Annual Review of Virology最新文献

Bacteriophages are enigmatic entities that defy definition. Classically, they are specialist viruses that exclusively parasitize bacterial hosts. Yet this definition becomes limiting when we consider their ubiquity in the body coupled with their vast capacity to directly interact with the mammalian host. While phages certainly do not infect nor replicate within mammalian cells, they do interact with and gain unfettered access to the eukaryotic cell structure. With the growing appreciation for the human virome, coupled with our increased application of phages to patients within clinical settings, the potential impact of phage-mammalian interactions is progressively recognized. In this review, we provide a detailed mechanistic overview of how phages interact with the mammalian cell surface, the processes through which said phages are internalized by the cell, and the intracellular processing and fate of the phages. We then summarize the current state-of-the-field with respect to phage-mammalian interactions and their associations with health and disease states.

Respiratory viruses, such as influenza viruses, cause significant morbidity and mortality worldwide through seasonal epidemics and sporadic pandemics. Influenza viruses transmit through multiple modes including contact (either direct or through a contaminated surface) and inhalation of expelled aerosols. Successful human to human transmission requires an infected donor who expels virus into the environment, a susceptible recipient, and persistence of the expelled virus within the environment. The relative efficiency of each mode can be altered by viral features, environmental parameters, donor and recipient host characteristics, and viral persistence. Interventions to mitigate transmission of influenza viruses can target any of these factors. In this review, we discuss many aspects of influenza virus transmission, including the systems to study it, as well as the impact of natural barriers and various nonpharmaceutical and pharmaceutical interventions.

From a farming family of 13 children in New Zealand, I graduated with a Master of Science degree in microbiology from the University of Otago (Dunedin, Otago, New Zealand). I established the first veterinary virology laboratory at Wallaceville Animal Research Station. I subsequently completed my PhD degree at Australian National University (Canberra, Australia) and a postdoctoral fellowship at the University of Michigan (Ann Arbor, Michigan). While in New South Wales, Australia, a walk on a beach littered with dead mutton birds (shearwaters) with Dr. Graeme Laver led to the surveillance of influenza in seabirds on the Great Barrier Reef Islands and my lifelong search for the origin of pandemic influenza viruses. Subsequent studies established that (a) aquatic birds are a natural reservoir of influenza A viruses, (b) these viruses replicate primarily in cells lining the intestinal tract, (c) reassortment in nature can lead to novel pandemic influenza viruses, and (d) live bird markets are one place where transmission of influenza virus from animals to humans occurs.

Plant viruses of the genus Tobamovirus cause significant economic losses in various crops. The emergence of new tobamoviruses such as the tomato brown rugose fruit virus (ToBRFV) poses a major threat to global agriculture. Upon infection, plants mount a complex immune response to restrict virus replication and spread, involving a multilayered defense system that includes defense hormones, RNA silencing, and immune receptors. To counter these defenses, tobamoviruses have evolved various strategies to evade or suppress the different immune pathways. Understanding the interactions between tobamoviruses and the plant immune pathways is crucial for the development of effective control measures and genetic resistance to these viruses. In this review, we discuss past and current knowledge of the intricate relationship between tobamoviruses and host immunity. We use this knowledge to understand the emergence of ToBRFV and discuss potential approaches for the development of new resistance strategies to cope with emerging tobamoviruses.

There are at least 21 families of enveloped viruses that infect mammals, and many contain members of high concern for global human health. All enveloped viruses have a dedicated fusion protein or fusion complex that enacts the critical genome-releasing membrane fusion event that is essential before viral replication within the host cell interior can begin. Because all enveloped viruses enter cells by fusion, it behooves us to know how viral fusion proteins function. Viral fusion proteins are also major targets of neutralizing antibodies, and hence they serve as key vaccine immunogens. Here we review current concepts about viral membrane fusion proteins focusing on how they are triggered, structural intermediates between pre- and postfusion forms, and their interplay with the lipid bilayers they engage. We also discuss cellular and therapeutic interventions that thwart virus-cell membrane fusion.

Two decades of metagenomic analyses have revealed that in many environments, small (∼5 kb), single-stranded DNA phages of the family Microviridae dominate the virome. Although the emblematic microvirus phiX174 is ubiquitous in the laboratory, most other microviruses, particularly those of the gokushovirus and amoyvirus lineages, have proven to be much more elusive. This puzzling lack of representative isolates has hindered insights into microviral biology. Furthermore, the idiosyncratic size and nature of their genomes have resulted in considerable misjudgments of their actual abundance in nature. Fortunately, recent successes in microvirus isolation and improved metagenomic methodologies can now provide us with more accurate appraisals of their abundance, their hosts, and their interactions. The emerging picture is that phiX174 and its relatives are rather rare and atypical microviruses, and that a tremendous diversity of other microviruses is ready for exploration.