortality in patients with COVID‐19. A systematic search was made of PubMed, Embase, Cochrane Library, and clinicaltrials.gov, without language restrictions. Randomized controlled trials on treatment of COVID‐19 with anakinra, compared with placebo or blank, were reviewed. Studies were pooled to risk ratios (RRs), with 95% confidence intervals (CIs). Five Randomized controlled trials (enrolling 1859 participants) met the inclusion criteria. There was no statistically significant difference in 14‐day mortality (RR 0.78, 95% CI 0.43–1.39;  = 0.40), 28‐day mortality (RR 1.06, 95% CI 0.89–1.26;  = 0.51), and 90‐day mortality (RR 1.01, 95% CI 0.73–1.39;  = 0.97) between the two groups. Sensitivity analyses further confirmed these results. Anakinra was not associated with reduced mortality in hospitalised patients with COVID‐19. Anakinra probably should not be used routinely in COVID‐19 patients.

The COVID‐19 pandemic caused by severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) has led to a global health emergency. There are many similarities between SARS‐CoV‐2 and influenza A virus (IAV); both are single‐stranded RNA viruses infecting airway epithelial cells and have similar modes of replication and transmission. Like IAVs, SARS‐CoV‐2 infections poses serious challenges due to the lack of effective therapeutic interventions, frequent appearances of new strains of the virus, and development of drug resistance. New approaches to control these infectious agents may stem from cellular factors or pathways that directly or indirectly interact with viral proteins to enhance or inhibit virus replication. One of the emerging concepts is that host cellular factors and pathways are required for maintaining viral genome integrity, which is essential for viral replication. Although IAVs have been studied for several years and many cellular proteins involved in their replication and pathogenesis have been identified, very little is known about how SARS‐CoV‐2 hijacks host cellular proteins to promote their replication. IAV induces apoptotic cell death, mediated by the B‐cell lymphoma‐2 (Bcl‐2) family proteins in infected epithelia, and the pro‐apoptotic members of this family promotes viral replication by activating host cell proteases. This review compares the life cycle and mode of replication of IAV and SARS‐CoV‐2 and examines the potential roles of host cellular proteins, belonging to the Bcl‐2 family, in SARS‐CoV‐2 replication to provide future research directions.

Publication date: Available online 19 April 2023 Source: Immunity Author(s): Marios Koutsakos, Ali H. Ellebedy …