Reviews in Medical Virology最新文献

Emerging viral pathogens, newly reported or rapidly evolving viruses, are a significant public health concern worldwide. Beyond their characteristic clinical presentations, emerging viruses, such as monkeypox virus (MPXV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have been increasingly implicated in the development of various neuropsychiatric complications including depression, mainly due to their ability to induce neuroinflammation, immune dysfunction, and neurotransmitter imbalances. Depression is a common mental health condition characterised by continuous low mood or sadness, pessimism, anxiety, and even a tendency to suicide as the main symptoms. Post viral depression commonly shows significant challenges, as traditional antidepressant agents exhibit suboptimal efficacy and prolonged onset of action. Regarding this, ketamine and its enantiomers, S-ketamine and R-ketamine, have recently received increasing attention as potential options in light of their potent and effective antidepressant properties. The present review describes the underlying pathophysiological mechanisms of depression associated with emerging viruses, highlighting the role of neuroinflammation and disturbances inneurotransmitter systems. It also discusses the antidepressant mechanisms of ketamine and its enantiomers, the current clinical evidence demonstrating their effectiveness and safety, especially in the case of treatment-resistant depression, and their growing relevance for mood complications linked to emerging viral infections, including depression. Although preliminary reports propose effectiveness, additional studies are needed to present optimal treatment strategies, long-term safety, and incorporation into clinical practice. Addressing these challenges will be critical for optimising the effectiveness of ketamine- and (S, R)-ketamine-containing therapeutic protocols in treating depression linked to emerging viral infections.

Acute respiratory infections (ARIs) stand as a significant cause of morbidity and mortality among children worldwide, contributing substantially to paediatric hospitalisation rates. ARIs stem from various pathogens, including bacteria, viruses, among others. With the advent of novel diagnostic techniques like molecular detection methods, the identification rate of multiple pathogens in paediatric ARIs is steadily rising. However, there is currently no consensus on the impact of mixed infections on the severity of respiratory infections in children. This narrative review summarises existing research indicating that the co-detection rate of multiple viruses among paediatric patients with ARIs ranged from 0.07% to 55%. Multi-virus coinfections did not appear to increase the severity of the disease in children because of viral interference, immune modulation, etc. Conversely, mixed infection of virus and bacteria may exacerbate disease severity through many mechanisms, such as synergistic activation of inflammation, diminished repair efficiency, increased transmission and release and so on. The insights provide aim to improve diagnostic precision and treatment strategies for paediatric ARIs, ultimately reducing complications and mortality rates associated with ARIs in children.

We performed an update (last search: 24 July 2023) of a systematic review on relative efficacy/effectiveness (rVE) and safety of newer/enhanced seasonal influenza vaccines in comparison with standard influenza vaccine or in head-to-head comparison. Eligible studies investigated adults aged ≥ 18 years, analysed the MF59-adjuvanted or high-dose or cell-based or recombinant or mRNA-based influenza vaccine and reported rVE or safety in randomised controlled trials (RCT) or non-randomised studies of interventions (NRSI). Of 1561 new entries identified, 17 studies were included. Together with 42 studies identified in the previous primary review they added up to 59 studies, all comparing newer/enhanced with standard seasonal influenza vaccines. Relative VE against laboratory-confirmed influenza was -30% (95%CI: -146% to 31%) to 88% (51%-100%; 7 NRSI) for the MF59-adjuvanted vaccine (low certainty of evidence, CoE); 24.2% (9.7%-36.5%; 1 RCT) and -9% (-158% to 54%) to 19% (-27% to 48%; 1 NRSI) for the high-dose vaccine (moderate CoE); -5.8% (-36.1% to 17.7%) to 21.4% (-7.3% to 42.4%; 2 NRSI) for the cell-based vaccine (low CoE); 30% (10%-47%; 1 RCT) and 3% (-31% to 28%) to 19% (-27% to 48%; 1 NRSI) for the recombinant vaccine (moderate CoE), respectively. Relative VE against laboratory-confirmed influenza-related hospitalisation was 59.2% (14.6%-80.5%; 1 NRSI) for the MF59-adjuvanted (moderate CoE); 27% (-1 to 48%; 1 NRSI) for the high-dose (low CoE); 8.5% (-75.9% to 52.3%; 1 NRSI) for the cell-based (low CoE); -7.3% (-52.1% to 24.4%) to 16.3% (-8.7% to 35.5%; 1 RCT) for the recombinant vaccine. No increased risk of serious adverse events was detected for any vaccine (12 RCT, 7 NRSI; low CoE). While all have a favourable safety profile, evidence on rVE of newer/enhanced vaccines is still limited, warranting further studies.

Chandipura virus (CHPV) is a single-stranded negative-sense RNA virus of the family Rhabdoviridae. CHPV is transmitted mainly through infected sandflies. CHPV paediatric encephalitis reported in 2003-2004 in central and south-western parts of India had a case fatality rate of ∼70%. CHPV infection leads to high-grade fever, vomiting, altered sensorium, generalised convulsions, decerebrate posture and coma. Neuroinflammation is the hallmark of CHPV infection and has a pronounced effect on cerebral and brainstem regions. Currently, there are no vaccines or treatments available for CHPV infection. Although previous studies have provided insights into the virus's pathology and host-pathogen interactions, the precise molecular mechanisms underlying CHPV pathogenesis are poorly understood. Understanding molecular pathogenesis is crucial for developing efficacious therapies and preventive measures. The review summarises CHPV epidemiology, transmission, genome structure, replication, pathogenesis and the latest antiviral therapies and vaccine developments.

Dengue, a widespread arthropod-borne viral disease, remains endemic in more than 100 nations, affecting over 40% of the world's population, with millions of cases reported annually, and has a major burden on global public health systems. The causative agent of this infection is the dengue virus which belongs to the Flaviviridae family of RNA viruses. The DENV infection leads to a broad spectrum of clinical symptoms, ranging from mild to severe, and even fatal in the cases of secondary infection. In the absence of promising antiviral therapies or vaccines to effectively combat the infection, understanding the interaction between the host and pathogen, along with the associated molecular mechanisms, is crucial. In this review, we focused on the specialised functions of various RNA-binding proteins (RBPs) and their roles at various stages of the viral life cycle. This review examines the intricate interplay between viral and host cellular factors. Notably, numerous host RBPs, including La, eIF2, PTBP1, YBX1, and other hnRNPs, interact with viral components, such as NS2A, NS2B, NS3, NS4A, NS4B and NS5, and most importantly, the viral UTRs (untranslated regions), to facilitate critical stages of the viral life cycle. We comprehensively compiled the specific roles of RBPs in the dengue virus life cycle, including viral entry, translation, transcription, and assembly, and further explored the therapeutic possibilities.

Studies with strong scientific evidence have demonstrated that comorbidities are associated with fatal outcomes in patients with SARS-CoV-2 infection. To aggregate the findings of these studies and assess the magnitude of the effect of different chronic diseases on COVID-19 mortality, we conducted a systematic review of reviews and meta-analysis. Six databases were searched to retrieve systematic reviews with meta-analysis published during the early years of the pandemic. Statistical analysis was performed using Stata v.12.0 software, and the risk ratio (RR) and odds ratio (OR), with a confidence interval of 95% (95% CI), were calculated. We selected 15 publications with 476 original articles and 2,135,888 patients. Our results indicated the following risk factors for COVID-19 mortality: diabetes mellitus (RR = 1.95; 95% CI:1.41-2.49); hypertension (RR = 1.88; 95% CI:1.51-2.26); cancer (RR = 1.84; 95% CI:1.24-2.43); cardiovascular (RR = 2.14; 95% CI:1.66-2.63), cerebrovascular (RR = 2.43; 95% CI:2.15-2.72), kidney (RR = 2.39; 95% CI:1.36-3.42), pulmonary (RR = 1.98; 95% CI:1.48-2.47) and liver diseases (OR = 1.56; 95% CI:1.18-1.94); obesity (OR = 1.15; 95% CI:1.04-1.26); smoking habits (OR = 1.18; 95% CI:1.13-1.22); and the male sex (OR = 1.69; 95% CI:1.65-1.73). Evidence has confirmed that underlying chronic conditions, which involve an imbalance in the immune response, significantly increase the risk of COVID-19 deaths.

In 2024, a novel recombinant of the Oropouche virus emerged as a potential threat. This virus has caused a significant outbreak in Brazil and Cuba, with imported cases subsequently reported in the USA and Europe. This review summarises the existing knowledge on the Oropouche virus, and discusses potential risk mitigation strategies for the transfusion community.

In the initial stage of the COVID-19 pandemic, high case fatality was noted. The case fatality during this was associated with the cytokine storm (CS) or cytokine storm syndrome (CSS). Sometimes, virus infections are due to the excessive secretion of pro-inflammatory cytokines, leading to cytokine storms, which might be directed to ARDS, multi-organ failure, and death. However, it was noted that several miRNAs are involved in regulating cytokines during SARS-CoV-2 and other viruses such as IFNs, ILs, GM-CSF, TNF, etc. The article spotlighted several miRNAs involved in regulating cytokines associated with the cytokine storm caused by SARS-CoV-2 and other viruses (influenza virus, MERS-CoV, SARS-CoV, dengue virus). Targeting those miRNAs might help in the discovery of novel therapeutics, considering CS or CSS associated with different virus infections.

SARS-CoV-2 is an oral pathogen that infects and replicates in mucosal and salivary epithelial cells, contributing to oral post-acute sequelae COVID-19 (PASC) and other oral and non-oral pathologies. While pre-existing inflammatory oral diseases provides a conducive environment for the virus, acute infection and persistence of SARS-CoV-2 can also results in oral microbiome dysbiosis that further worsens poor oral mucosal health. Indeed, oral PASC includes periodontal diseases, dysgeusia, xerostomia, pharyngitis, oral keratoses, and pulpitis suggesting significant bacterial contributions to SARS-CoV-2 and oral tissue tropism. Dysbiotic microbiome-induced inflammation can promote viral entry via angiotensin-converting enzyme receptor-2 (ACE2), serine transmembrane TMPRSS2 and possibly other non-canonical pathways. Additionally, metabolites derived from a dysbiotic microbiome can alter the physiological and biochemical pathways related to the metabolism of lipids, carbohydrates, and amino acids. This may promote a pro-inflammatory microenvironment, leading to immune exhaustion, loss of tolerance, and susceptibility to a variety of oral pathogens, causing acute and later chronic inflammation. Microbial release of mimics of host metallopeptidases related to furin, ADAM17 (A disintegrin and metalloproteinase 17), and glycoprotein metabolites can further aid viral attachment to T cell immunoglobulin-like (TIMs), enhancing viral entry while simultaneously depressing oral mucosal immune resistance and clearance. Membrane reorganization characterised by neuroproteins, such as neuropilins, also functionally assists with SARS-CoV-2 entry and extends the pathogenesis of PASC from the oral cavity to the brain, gut, or other non-oral tissues. Thus, poor oral health, characterised by disrupted oral microbiomes can promote viral tropism, weaken antiviral resistance, and heightens susceptibility to SARS-CoV-2 infection. This immune dysfunction also increases the risk of additional viral infections, exacerbating oral conditions like periodontal and endodontic diseases. These persistent oral health issues can contribute to systemic inflammation, creating bidirectional effects between oral and non-oral tissues, potentially leading to Post-Acute Sequelae of COVID-19 (PASC).

Arboviral infections in paediatric populations present unique challenges due to distinct pathophysiological mechanisms influenced by developmental and immunological differences. Commonly implicated arboviruses include dengue virus (DENV), Zika virus (ZIKV), chikungunya virus (CHIKV), West Nile virus (WNV), and yellow fever virus (YFV). These viruses exhibit specific tropisms, targeting organs such as the central nervous system (CNS), liver, and vasculature. Immune responses in children, characterised by an underdeveloped adaptive system and enhanced innate immunity, can exacerbate inflammation and increase susceptibility to severe outcomes such as dengue hemorrhagic fever (DHF), congenital Zika syndrome (CZS), and neuroinvasive complications. Maternal antibodies, antibody-dependent enhancement (ADE), and immature barriers, such as the blood-brain barrier, further contribute to disease severity. This review highlights the virological and immunological nuances of arboviral pathophysiology in paediatric patients, emphasising the need for age-specific diagnostic, therapeutic, and preventive strategies to mitigate the burden of these infections.