Current opinion in virology最新文献

The 2013–2016 Ebola virus disease epidemic and the coronavirus disease 2019 pandemic galvanized tremendous growth in models for emerging zoonotic and vector-borne viruses. Therefore, we have reviewed the main goals and methods of models to guide scientists and decision-makers. The elements of models for emerging viruses vary across spectrums: from understanding the past to forecasting the future, using data across space and time, and using statistical versus mechanistic methods. Hybrid/ensemble models and artificial intelligence offer new opportunities for modeling. Despite this progress, challenges remain in translating models into actionable decisions, particularly in areas at highest risk for viral disease outbreaks. To address this issue, we must identify gaps in models for specific viruses, strengthen validation, and involve policymakers in model development.

The koala retrovirus, KoRV, is one of the few models for understanding the health consequences of retroviral colonization of the germline. Such colonization events transition exogenous infectious retroviruses to Mendelian traits or endogenous retroviruses (ERVs). KoRV is currently in a transitional state from exogenous retrovirus to ERV, which in koalas (Phascolarctos cinereus) has been associated with strongly elevated levels of neoplasia. In this review, we describe what is currently known about the associations and underlying mechanisms of KoRV-induced neoplasia.

Oncogenic viruses play a pivotal role in oncology due to their unique role in unraveling the complexities of cancer development. Understanding the role viruses play in specific cancers is important to provide basic insights into the transformation process, which will help identify potential cellular targets for treatment. This review discusses the diverse role of animal herpesviruses in initiating and promoting various forms of cancer. We will summarize the mechanisms that underlie the development of animal herpesvirus-induced cancer that may provide a basis for developing potential therapeutic interventions or preventative strategies in the future.

Chronic hepatitis C virus (HCV) infection is a major cause of hepatic fibrosis and cirrhosis, with a risk for the development of hepatocellular carcinoma (HCC). Although highly effective direct-acting antivirals (DAAs) are available, the incidence, morbidity, and mortality of HCV-associated HCC are still high. This article reviews the current knowledge of the mechanisms of HCV-induced carcinogenesis with a special focus on those processes that continue after virus clearance and outlines implications for patient surveillance after DAA treatment.

Oncogenic viruses contribute to 15% of global human cancers. To achieve that, virus-encoded oncoproteins deregulate cellular transcription, antagonize common cellular pathways, and thus drive cell transformation. Notably, adenoviruses were the first human viruses proven to induce cancers in diverse animal models. Over the past decades, human adenovirus (HAdV)-mediated oncogenic transformation has been pivotal in deciphering underlying molecular mechanisms. Key adenovirus oncoproteins, encoded in early regions 1 (E1) and 4 (E4), co-ordinate these processes. Among the different adenovirus species, the most extensively studied HAdV-C5 displays lower oncogenicity than HAdV-A12. A complete understanding of the different HAdV-A12 and HAdV-C5 oncoproteins in virus-mediated cell transformation, as summarized here, is relevant for adenovirus research and offers broader insights into viral transformation and oncogenesis.

Mucosal-associated invariant T (MAIT) cells are an unconventional T cell population that are highly abundant in humans. They possess a semi-invariant T cell receptor (TCR) that recognises microbial metabolites formed during riboflavin biosynthesis, presented on a nonpolymorphic MHC-like molecule MR1. MAIT cells possess an array of effector functions, including type 1, type 17, and tissue repair activity. Deployment of these functions depends on the stimuli they receive through their TCR and/or cytokine receptors. Strong cytokine signalling, such as in response to vaccination, can bypass TCR triggering and provokes a strong proinflammatory response. Although data are still emerging, multiple aspects of MAIT cell biology are associated with modulation of immunity induced by the coronavirus disease 2019 mRNA and adenovirus vector vaccines. In this review, we will address how MAIT cells may play a role in immunogenicity of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and how these cells can be harnessed as cellular adjuvants.

Viral infections, including those affecting the respiratory tract, can alter the composition of the intestinal microbiota, which, in turn, can significantly influence both innate and adaptive immune responses, resulting in either enhanced pathogen clearance or exacerbation of the infection, possibly leading to inflammatory complications. A deeper understanding of the interplay between the intestinal microbiota and host immune responses in the context of respiratory viral infections (i.e. the gut–lung axis) is necessary to develop new treatments. This review highlights key mechanisms by which the intestinal microbiota, including its metabolites, can act locally or at distant organs to combat respiratory viruses. Therapeutics aimed at harnessing the microbiota to prevent and/or help treat respiratory viral infections represent a promising avenue for future investigation.

Virus infection activates specific pattern recognition receptors and immune signal transduction, resulting in pro-inflammatory cytokine production and activation of innate immunity. We describe here the molecular organization of early signaling pathways downstream of viral recognition, including conformational changes, post-translational modifications, formation of oligomers, and generation of small-molecule second messengers. Such molecular organization allows tight regulation of immune signal transduction, characterized by swift but transient responses, nonlinearity, and signal amplification. Pathologies of early immune signaling caused by genomic mutations illustrate the fine regulation of the immune transduction cascade.

Bacille Calmette-Guérin (BCG) remains the sole licensed vaccine against tuberculosis (TB), despite its variable efficacy in protecting against pulmonary TB. The development of effective TB vaccines faces significant challenges, marked by the absence of validated correlates of protection and predictive animal models. Strategic approaches to enhance TB vaccines and augment BCG efficacy include utilising prime-boost strategies with viral-vectored vaccines and exploring innovative delivery techniques, such as mucosal vaccine administration. Viral vectors offer numerous advantages, including the capacity to accommodate genes encoding extensive antigenic fragments and the induction of robust immune responses. Aerosol delivery aligns with the route of Mycobacterium tuberculosis infection and holds the potential to enhance protective mucosal immunity. Aerosolised viral-vectored vaccines overcome anti-vector immunity, facilitating repeated aerosol deliveries.