Annual Review of Virology最新文献

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.

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.

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.

Protein synthesis by the ribosome is the final stage of biological information transfer and represents an irreversible commitment to gene expression. Accurate translation of messenger RNA is therefore essential to all life, and spontaneous errors by the translational machinery are highly infrequent (∼1/100,000 codons). Programmed -1 ribosomal frameshifting (-1PRF) is a mechanism in which the elongating ribosome is induced at high frequency to slip backward by one nucleotide at a defined position and to continue translation in the new reading frame. This is exploited as a translational regulation strategy by hundreds of RNA viruses, which rely on -1PRF during genome translation to control the stoichiometry of viral proteins. While early investigations of -1PRF focused on virological and biochemical aspects, the application of X-ray crystallography and cryo-electron microscopy (cryo-EM), and the advent of deep sequencing and single-molecule approaches have revealed unexpected structural diversity and mechanistic complexity. Molecular players from several model systems have now been characterized in detail, both in isolation and, more recently, in the context of the elongating ribosome. Here we provide a summary of recent advances and discuss to what extent a general model for -1PRF remains a useful way of thinking.

Negative-stranded RNA viruses are a large group of viruses that encode their genomes in RNA across multiple segments in an orientation antisense to messenger RNA. Their members infect broad ranges of hosts, and there are a number of notable human pathogens. Here, we examine the development of reverse genetic systems as applied to these virus families, emphasizing conserved approaches illustrated by some of the prominent members that cause significant human disease. We also describe the utility of their genetic systems in the development of reporter strains of the viruses and some biological insights made possible by their use. To conclude the review, we highlight some possible future uses of reporter viruses that not only will increase our basic understanding of how these viruses replicate and cause disease but also could inform the development of new approaches to therapeutically intervene.