世界病毒学杂志(英文版)最新文献

The coronavirus disease 2019 (COVID-19) pandemic caused by the novel beta coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) crippled the whole world and has resulted in large number of morbidity and mortality. The origin of the SARS-CoV-2 is still disputed. The risk of infection with SARS-CoV-2 is dependent on several risk factors as observed in many studies. The severity of the disease depends on many factors including the viral strain, host immunogenetics, environmental factors, host genetics, host nutritional status and presence of comorbidities like hypertension, diabetes, Chronic Obstructive Pulmonary Disease, cardiovascular disease, renal impairment. Diabetes is a metabolic disorder mainly characterized by hyperglycemia. Diabetic individuals are intrinsically prone to infections. SARS-CoV-2 infection in patients with diabetes result in β-cell damage and cytokine storm. Damage to the cells impairs the equilibrium of glucose, leading to hyperglycemia. The ensuing cytokine storm causes insulin resistance, especially in the muscles and liver, which also causes a hyperglycemic state. All of these increase the severity of COVID-19. Genetics also play pivotal role in disease pathogenesis. This review article focuses from the probable sources of coronaviruses and SARS-CoV-2 to its impacts on individuals with diabetes and host genetics in pre- and post-pandemic era.

Viral gastroenteritis is the most common viral illness that affects the gastrointestinal (GI) tract, causing inflammation and irritation of the lining of the stomach and intestines. Common signs and symptoms associated with this condition include abdominal pain, diarrhea, and dehydration. The infections commonly involved in viral gastroenteritis are rotavirus, norovirus, and adenovirus, which spread through the fecal-oral and contact routes and cause non-bloody diarrhea. These infections can affect both immunocompetent and immunocompromised individuals. Since the pandemic in 2019, coronavirus gastroenteritis has increased in incidence and prevalence. Morbidity and mortality rates from viral gastroenteritis have declined significantly over the years due to early recognition, treatment with oral rehydration salts, and prompt vaccination. Improved sanitation measures have also played a key role in reducing the transmission of infection. In addition to viral hepatitis causing liver disease, herpes virus, and cytomegalovirus are responsible for ulcerative GI disease. They are associated with bloody diarrhea and commonly occur in im-munocompromised individuals. Hepatitis viruses, Epstein-Barr virus, herpesvirus 8, and human papillomavirus have been involved in benign and malignant diseases. This mini review aims to list different viruses affecting the GI tract. It will cover common symptoms aiding in diagnosis and various important aspects of each viral infection that can aid diagnosis and management. This will help primary care physicians and hospitalists diagnose and treat patients more easily.

Background: Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). HBV DNA can get integrated into the hepatocyte genome to promote carcinogenesis. However, the precise mechanism by which the integrated HBV genome promotes HCC has not been elucidated.

Aim: To analyze the features of HBV integration in HCC using a new reference database and integration detection method.

Methods: Published data, consisting of 426 Liver tumor samples and 426 paired adjacent non-tumor samples, were re-analyzed to identify the integration sites. Genome Reference Consortium Human Build 38 (GRCh38) and Telomere-to-Telomere Consortium CHM13 (T2T-CHM13 (v2.0)) were used as the human reference genomes. In contrast, human genome 19 (hg19) was used in the original study. In addition, GRIDSS VIRUSBreakend was used to detect HBV integration sites, whereas high-throughput viral integration detection (HIVID) was applied in the original study (HIVID-hg19).

Results: A total of 5361 integration sites were detected using T2T-CHM13. In the tumor samples, integration hotspots in the cancer driver genes, such as TERT and KMT2B, were consistent with those in the original study. GRIDSS VIRUSBreakend detected integrations in more samples than by HIVID-hg19. Enrichment of integration was observed at chromosome 11q13.3, including the CCND1 pro-moter, in tumor samples. Recurrent integration sites were observed in mitochondrial genes.

Conclusion: GRIDSS VIRUSBreakend using T2T-CHM13 is accurate and sensitive in detecting HBV integration. Re-analysis provides new insights into the regions of HBV integration and their potential roles in HCC development.

Autism spectrum disorder (ASD) is a group of heterogeneous, multi-factorial, neurodevelopmental disorders resulting from genetic and environmental factors interplay. Infection is a significant trigger of autism, especially during the critical developmental period. There is a strong interplay between the viral infection as a trigger and a result of ASD. We aim to highlight the mutual relationship between autism and viruses. We performed a thorough literature review and included 158 research in this review. Most of the literature agreed on the possible effects of the viral infection during the critical period of development on the risk of developing autism, especially for specific viral infections such as Rubella, Cytomegalovirus, Herpes Simplex virus, Varicella Zoster Virus, Influenza virus, Zika virus, and severe acute respiratory syndrome coronavirus 2. Viral infection directly infects the brain, triggers immune activation, induces epigenetic changes, and raises the risks of having a child with autism. At the same time, there is some evidence of increased risk of infection, including viral infections in children with autism, due to lots of factors. There is an increased risk of developing autism with a specific viral infection during the early developmental period and an increased risk of viral infections in children with autism. In addition, children with autism are at increased risk of infection, including viruses. Every effort should be made to prevent maternal and early-life infections and reduce the risk of autism. Immune modulation of children with autism should be considered to reduce the risk of infection.

The main etiopathogenic theories of long coronavirus disease (COVID) are listed and a conjunction of them is carried out with the objective of deciphering the pathophysiology of the entity, finally the main lines of treatment existing in real life are discussed (Paxlovid, use of antibiotics in dysbiosis, triple anticoagulant therapy, temelimab).

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been a major challenge to be faced in recent years. While adults suffered the highest morbidity and mortality rates of coronavirus disease 2019, children were thought to be exclusively asymptomatic or to present with mild conditions. However, around April 2020, there was an outbreak of a new clinical syndrome related to SARS-CoV-2 in children - multisystemic inflammatory syndrome in children (MIS-C) - which comprises a severe and uncon-trolled hyperinflammatory response with multiorgan involvement. The Centers for Disease Control and Prevention considers a suspected case of MIS-C an individual aged < 21 years presenting with fever, high inflammatory markers levels, and evidence of clinically severe illness, with multisystem (> 2) organ involvement, no alternative plausible diagnoses, and positive for recent SARS-CoV-2 infection. Despite its severity, there are no definitive disease management guidelines for this condition. Conversely, the complex pathogenesis of MIS-C is still not completely understood, although it seems to rely upon immune dysregulation. Hence, in this study, we aim to bring together current evidence regarding the pathogenic mechanisms of MIS-C, clinical picture and management, in order to provide insights for clinical practice and implications for future research directions.

The relationship between coronavirus disease-19 (COVID-19) and cardiovascular diseases has been an important issue. Therefore, cardiac biomarkers and cardiac imaging have an important place in the diagnostic phase. It is important to know the relationship of biomarkers in COVID-19 so that we can understand the diagnosis of the disease, the predicted course and results after diagnosis.

Liver injury secondary to vaccination is a rare adverse event that has recently come under attention thanks to the continuous pharmacovigilance following the widespread implementation of coronavirus disease 2019 (COVID-19) vaccination protocols. All three most widely distributed severe acute respiratory syndrome coronavirus 2 vaccine formulations, e.g., BNT162b2, mRNA-1273, and ChAdOx1-S, can induce liver injury that may involve immune-mediated pathways and result in autoimmune hepatitis-like presentation that may require therapeutic intervention in the form of corticosteroid administration. Various mechanisms have been proposed in an attempt to highlight immune checkpoint inhibition and thus establish causality with vaccination. The autoimmune features of such a reaction also prompt an in-depth investigation of the newly employed vaccine technologies. Novel vaccine delivery platforms, e.g., mRNA-containing lipid nanoparticles and adenoviral vectors, contribute to the inflammatory background that leads to an exaggerated immune response, while patterns of molecular mimicry between the spike (S) protein and prominent liver antigens may account for the autoimmune presentation. Immune mediators triggered by vaccination or vaccine ingredients per se, including autoreactive antibodies, cytokines, and cytotoxic T-cell populations, may inflict hepatocellular damage through well-established pathways. We aim to review available data associated with immune-mediated liver injury associated with COVID-19 vaccination and elucidate potential mechanisms underlying its pathogenesis.

The intestinal lumen harbors a diverse consortium of microorganisms that participate in reciprocal crosstalk with intestinal immune cells and with epithelial and endothelial cells, forming a multi-layered barrier that enables the efficient absorption of nutrients without an excessive influx of pathogens. Despite being a lung-centered disease, severe coronavirus disease 2019 (COVID-19) affects multiple systems, including the gastrointestinal tract and the pertinent gut barrier function. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can inflict either direct cytopathic injury to intestinal epithelial and endothelial cells or indirect immune-mediated damage. Alternatively, SARS-CoV-2 undermines the structural integrity of the barrier by modifying the expression of tight junction proteins. In addition, SARS-CoV-2 induces profound alterations to the intestinal microflora at phylogenetic and metabolomic levels (dysbiosis) that are accompanied by disruption of local immune responses. The ensuing dysregulation of the gut-lung axis impairs the ability of the respiratory immune system to elicit robust and timely responses to restrict viral infection. The intestinal vasculature is vulnerable to SARS-CoV-2-induced endothelial injury, which simultaneously triggers the activation of the innate immune and coagulation systems, a condition referred to as "immunothrombosis" that drives severe thrombotic complications. Finally, increased intestinal permeability allows an aberrant dissemination of bacteria, fungi, and endotoxin into the systemic circulation and contributes, to a certain degree, to the over-exuberant immune responses and hyper-inflammation that dictate the severe form of COVID-19. In this review, we aim to elucidate SARS-CoV-2-mediated effects on gut barrier homeostasis and their implications on the progression of the disease.

Background: Understanding the transmission dynamics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection among healthcare workers (HCWs) and their social contacts is crucial to plan appropriate risk-reduction measures.

Aim: To analyze the socio-demographic risk factors and transmission of SARS-CoV-2 infection among HCWs in two tertiary care hospitals in Dubai, United Arab Emirates.

Methods: The demographic and clinical characteristics were available for all HCWs in both facilities from the human resources department. A cross-sectional survey was conducted from January-April 2022 among HCWs who tested positive through Reverse Transcriptase Polymerase Chain Reaction of the nasopharyngeal swab for SARS-CoV-2 between March 2020 and August 2021 in two tertiary-level hospitals. The survey included questions on demographics, work profile, characteristics of coronavirus disease 2019 (COVID-19), and infection among their household or co-workers. The survey also checked the knowledge and perception of participants on the infection prevention measures related to SARS-CoV-2.

Results: Out of a total of 346 HCWs infected with SARS-CoV-2, 286 (82.7%) HCWs consented to participate in this study. From the sample population, 150 (52.5%) of participants were female, and a majority (230, 80.4%) were frontline HCWs, including 121 nurses (121, 42.4%). Only 48 (16.8%) participants were fully vaccinated at the time of infection. Most infected HCWs (85%) were unaware of any unprotected exposure and were symptomatic at the time of testing (225, 78.7%). Nearly half of the participants (140, 49%) had co-infection among household, and nearly one-third (29.5%) had co-infection among three or more household. Another 108 (37.8%) participants reported cross-infection among co-workers. The frontline HCWs were significantly more infected (25.1% vs 8.6%, P < 0.001) compared to non-frontline HCWs. Another significant risk factor for a high infection rate was male sex (P < 0.001). Among the infected frontline HCWs, a significantly higher proportion were male and shared accommodation with family (P < 0.001). COVID-19 vaccination significantly reduced the infection rate (83.2% vs 16.8, P < 0.001) among HCWs. Most participants (99.3%) were aware about importance of appropriate use of personal protective equipment. However, only 70% agreed with the efficacy of the COVID-19 vaccination in preventing an infection and severe disease.

Conclusion: The risk profiling of the HCWs infected with SARS-CoV-2 found that working at frontline and being male increase the rate of infection. COVID-19 vaccination can effectively reduce the rate of transmission of SARS-CoV-2 among HCWs.