Reviews in Medical Virology最新文献

Respiratory syncytial virus (RSV) represents a significant burden on older adults (aged ≥ 50 years) globally and can lead to acute respiratory tract infections with substantial morbidity and mortality. However, there is a significant gap in knowledge regarding RSV infection in older adults, particularly in the Asia-Pacific region. This knowledge gap underscores the need for targeted and comprehensive studies to fully understand the nuanced epidemiology of RSV in ageing populations. This review synthesises data from various countries, emphasising the impact of RSV on older populations in the Asia-Pacific region. The overall proportions of RSV-related ARIs among older patients ranged from 0.2% to 5.6%. Among older adult patients with CAP, RSV accounted for 1.1%-10.3% of cases. However, it is crucial to note that the diversity in reported percentages highlights the influence of factors such as geographic location, health care settings and diagnostic practices. The most common symptoms observed in older adults with RSV infection were cough, sputum production and fever, followed by dyspnoea, sore throat and rhinorrhoea. Most of the old adults with RSV infection had underlying diseases, and RSV can cause significant morbidity and mortality in old adults. Treatment of RSV infections predominantly involve supportive care, with aerosolised ribavirin reserved for severe cases, especially immunocompromised patients. Emerging antiviral agents, including fusion and nucleoprotein inhibitors, offer promising avenues for future therapeutics. The recent approval of the bivalent RSV prefusion F protein-based vaccine for individuals aged 60 and older represents a milestone in preventive strategies. In conclusion, RSV infection remains a significant threat to older adults in the Asia-Pacific region, necessitating ongoing research and surveillance efforts. The recent vaccine approval marks a positive milestone, but further studies are crucial for refining prevention and treatment approaches.

Infertility affects approximately one-sixth of couples worldwide, with male factors contributing to half of all cases. However, infections, particularly those of reproductive tract, are increasingly recognized as important contributors to male infertility. Therefore, in this meta-analysis, we focused on the impact of various viral infections on male infertility. We searched PubMed, Embase, Web of Science and Cochrane Library on 20 October 2023. And included 135 studies involving 30,298 men of reproductive age. We found that the human papilloma virus (HPV)-infected group had a significantly higher DNA fragmentation index (DFI) than the non-infected group, with a mean difference (MD) of 5.64 (95% CI: 3.74-7.54). Conversely, the HPV-infected group had significantly lower sperm count, concentration, viability and normal morphology. Other viruses that affect semen quality include hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). HBV significantly decreased fertilization rate, with an odds ratio (OR) of 0.86 (95% CI: 0.76-0.99). HPV associated with lower clinical pregnancy rate (OR: 0.31 [95% CI: 0.16-0.62]) and higher miscarriage rate (OR: 5.28 [95% CI: 2.02-13.78]). Additionally, the fertility treatment group had a significantly higher rate of HPV infection (OR: 1.85 [95% CI: 1.10-3.12]) and adeno-associated virus (AAV) infection (OR: 8.49 [95% CI: 2.66-27.10]) than the fertility group. Conclusively, most viral infections affect semen quality, while HBV and HPV may affect assisted reproductive technology (ART) outcomes. HPV and AAV are risk factors for infertility.

The World Health Organisation has set targets of reducing the transmission of new hepatitis C (HCV) infections by 90%, and ending human immunodeficiency virus-1 (HIV) as a public health threat, by 2030. To achieve this, efficient and timely viral surveillance, and effective public health interventions, are required. Traditional epidemiological methods are largely dependent on the recognition of incident cases with symptomatic illness; acute HIV and HCV infections are commonly asymptomatic, which may lead to delays in the recognition of such new infections. Instead, for these viruses, molecular epidemiology may improve the detection of, and response to, clusters of viral transmission. Molecular epidemiology using historical datasets has highlighted key populations that may have benefitted from a timely intervention. Similar analyses performed on contemporary samples are needed to underpin the 2030 targets, but this requires the generation of a cohesive dataset of viral genome sequences in near-real-time. To generate such data, methodologies harnessing next-generation sequencing (NGS) should be utilised. Here we discuss the opportunity presented by NGS for public health surveillance of HIV and HCV, and discuss three methods that can generate sequences for such analysis. These include full-length genome amplification, utilised for analysis of HCV in the research space; tiling PCR, which was the method of choice for many diagnostic laboratories in the SARS-CoV-2 pandemic; and bait-capture hybridisation, which has been utilised in local HIV outbreaks. These techniques could be applied for near-real-time HIV and HCV surveillance, informing public health strategies that will be key to achieving 2030 targets.

The persistent challenge posed by viruses that infect the central nervous system lies in their sophisticated ability to evade the host immune system. This review explores into the complex mechanisms of immune evasion employed by these neurotropic viruses, focussing on their modulation of host immune responses, evasion of adaptive immunity, and the cellular and molecular strategies that enable their persistence. Key areas explored include viral latency and reactivation, the inhibition of apoptosis, and antigenic variation, with a detailed examination of viral proteins and their interactions with host cellular processes.

Viral myocarditis, characterised by inflammation of the heart muscle, presents a significant challenge to global public health, particularly affecting younger individuals and often progressing to dilated cardiomyopathy (DCM), a leading cause of heart failure. Despite ongoing research efforts, viable treatments for this condition remain elusive. Recent studies have shed light on the complex interplay between the innate immune response and autophagy mechanisms, revealing their pivotal roles in the pathogenesis of viral myocarditis and subsequent DCM development. This review aims to delve into the recent advancements in understanding the molecular mechanisms and pathways that intersect innate immunity and autophagy in the context of viral myocarditis. Furthermore, it explores the potential therapeutic implications of these findings, offering insights into promising avenues for the management and treatment of this debilitating condition.

Several Flaviviridae constitute an emerging threat to global health because of their continuing spread and the expansion of vector habitats, largely driven by climate change and intensified global travel. Infections can result in severe neurological or visceral pathologies. The relationship between oxidative stress (OS), an imbalance between generated reactive oxygen species and the antioxidant defences of the host, and flavivirus infection has been repeatedly demonstrated in in vitro and animal studies, but measuring biomarkers of oxidative stress in vivo could prove useful in clinical patient management. We summarise the knowledge and prospects of measuring peripheral OS biomarker levels for clinical case management and correlation with disease severity in six important human flavivirus infections (dengue virus (DENV), Japanese encephalitis virus, West Nile virus (WNV), tick-borne encephalitis virus (TBEV), yellow fever virus and zika virus). We searched the Medline and Web of Science databases for 'Oxidative Stress' AND 'Biomarkers' AND 'Flavivirus', combined with 'clinical', 'in vivo/in vivo', 'patient' and/or 'disease' and included 43 peer-reviewed publications. Correlation between OS and infection has been studied in all six Flaviviridae, but most clinically relevant data are available for DENV, TBEV and WNV. Plasma protein carbonyls, glutathione peroxidase activity and nitrogen monoxide are promising prognostic markers, but their measurement would benefit from methodological harmonisation. Future studies should investigate a broad range of OS biomarkers as predictors of clinically relevant outcomes. We advocate the validation and use of universal or disease-specific oxidative stress indexes that incorporate the most significant outcomes into one, easy-to-use clinical determinant.

Human parainfluenza virus type 2 (hPIV2), one of the causative agents of infantile common cold, is a non-segmented negative-sense RNA virus with a robust gene expression system. It infects recurrently throughout human life without causing severe disease. Because hPIV2 has a viral envelope that can carry ectopic proteins, we developed a non-propagative RNA/protein-carrying vector BC-PIV by deleting the F gene from hPIV2. BC-PIV can be vigorously proliferated in the stable packaging cell line Vero/BC-F cells expressing the hPIV2 F gene but not in other cells. BC-PIV can deliver exogenous gene(s) on a multigenic RNA genome as an inserted gene fragment(s) and simultaneously deliver exogenous protein(s) on its envelope in a membrane-anchored form. For example, influenza virus M2e protein, Ebola virus GP protein, and severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) spike protein were shown to be highly expressed in packaging cells and incorporated into the virion. The Ebola virus GP protein and SARS-CoV-2 spike protein, each delivered via BC-PIV, efficiently induced neutralising antibodies against each virus, even after prior treatment with recombinant BC-PIV in mice and hamsters, respectively. In this review, we describe the properties of BC-PIV as a promising vaccine vector, and also demonstrate its application as an anti-tumour virus.

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019 triggered a swift global spread, leading to a devastating pandemic. Alarmingly, approximately one in four individuals diagnosed with coronavirus disease 2019 (COVID-19) experience varying degrees of cognitive impairment, raising concerns about a potential increase in neurological sequelae cases. Neuroinflammation seems to be the key pathophysiological hallmark linking mild respiratory COVID-19 to cognitive impairment, fatigue, and neurological sequelae in COVID-19 patients, highlighting the interaction between the nervous and immune systems following SARS-CoV-2 infection. Several hypotheses have been proposed to explain how the virus disrupts physiological pathways to trigger inflammation within the CNS, potentially leading to neuronal damage. These include neuroinvasion, systemic inflammation, disruption of the lung and gut-brain axes, and reactivation of latent viruses. This review explores the potential origins of neuroinflammation and the underlying neuroimmune cross-talk, highlighting important unanswered questions in the field. Addressing these fundamental issues could enhance our understanding of the virus's impact on the CNS and inform strategies to mitigate its detrimental effects.