Emergence Of RNA Viruses Research Articles

Impact of Predator Exclusion and Habitat on Seroprevalence of New World Orthohantavirus Harbored by Two Sympatric Rodents within the Interior Atlantic Forest.

Understanding how perturbations to trophic interactions influence virus–host dynamics is essential in the face of ongoing biodiversity loss and the continued emergence of RNA viruses and their associated zoonoses. Herein, we investigated the role of predator exclusion on rodent communities and the seroprevalence of hantaviruses within the Reserva Natural del Bosque Mbaracayú (RNBM), which is a protected area of the Interior Atlantic Forest (IAF). In the IAF, two sympatric rodent reservoirs, Akodon montensis and Oligoryzomys nigripes, harbor Jaborá and Juquitiba hantavirus (JABV, JUQV), respectively. In this study, we employed two complementary methods for predator exclusion: comprehensive fencing and trapping/removal. The goal of exclusion was to preclude the influence of predation on small mammals on the sampling grids and thereby potentially reduce rodent mortality. Following baseline sampling on three grid pairs with different habitats, we closed the grids and began predator removal. By sampling three habitat types, we controlled for habitat-specific effects, which is important for hantavirus–reservoir dynamics in neotropical ecosystems. Our six-month predator exclusion experiment revealed that the exclusion of terrestrial mammalian predators had little influence on the rodent community or the population dynamics of A. montensis and O. nigripes. Instead, fluctuations in species diversity and species abundances were influenced by sampling session and forest degradation. These results suggest that seasonality and landscape composition play dominant roles in the prevalence of hantaviruses in rodent reservoirs in the IAF ecosystem.

Existing Host Range Mutations Constrain Further Emergence of RNA Viruses.

RNA viruses are capable of rapid host shifting, typically due to a point mutation that confers expanded host range. As additional point mutations are necessary for further expansions, epistasis among host range mutations can potentially affect the mutational neighborhood and frequency of niche expansion. We mapped the mutational neighborhood of host range expansion using three genotypes of the double-stranded RNA (dsRNA) bacteriophage φ6 (wild type and two isogenic host range mutants) on the novel host Pseudomonas syringae pv. atrofaciens. Both Sanger sequencing of 50 P. syringae pv. atrofaciens mutant clones for each genotype and population Illumina sequencing revealed the same high-frequency mutations allowing infection of P. syringae pv. atrofaciens. Wild-type φ6 had at least nine different ways of mutating to enter the novel host, eight of which are in p3 (host attachment protein gene), and 13/50 clones had unchanged p3 genes. However, the two isogenic mutants had dramatically restricted neighborhoods: only one or two mutations, all in p3. Deep sequencing revealed that wild-type clones without mutations in p3 likely had changes in p12 (morphogenic protein), a region that was not polymorphic for the two isogenic host range mutants. Sanger sequencing confirmed that 10/13 of the wild-type φ6 clones had nonsynonymous mutations in p12, and 2 others had point mutations in p9 and p5. None of these genes had previously been associated with host range expansion in φ6. We demonstrate, for the first time, epistatic constraint in an RNA virus due to host range mutations themselves, which has implications for models of serial host range expansion.IMPORTANCE RNA viruses mutate rapidly and frequently expand their host ranges to infect novel hosts, leading to serial host shifts. Using an RNA bacteriophage model system (Pseudomonas phage φ6), we studied the impact of preexisting host range mutations on another host range expansion. Results from both clonal Sanger and Illumina sequencing show that extant host range mutations dramatically narrow the neighborhood of potential host range mutations compared to that of wild-type φ6. This research suggests that serial host-shifting viruses may follow a small number of molecular paths to enter additional novel hosts. We also identified new genes involved in φ6 host range expansion, expanding our knowledge of this important model system in experimental evolution.

The Evolution and Emergence of RNA Viruses

The Evolution and Emergence of RNA Viruses

The Evolution and Emergence of RNA Viruses

This impressive monograph by Edward Holmes opens with a quotation from La Peste, by Albert Camus: “Everyone knows that pestilences have a way of recurring in the world; yet somehow we find it hard to believe in ones that crash down on our heads from a blue sky.” This apt quotation might lead the reader to believe that the evolution and emergence of RNA viruses in causing new diseases would be discussed, but in fact the book, as its title suggests, concentrates on how RNA viruses evolve and emerge at the molecular level, not how they cause disease. In addition to explaining what is currently known about the origins of RNA viruses, the book describes the mechanisms of RNA virus evolution, RNA virus quasispecies, and comparative genomics, as well as interesting new concepts, such as phylogeography. This term refers to the spatial movement of a phylogenetic species, which can be described in various ways (Holmes lists 5), two of which are the gravity model and the strong spatial subdivision model. In the former, patterns of transmission are driven by major population centers before moving out to smaller populations (influenza virus). In the spatial subdivision model, no clear evidence of migration among populations is presented (hepatitis C virus), and genomic diversity is partitioned into a series of clades (types and subtypes). Holmes argues persuasively that research in this area is limited by the size and detail of genome databases, combined with relevant epidemiologic and clinical information, such as precise geographic location, exact date of sampling, and transmission dynamics of the disease. The book is fully referenced and has a useful index, and I recommend it to those who have knowledge of and interest in the molecular biology of RNA viruses.