世界病毒学杂志(英文版)最新文献

Background: Cholangiocarcinoma is the second most common primary liver malignancy. Its incidence and mortality rates have been increasing in recent years. Hepatitis C virus (HCV) infection is a risk factor for development of cirrhosis and cholangiocarcinoma. Currently, surgical resection remains the only curative treatment option for cholangiocarcinoma. We aim to study the impact of HCV infection on outcomes of liver resection (LR) in intrahepatic cholangiocarcinoma (ICC).

Aim: To study the outcomes of curative resection of ICC in patients with HCV (i.e., HCV+) compared to patients without HCV (i.e., HCV-).

Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) and observational studies to assess the outcomes of LR in ICC in HCV+ patients compared to HCV- patients in tertiary care hospitals. PubMed, EMBASE, The Cochrane Library and Scopus were systematically searched from inception till August 2023. Included studies were RCTs and non-RCTs on patients ≥ 18 years old with a diagnosis of ICC who underwent LR, and compared outcomes between patients with HCV+ vs HCV-. The primary outcomes were overall survival (OS) and recurrence-free survival. Secondary outcomes include perioperative mortality, operation duration, blood loss, intrahepatic and extrahepatic recurrence.

Results: Seven articles, published between 2004 and 2021, fulfilled the selection criteria. All of the studies were retrospective studies. Age, incidence of male patients, albumin, bilirubin, platelets, tumor size, incidence of multiple tumors, vascular invasion, bile duct invasion, lymph node metastases, and stage 4 disease were comparable between HCV+ and HCV- group. Alanine transaminase [MD 22.20, 95%confidence interval (CI): 13.75, 30.65, P < 0.00001] and aspartate transaminase levels (MD 27.27, 95%CI: 20.20, 34.34, P < 0.00001) were significantly higher in HCV+ group compared to HCV- group. Incidence of cirrhosis was significantly higher in HCV+ group [odds ratio (OR) 5.78, 95%CI: 1.38, 24.14, P = 0.02] compared to HCV- group. Incidence of poorly differentiated disease was significantly higher in HCV+ group (OR 2.55, 95%CI: 1.34, 4.82, P = 0.004) compared to HCV- group. Incidence of simultaneous hepatocellular carcinoma lesions was significantly higher in HCV+ group (OR 8.31, 95%CI: 2.36, 29.26, P = 0.001) compared to HCV- group. OS was significantly worse in the HCV+ group (hazard ratio 2.05, 95%CI: 1.46, 2.88, P < 0.0001) compared to HCV- group.

Conclusion: This meta-analysis demonstrated significantly worse OS in HCV+ patients with ICC who underwent curative resection compared to HCV- patients.

Background: Alcohol-associated cirrhosis (AC) contributes to significant liver-related mortality in the United States. It is known to cause immune dysfunction and coagulation abnormalities. Patients with comorbid conditions like AC are at risk of worse clinical outcomes from coronavirus disease 2019 (COVID-19). The specific association between AC and COVID-19 mortality remains inconclusive, given the lack of robust clinical evidence from prior studies.

Aim: To study the predictors of mortality and the outcomes of AC in patients hospitalized with COVID-19 in the United States.

Methods: We conducted a retrospective cohort study using the National Inpatient Sample (NIS) database 2020. Patients were identified with primary COVID-19 hospitalizations based on an underlying diagnosis of AC. A matched comparison cohort of COVID-19 patients without AC was identified after 1:N propensity score matching based on baseline sociodemographic characteristics and Elixhauser comorbidities. Primary outcomes included median length of stay, median inpatient charges, and in-hospital mortality. Secondary outcomes included a prevalence of systemic complications.

Results: A total of 1325 COVID-19 patients with AC were matched to 1135 patients without AC. There was no difference in median length of stay and hospital charges in COVID-19 patients with AC compared to non-AC (P > 0.05). There was an increased prevalence of septic shock (5.7% vs 4.1%), ventricular fibrillation/ventricular flutter (0.4% vs 0%), atrial fibrillation (13.2% vs 8.8%), atrial flutter (8.7% vs 4.4%), first-degree atrioventricular nodal block (0.8% vs 0%), upper extremity venous thromboembolism (1.5% vs 0%), and variceal bleeding (3.8% vs 0%) in the AC cohort compared to the non-AC cohort (P < 0.05). There was no difference in inpatient mortality in COVID-19 patients with non-AC compared to AC, with an odds ratio of 0.97 (95% confidence interval: 0.78-1.22, P = 0.85). Predictors of mortality included advanced age, cardiac arrhythmias, coagulopathy, protein-calorie malnutrition, fluid and electrolyte disorders, septic shock, and upper extremity venous thromboembolism.

Conclusion: AC does not increase mortality in patients hospitalized with COVID-19. There is an increased association between inpatient complications among COVID-19 patients with AC compared to non-AC.

Background: Hepatitis B virus (HBV) and hepatitis C virus (HCV) viral load (VL) estimation is essential for the management of both HBV and HCV infections. Due to a longer turnaround time for VL estimation, many patients drop out from the cascade of care. To achieve the global goals of reducing morbidity and mortality due to HBV/HCV and moving towards their elimination by 2030, molecular diagnostic platforms with faster and random (i.e. single sample) access are needed.

Aim: To evaluate the performance of the recently launched NeuMoDx 96 random access system with the conventional COBAS^®AmpliPrep/COBAS TaqMan system for HBV and HCV VL estimation.

Methods: Archived once-thawed plasma samples were retrieved and tested on both platforms. Correlation between the assays was determined by linear regression and Bland-Altman analysis. The study included samples from 186 patients, 99 for HBV of which 49 were true infected HBV cases (hepatitis B surface antigen, anti-hepatitis B core antibody, and HBV DNA-positive) and 87 for HCV assay in which 39 were true positives for HCV infection (anti-HCV and HCV RNA-positive).

Results: The median VL detected by NeuMoDx for HBV was 2.9 (interquartile range [IQR]: 2.0-4.3) log₁₀ IU/mL and by COBAS it was 3.70 (IQR: 2.28-4.56) log₁₀ IU/mL, with excellent correlation (R² = 0.98). In HCV, the median VL detected by NeuMoDx was 4.9 (IQR: 4.2-5.4) log₁₀ IU/mL and by COBAS it was 5.10 (IQR: 4.07-5.80) log₁₀ IU/mL with good correlation (R² = 0.96).

Conclusion: The overall concordance between both the systems was 100% for both HBV and HCV VL estimation. Moreover, no genotype-specific bias for HBV/HCV VL quantification was seen in both the systems. Our findings reveal that NeuMoDx HBV and HCV quantitative assays have shown overall good clinical performance and provide faster results with 100% sensitivity and specificity compared to the COBAS AmpliPrep/COBAS TaqMan system.

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.