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First characterization of Staphylococcus felis in diabetic foot osteomyelitis: from intracellular persistence to phage treatment.

Staphylococcus felis is a coagulase-negative Staphylococcus (CoNS) primarily associated with the feline microbiota and only rarely reported in human disease. Here, we report its implication in diabetic foot osteomyelitis, and provide the first comprehensive characterization of its pathogenic potential. Two isolates (NSF001 and NSF002), recovered 5 months apart from bone biopsies of the same patient, were analyzed for growth kinetics, biofilm formation, and intracellular persistence in macrophages and osteoblasts. Both isolates proliferated efficiently, produced robust biofilm, and persisted within host cells, most markedly in osteoblasts. In a zebrafish embryo infection model, both isolates caused significant mortality, confirming their pathogenic potential in vivo. Whole-genome sequencing revealed conserved virulence determinants, a narrow resistome, and strain-specific genomic variations affecting genes involved in virulence regulation, phage defense, and iron acquisition. The lytic phage SAVM02, previously characterized for activity against other Staphylococcus species, effectively inhibited S. felis growth in vitro and conferred protection in vivo against lethal infection. Notably, the two sequential isolates differed in their in vivo virulence and phage susceptibility, paralleling these within-host microevolutionary changes and illustrating bacterial adaptation during chronic infection. Altogether, this study establishes S. felis as a CoNS capable of intracellular persistence, biofilm formation, and in vivo virulence in chronic human infection. Our findings also highlight the therapeutic potential of lytic phages against virulent CoNS species and support further investigation of phage therapy for chronic staphylococcal infections.IMPORTANCECoagulase-negative staphylococci (CoNS) are increasingly recognized as genuine agents of chronic infection, yet the pathogenic capacity of most individual species remains undefined. Staphylococcus felis, a commensal of cats only exceptionally reported in humans, had never been implicated in a chronic human infection. Here, we describe two sequential S. felis isolates recovered from bone biopsies of a patient with diabetic foot osteomyelitis and show that this species combines biofilm formation, intracellular persistence in macrophages and osteoblasts, and lethality in a zebrafish embryo model. Whole-genome comparison of the two isolates uncovered microevolutionary changes, most notably in iron-acquisition and genome-defense loci, that paralleled differences in virulence and phage susceptibility. These findings extend the list of CoNS capable of causing invasive human disease and provide a rationale for lytic phage therapy against emerging, difficult-to-treat staphylococcal pathogens.

Staphylococcus felis↗

Genomic-scale analysis of bacterial gene and protein expression in the host.

The developing complementary technologies of DNA microarrays and proteomics are allowing the response of bacterial pathogens to different environments to be probed at the whole genome level. Although using these technologies to analyze pathogens within a host is still in its infancy, initial studies indicate that these technologies will be valuable tools for understanding how the pathogen reacts to the in vivo microenvironment. Some bacterial pathogens have been shown to substantially modify their surface components in response to the host immune system and modify their energy metabolism and transport pathways to allow efficient growth within the host. Further detailed analyses of these responses will increase understanding of the molecular mechanisms of pathogenesis, identify new bacterial virulence factors, and aid in the design of new vaccines.

Bacteria↗

Rational identification of new antibacterial drug targets that are essential for viability using a genomics-based approach.

In the last two decades, the search for completely novel antibacterial agents has acquired a new sense of urgency due to the remarkable rise of antibiotic resistance among key bacterial pathogens. More recently, the advent of bacterial genomics has provided investigators with the data and bioinformatic tools to rationally identify novel antibacterial targets and the genome-scaled methodologies to validate them. Only 6 years have elapsed since the publication of the first complete bacterial genome sequence, but more than 50 complete microbial genome sequences are now available. This review will discuss the advantages and limitations of the existing bacterial genome dataset for the rational identification of novel antibacterial targets. Since the ability to rapidly identify essential genes where loss of function is coincident with loss of viability is the most important task of genomics-based target validation, essentiality testing methodologies (in which molecular genetic techniques are used to determine whether or not a gene product is required for viability of the parent cell) will be surveyed and their amenability to genome-scaled analysis assessed. Finally, we will discuss the impact of bacterial genomics to date on the development of novel and effective antibiotics.

Anti-Infective Agents↗

The mosquito genome--a turning point?

Of the insects that serve as vectors for parasitic diseases, the genus Anopheles is the most important. Of the approximately 400 species, about twelve serve as vectors for human pathogens. Months have passed since the sequenced genomes of the malaria parasite, Plasmodium falciparum, and its vector, Anopheles gambiae, were published. Sequences were compared, gene and protein predictions were made, new research areas evolved and many ongoing projects gained new momentum. A general belief is that we are at a turning point: we are now in a position to tackle both the parasite and the vector from new angles and with new force, for example, by identifying new drug targets and obtaining a deeper insight into molecular mechanisms of the insect, the parasite and the interactions between them.

Animals↗

The MA (p15) and p12 regions of the gag gene are sufficient for the pathogenicity of the murine AIDS virus.

Inoculation of the replication-defective retrovirus DEF27 (BM5d), packaged as an amphotropic virus pseudotype, into C57BL/6J mice leads to development of murine AIDS. Disease development showed a long incubation period (20 to 24 weeks), was associated with amplification of the BM5d provirus in splenocytes and lymph nodes, and was independent of the presence of exogenous or endogenous replication-competent helper viruses. However, both the onset of disease and amplification of the defective provirus were significantly enhanced by coinfection with the replication-competent B-cell-tropic ecotropic helper virus BM5e. The part of the BM5d viral genome that was essential for the pathogenicity was determined by making precisely engineered alterations in the reading frame of the gag and pol genes of BM5d proviral DNA and examining the ability of the altered amphotropic BM5d pseudotypes to induce the disease in C57BL/6J mice. The results show that expression of the MA (p15) and p12 regions of the gag gene is sufficient for pathogenicity of the BM5d retrovirus.

Animals↗

Risk assessment prediction from genome sequences: promises and dreams.

The application of bacterial genomics opens new avenues of research on foodborne pathogens. Foodborne pathogens must be able to colonize their hosts and survive transmission from host to host. Different groups of genes are involved in the processes of survival, colonization, and virulence, and such genes are potential targets for risk assessment and intervention strategies. Filtering from genome sequences the genes relevant to these processes is a major challenge, and although many tools are already available for analyses, this type of data mining is just beginning. For the simplest application, gene comparison, it is important to know how gene function, for instance in virulence, is being defined and tested. In other genomic applications, reserachers look for specific properties or characteristics of (virulence) genes to identify novel gene candidates. Each approach has pitfalls, and gene candidates must be tested in the lab to confirm their function. Models for colonization and virulence are available for most although not all pathogens. Models for survival and stress responses are needed to increase the utilization of genomic approaches to risk assessment. Here, I discuss how genome sequences are likely to help in microbial risk assessment of foodborne pathogens and how dreams may become promises.

Animals↗

A genomic view of immunology.

The outstanding problems facing immunology are whole system issues: curing allergic and autoimmune disease and developing vaccines to stimulate stronger immune responses against pathogenic organisms and cancer. We hope that the human genome sequence will reveal the molecular checks and balances that ensure both an effective immunogenic response against pathogenic microorganisms and a suitably tolerogenic response to self antigens and innocuous environmental antigens. Three synergistic approaches--sequence homology searches, messenger RNA expression profiling on microarrays, and mutagenesis in mice--provide the best opportunities to reveal, in the genome sequence, key proteins and pathways for targeting by new immunomodulatory treatments.

Animals↗

Temporal and geographical lineage dynamics of invasive Streptococcus pyogenes in Australia from 2011 to 2023: a retrospective, multicentre, clinical and genomic epidemiology study.

BACKGROUND: Defining the temporal dynamics of invasive Streptococcus pyogenes (group A Streptococcus) and differences between hyperendemic and lower-incidence regions provides crucial insights into pathogen evolution and, in turn, informs preventive measures. We aimed to examine the clinical and temporal lineage dynamics of S pyogenes across different disease settings in Australia to improve understanding of drivers of pathogen diversity. METHODS: In this retrospective, multicentre, clinical and genomic epidemiology study, we identified cases of invasive S pyogenes infection from normally sterile sites between Jan 1, 2011, and Feb 28, 2023. Data were collected from five hospital networks across low-incidence regions in temperate southeast Australia and the hyperendemic, tropical, and largely remote Top End of the Northern Territory of Australia. The crude incidence rate ratio (IRR) of bloodstream S pyogenes infection comparing the Top End and southeast Australia and in First Nations people compared with non-First Nations people was estimated by quasi-Poisson regression. We estimated odds ratios (ORs) of intensive care unit (ICU) admission, in-hospital mortality, and 30-day mortality for the Top End versus southeast Australia using logistic regression. Retrieved and successfully sequenced isolates were assigned lineages at whole-genome resolution. Temporal trends in the composition of co-circulating lineages were compared between the two regions. We used an S pyogenes-specific multistrain simulated transmission model to examine the relationship between host population-specific parameters and observed pathogen lineage dynamics. The prevalence of accessory genes (those present in 5-95% of all genomes) was compared across geographies and temporal periods to investigate genomic drivers of diversity. FINDINGS: We identified 500 cases of invasive S pyogenes infection in patients in the Top End and 495 cases in patients in southeast Australia. The crude IRR of bloodstream infection for the Top End compared with southeast Australia was 5·97 (95% CI 4·61-7·73) across the entire study period; in the Top End, infection disproportionately affected First Nations people compared with non-First Nations people (5·41, 4·28-6·89). The odds of in-hospital mortality (OR 0·43, 95% CI 0·26-0·70), 30-day mortality (0·38, 0·23-0·63), and ICU admission (0·42, 0·30-0·59) were lower in the Top End than in southeast Australia. Longitudinal lineage analysis of 642 S pyogenes genomes identified waves of replacement with distinct lineages in the Top End, whereas southeast Australia had a small number of dominant lineages that persisted and cycled in frequency. The transmission model qualitatively reproduced a similar pattern of replacement with distinct lineages when using a high transmission rate, small population size, and high levels of human movement-characteristics similar to those of communities in the hyperendemic Top End. Using a lower transmission rate, larger population size, and lower levels of migration similar to those of communities in urbanised southeast Australia, the transmission model qualitatively reproduced a pattern of dominant lineages that cycled in frequency. Despite distinct circulating lineages, the prevalence of accessory genes in the bacterial population was maintained across geographies and temporal periods. INTERPRETATION: In a hyperendemic setting, the replacement of distinct S pyogenes lineages occurred in waves, which could be linked to the disproportionate burden of disease and sparse human population in this setting. The maintenance of bacterial gene frequency could be consistent with multilocus selection. These findings suggest that lineage-specific interventions-such as vaccines under development-should consider disease setting and, without broad cross-protection, might lead to lineage replacement. FUNDING: National Health and Medical Research Council, and Leducq Foundation.

Humans↗

Genome-wide comparison reveals great inter- and intraspecies variability in B. pseudomallei and B. mallei pathogens.

Burkholderia mallei and B. pseudomallei, closely related Gram-negative bacteria, are causative agents of serious infectious diseases of humans and animals: glanders and melioidosis, respectively. Despite numerous studies of these pathogens, the detailed mechanism of their pathogenesis is still unknown. The problem is even more complicated due to natural variability of B. pseudomallei and B. mallei strains, the understanding of which is a prerequisite for rational design of tools for diagnostics, prophylaxis and therapy of the diseases. Using a subtractive hybridization technique, we compared the genomes of B. pseudomallei C-141 and B. mallei C-5 strains. A subtracted library of DNA fragments specific for B. pseudomallei C-141 and absent from B. mallei C-5 was obtained and analyzed. A variety of differences have been detected and mapped on the recently sequenced genome of B. pseudomallei K96243. A comparative sequence analysis also revealed considerable genomic differences between B. pseudomallei C-141 and B. mallei ATCC 23344 strains sequenced at The Institute for Genomic Research (TIGR). We also observed significant genomic differences between B. pseudomallei C-141 and B. pseudomallei K96243. Some of the differential DNA fragments displayed similarity to different mobile elements which have not yet been described for B. pseudomallei, whereas the others matched various prophage components, components of active transport systems, different enzymes and transcription regulators. A substantial proportion of the differential clones had no database matches either at the nucleotide or protein level. The results provide evidence for great genome-wide variability of B. pseudomallei, further confirmed by Southern blot analysis of various B. pseudomallei strains. The data obtained can be useful for future development of efficient diagnostic tools allowing rapid identification of species, strains and isolates of B. mallei and B. pseudomallei.

Bacterial Typing Techniques↗

Sequence analysis of both genome segments of two very virulent infectious bursal disease virus field isolates with distinct pathogenicity.

The deduced amino acid sequences of segment A and B of two very virulent Infectious bursal disease virus (vvIBDV) isolates, UPM94/273 and UPM97/61 were compared with 25 other IBDV strains. Twenty amino acid residues (8 in VP1, 5 in VP2, 2 in VP3, 4 in VP4, 1 in VP5) that were common to vvIBDV strains were detected. However, UPM94/273 is an exceptional vvIBDV with usual amino acid substitutions. The differences in the divergence of segment A and B indicated that the vvIBDV strains may have been derived from genetic reassortment of a single ancestral virus or both segments have different ability to undergo genetic variation due to their different functional constraints.

Amino Acid Sequence↗

A new regulatory DNA motif of the gamma subclass Proteobacteria: identification of the LexA protein binding site of the plant pathogen Xylella fastidiosa.

Escherichia coli LexA protein is the repressor of a gene network whose members are directly involved in the repair of damaged DNA and in the survival of bacterial cells until DNA lesions have been eliminated. The lexA gene is widely present in bacteria, although the sequences of only three LexA-binding sites are known: Gram-positive, alpha Proteobacteria and some members of gamma Proteobacteria represented by E. coli. Taking advantage of the fact that the genome sequence of the plant-pathogenic bacterium Xylella fastidiosa has been determined, its lexA gene has been cloned and overexpressed in E. coli to purify its product. After demonstration that X. fastidiosa lexA and recA genes are co-transcribed, gel mobility shift assays and directed mutagenesis experiments using the promoter of the lexA-recA transcriptional unit demonstrated that the X. fastidiosa LexA protein specifically binds the imperfect palindrome TTAGN(6)TACTA. This is the first LexA binding sequence identified in the gamma Proteobacteria differing from the E. coli-like LexA box. Although a computational search has revealed the presence of TTAGN(6)TACTA-like motifs upstream of X. fastidiosa genes other than lexA, X. fastidiosa LexA only binds the promoter of one of them, XF2313, encoding a putative DNA-modification methylase. Moreover, X. fastidiosa LexA protein does not bind any of the other genes whose homologues are regulated by the LexA repressor in E. coli (uvrA, uvrB, ssb, ruvAB, ftsK, dinG, recN and ybfE). RT-PCR quantitative analysis has also demonstrated that lexA-recA and XF2313 genes, as well as the X. fastidiosa genes which are homologues to those of E. coli belonging to the LexA regulon, with the exception of ssb, are DNA damage-inducible in X. fastidiosa.

Bacterial Proteins↗

System-wide genomic and biochemical comparisons of sialic acid biology among primates and rodents: Evidence for two modes of rapid evolution.

Numerous vertebrate genes are involved in the biology of the oligosaccharide chains attached to glycoconjugates. These genes fall into diverse groups within the conventional Gene Ontology classification. However, they should be evaluated together from functional and evolutionary perspectives in a "biochemical systems" approach, considering each monosaccharide unit's biosynthesis, activation, transport, modification, transfer, recycling, degradation, and recognition. Sialic acid (Sia) residues are monosaccharides at the outer end of glycans on the cell-surface and secreted molecules of vertebrates, mediating recognition by intrinsic or extrinsic (pathogen) receptors. The availability of multiple genome sequences allows a system-wide comparison among primates and rodents of all genes directly involved in Sia biology. Taking this approach, we present further evidence for accelerated evolution in Sia-binding domains of CD33-related Sia-recognizing Ig-like lectins. Other gene classes are more conserved, including those encoding the sialyltransferases that attach Sia residues to glycans. Despite this conservation, tissue sialylation patterns are shown to differ widely among these species, presumably because of rapid evolution of sialyltransferase expression patterns. Analyses of N- and O-glycans of erythrocyte and plasma glycopeptides from these and other mammalian taxa confirmed this phenomenon. Sia modifications on these glycopeptides also appear to be undergoing rapid evolution. This rapid evolution of the sialome presumably results from the ongoing need of organisms to evade microbial pathogens that use Sia residues as receptors. The rapid evolution of Sia-binding domains of the inhibitory CD33-related Sia-recognizing Ig-like lectins is likely to be a secondary consequence, as these inhibitory receptors presumably need to keep up with recognition of the rapidly evolving "self"-sialome.

Amino Acid Sequence↗

Nucleotide sequence and genomic organization of Aleutian mink disease parvovirus (ADV): sequence comparisons between a nonpathogenic and a pathogenic strain of ADV.

A DNA sequence of 4,592 nucleotides (nt) was derived for the nonpathogenic ADV-G strain of Aleutian mink disease parvovirus (ADV). The 3'(left) end of the virion strand contained a 117-nt palindrome that could assume a Y-shaped configuration similar to, but less stable than, that of other parvoviruses. The sequence obtained for the 5' end was incomplete and did not contain the 5' (right) hairpin structure but ended just after a 25-nt A + T-rich direct repeat. Features of ADV genomic organization are (i) major left (622 amino acids) and right (702 amino acids) open reading frames (ORFs) in different translational frames of the plus-sense strand, (ii) two short mid-ORFs, (iii) eight potential promoter motifs (TATA boxes), including ones at 3 and 36 map units, and (iv) six potential polyadenylation sites, including three clustered near the termination of the right ORF. Although the overall homology to other parvoviruses is less than 50%, there are short conserved amino acid regions in both major ORFs. However, two regions in the right ORF allegedly conserved among the parvoviruses were not present in ADV. At the DNA level, ADV-G is 97.5% related to the pathogenic ADV-Utah 1. A total of 22 amino acid changes were found in the right ORF; changes were found in both hydrophilic and hydrophobic regions and generally did not affect the theoretical hydropathy. However, there is a short heterogeneous region at 64 to 65 map units in which 8 out of 11 residues have diverged; this hypervariable segment may be analogous to short amino acid regions in other parvoviruses that determine host range and pathogenicity. These findings suggested that this region may harbor some of the determinants responsible for the differences in pathogenicity of ADV-G and ADV-Utah 1.

Aleutian Mink Disease Virus↗

Complete genome sequence and analysis of Wolinella succinogenes.

To understand the origin and emergence of pathogenic bacteria, knowledge of the genetic inventory from their nonpathogenic relatives is a prerequisite. Therefore, the 2.11-megabase genome sequence of Wolinella succinogenes, which is closely related to the pathogenic bacteria Helicobacter pylori and Campylobacter jejuni, was determined. Despite being considered nonpathogenic to its bovine host, W. succinogenes holds an extensive repertoire of genes homologous to known bacterial virulence factors. Many of these genes have been acquired by lateral gene transfer, because part of the virulence plasmid pVir and an N-linked glycosylation gene cluster were found to be syntenic between C. jejuni and genomic islands of W. succinogenes. In contrast to other host-adapted bacteria, W. succinogenes does harbor the highest density of bacterial sensor kinases found in any bacterial genome to date, together with an elaborate signaling circuitry of the GGDEF family of proteins. Because the analysis of the W. succinogenes genome also revealed genes related to soil- and plant-associated bacteria such as the nif genes, W. succinogenes may represent a member of the epsilon proteobacteria with a life cycle outside its host.

Bacterial Proteins↗

Molecular biology and pathogenicity of mycoplasmas.

The recent sequencing of the entire genomes of Mycoplasma genitalium and M. pneumoniae has attracted considerable attention to the molecular biology of mycoplasmas, the smallest self-replicating organisms. It appears that we are now much closer to the goal of defining, in molecular terms, the entire machinery of a self-replicating cell. Comparative genomics based on comparison of the genomic makeup of mycoplasmal genomes with those of other bacteria, has opened new ways of looking at the evolutionary history of the mycoplasmas. There is now solid genetic support for the hypothesis that mycoplasmas have evolved as a branch of gram-positive bacteria by a process of reductive evolution. During this process, the mycoplasmas lost considerable portions of their ancestors' chromosomes but retained the genes essential for life. Thus, the mycoplasmal genomes carry a high percentage of conserved genes, greatly facilitating gene annotation. The significant genome compaction that occurred in mycoplasmas was made possible by adopting a parasitic mode of life. The supply of nutrients from their hosts apparently enabled mycoplasmas to lose, during evolution, the genes for many assimilative processes. During their evolution and adaptation to a parasitic mode of life, the mycoplasmas have developed various genetic systems providing a highly plastic set of variable surface proteins to evade the host immune system. The uniqueness of the mycoplasmal systems is manifested by the presence of highly mutable modules combined with an ability to expand the antigenic repertoire by generating structural alternatives, all compressed into limited genomic sequences. In the absence of a cell wall and a periplasmic space, the majority of surface variable antigens in mycoplasmas are lipoproteins. Apart from providing specific antimycoplasmal defense, the host immune system is also involved in the development of pathogenic lesions and exacerbation of mycoplasma induced diseases. Mycoplasmas are able to stimulate as well as suppress lymphocytes in a nonspecific, polyclonal manner, both in vitro and in vivo. As well as to affecting various subsets of lymphocytes, mycoplasmas and mycoplasma-derived cell components modulate the activities of monocytes/macrophages and NK cells and trigger the production of a wide variety of up-regulating and down-regulating cytokines and chemokines. Mycoplasma-mediated secretion of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-1 (IL-1), and IL-6, by macrophages and of up-regulating cytokines by mitogenically stimulated lymphocytes plays a major role in mycoplasma-induced immune system modulation and inflammatory responses.

Animals↗

A One Health approach to Antimicrobial Resistance: Concepts, challenges, and advances in omics.

Antimicrobial resistance (AMR) is a global threat driven by the interplay between microbial evolution and human activity. Antimicrobial use in human and veterinary medicine, as well as in agriculture, accelerates the selection and dissemination of resistant bacteria and genes across interconnected human, animal, and environmental reservoirs. These dynamic exchanges render single-sector interventions ineffective. A One Health approach integrating human, animal, and environmental health is therefore essential to understand and mitigate the emergence and spread of AMR. This chapter focuses on bacterial antimicrobial resistance, addressing key concepts, major challenges, and emerging technologies within a One Health framework. Advances in next-generation sequencing and omics technologies have transformed our capacity to resolve AMR at unprecedented scale and resolution. These tools enable the tracking of resistance genes and high-risk clones across ecosystems, uncover transmission pathways, and identify key drivers of dissemination. Such insights support real-time epidemiological surveillance, outbreak detection, and targeted interventions. However, translating these advances into routine practice remains a major challenge, requiring harmonized methodologies, data integration, and cross-sector coordination. Addressing AMR demands sustained collaboration across disciplines and stakeholders, including clinicians, veterinarians, farmers, researchers, policymakers, industry, and the public. And framing AMR as a shared ecological and societal responsibility underscores the urgency of coordinated global action. We call for the urgent integration of One Health principles into surveillance, policy, and innovation to preserve antimicrobial effectiveness and safeguard future health.

Humans↗

Genome-wide operon prediction in Staphylococcus aureus.

Identification of operon structure is critical to understanding gene regulation and function, and pathogenesis, and for identifying targets towards the development of new antibiotics in bacteria. Recently, the complete genome sequences of a large number of important human bacterial pathogens have become available for computational analysis, including the major human Gram-positive pathogen Staphylococcus aureus. By annotating the predicted operon structure of the S.aureus genome, we hope to facilitate the exploration of the unique biology of this organism as well as the comparative genomics across a broad range of bacteria. We have integrated several operon prediction methods and developed a consensus approach to score the likelihood of each adjacent gene pair to be co-transcribed. Gene pairs were separated into distinct operons when scores were equal to or below an empirical threshold. Using this approach, we have generated a S.aureus genome map with scores annotated at the intersections of every adjacent gene pair. This approach predicted about 864 monocistronic transcripts and 533 polycistronic operons from the protein-encoding genes in the S.aureus strain Mu50 genome. When compared with a set of experimentally determined S.aureus operons from literature sources, this method successfully predicted at least 91% of gene pairs. At the transcription unit level, this approach correctly identified at least 92% of complete operons in this dataset. This consensus approach has enabled us to predict operons with high accuracy from a genome where limited experimental evidence for operon structure is available.

Chromosome Mapping↗

Characterization of two avian reoviruses that exhibit strain-specific quantitative differences in their syncytium-inducing and pathogenic capabilities.

We previously proposed that the conservation of the nonessential syncytium-inducing phenotype among all reported avian reovirus (ARV) isolates may reflect a mechanism for enhanced virus dissemination in vivo, which in turn could contribute to the natural pathogenicity of ARV. Direct testing of this hypothesis has been hampered by the lack of available virus strains with defined differences in their fusion-inducing capability. We now report on the characterization of two ARV strains, ARV-176 and ARV-138, that exhibited strain-specific differences in their fusogenic properties, which correlated with their pathogenic potential in embryonated eggs. Moreover, both virus strains possessed similar replicative abilities in cell culture, suggesting that the weakly fusogenic ARV-138 virus is specifically inhibited in its syncytium-inducing ability. To test the use of these viruses for reassortant studies aimed at assessing the role of cell fusion in viral pathogenesis, a preliminary genetic analysis was undertaken using a monoreassortant that contained nine genome segments from the parental ARV-138 virus and the S1 genome segment from the highly fusogenic and pathogenic ARV-176 parental virus. The monoreassortant possessed the full fusogenic potential of the ARV-176 parental virus and displayed enhanced embryo pathogenicity, providing the first genetic evidence implicating the ARV S1 genome segment in both syncytium formation and viral pathogenesis.

Animals↗