Journal articles: 'Host-virus relationships'

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Lal, Sunil K. "Influenza A Virus: Host–Virus Relationships." Viruses 12, no. 8 (August 9, 2020): 870. http://dx.doi.org/10.3390/v12080870.

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We are in the midst of a pandemic where the infective agent has been identified, but how it causes mild disease in some and fatally severe disease in other infected individuals remains a mystery [...]

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Mansour, A., and A. Al-Musa. "Cucumber Vein Yellowing Virus; Host Range and Virus Vector Relationships." Journal of Phytopathology 137, no. 1 (January 1993): 73–78. http://dx.doi.org/10.1111/j.1439-0434.1993.tb01327.x.

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López‐Lastra, Marcelo. "Host–virus relationships: a sum of many battles." FEBS Open Bio 12, no. 6 (June 2022): 1094–95. http://dx.doi.org/10.1002/2211-5463.13420.

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Dusi, A. N., and D. Peters. "Beet mosaic virus: its Vector and Host Relationships." Journal of Phytopathology 147, no. 5 (May 1999): 293–98. http://dx.doi.org/10.1111/j.1439-0434.1999.tb03833.x.

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Xu, Feng, Chen Zhao, Yuhua Li, Jiang Li, Youping Deng, and Tieliu Shi. "Exploring virus relationships based on virus-host protein-protein interaction network." BMC Systems Biology 5, Suppl 3 (2011): S11. http://dx.doi.org/10.1186/1752-0509-5-s3-s11.

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MANSOUR, A., and A. AL-MUSA. "Tomato yellow leaf curl virus: host range and virus-vector relationships." Plant Pathology 41, no. 2 (April 1992): 122–25. http://dx.doi.org/10.1111/j.1365-3059.1992.tb02328.x.

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Scharninghausen, Jerrold J., Michael Faulde, and Semra Cavaljuga. "Hantavirus host/virus interactions within Southeast Europe." Bosnian Journal of Basic Medical Sciences 4, no. 4 (November 20, 2004): 13–18. http://dx.doi.org/10.17305/bjbms.2004.3353.

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Viral studies have historically approached their phylogenetic analysis without consideration of the impact of the role the host plays in evolution. Our study examines host/viral interactions through analysis of the phylogenetic relationship between hantavirus genetic sequences and host cytochrome B sequences. Phylogenetic analysis of known Hantavirus genetic sequences were performed using PAUP 3.1.1 (vers. 4.0.0d64). Only sequences available through GENBANK were analyzed. Phylogenetic analysis of hantavirus sequences revealed distinct patterns based upon geographic area. These patterns coincided with the known ranges of reservoir hosts. Multiple hosts for individual viruses and multiple viruses in a single host species for hantaviruses have been described. This may be due to accidental exposure, host-switching, co-speciation, or broad co-accommodation. Since the host is the actual environment that the virus survives in, changes in the host over time could potentially directly influence changes in the virus. Multiple viruses and hosts collide in Southeastern Europe increasing the prospect of finding distinct viral/host relationships. Rodent Cytochrome B is very well conserved and can be used to tract host lineage. By tracking the relationship of infected hosts, we theorize that patterns in host DNA will emerge that will mirror patterns in viral sequences. This analysis of the host DNA could provide an understanding into the causes of variation in hantaviral sequences, pathogenicity, transmissibility, infectivity, viral range and expand our knowledge of viral/host interactions. Surveillance for viruses in the field should include analysis of the host DNA in combination with the viral analysis.

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Hunziker, Lukas, Mike Recher, Adrian Ciurea, Marianne M. A. Martinic, Bernhard Odermatt, Hans Hengartner, and Rolf M. Zinkernagel. "Antagonistic Variant Virus Prevents Wild-type Virus-induced Lethal Immunopathology." Journal of Experimental Medicine 196, no. 8 (October 21, 2002): 1039–46. http://dx.doi.org/10.1084/jem.20012045.

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Altered peptide ligands (APLs) and their antagonistic or partial agonistic character–influencing T cell activation have mainly been studied in vitro Some studies have shown APLs as a viral escape mechanism from cytotoxic CD8+ T cell responses in vivo. However, whether infection or superinfection with a virus displaying an antagonistic T cell epitope can alter virus–host relationships via inhibiting T cell–mediated immunopathology is unclear. Here, we evaluated a recently described CD4+ T cell escape lymphocytic choriomeningitis virus (LCMV) variant that in vitro displayed antagonistic characteristics for the major histocompatibility complex class II–restricted mutated epitope. Mice transgenic for the immunodominant LCMV-specific T helper epitope that usually succumb to wild-type LCMV-induced immunopathology, survived if they were simultaneously coinfected with antagonistic variant but not with control virus. The results illustrate that a coinfecting APL-expressing virus can shift an immunopathological virus–host relationships in favor of host survival. This may play a role in poorly cytopathic long-lasting virus carrier states in humans.

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Brown, J. K. "Host Range and Vector Relationships of Cotton Leaf Crumple Virus." Plant Disease 71, no. 6 (1987): 522. http://dx.doi.org/10.1094/pd-71-0522.

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McLeish, Michael, Soledad Sacristán, Aurora Fraile, and Fernando García-Arenal. "Scale dependencies and generalism in host use shape virus prevalence." Proceedings of the Royal Society B: Biological Sciences 284, no. 1869 (December 20, 2017): 20172066. http://dx.doi.org/10.1098/rspb.2017.2066.

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Processes that generate the distribution of pathogens and their interactions with hosts are not insensitive to changes in spatial scale. Spatial scales and species traits are often selected intentionally, based on practical considerations, ignoring biases that the scale and type of observation may introduce. Specifically, these biases might change the interpretation of disease–diversity relationships that are reported as either ‘dilution’ or ‘amplification’ effects. Here, we combine field data of a host–pathogen community with empirical models to test the effects that (i) spatial scale and (ii) host range have on the relationship between plant–virus infection prevalence and diversity. We show that prevalence–diversity relationships are scale-dependent and can produce opposite effects associated with different habitats at sub-ecosystem scales. The total number of host species of each virus reflected generalism at the ecosystem scale. However, plasticity in host range resembled habitat-specific specialization and also changed model predictions. We show that habitat heterogeneity, ignored at larger (ecosystem) spatial scales, influences pathogen distributions. Hence, understanding disease distributions and the evolution of pathogens requires reconciling specific hypotheses of the study with an appropriate spatial scale, or scales, and consideration of traits, such as host range, that might strongly contribute to biotic interactions.

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Tomaru, Yuji, and Kei Kimura. "Novel Protocol for Estimating Viruses Specifically Infecting the Marine Planktonic Diatoms." Diversity 12, no. 6 (June 4, 2020): 225. http://dx.doi.org/10.3390/d12060225.

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Since their discovery, at least 15 diatom viruses have been isolated and characterised using a culture method with two cycles of extinction dilution. However, the method is time consuming and laborious, and it isolates only the most dominant virus in a water sample. Recent studies have suggested inter-species host specificity of diatom viruses. Here, we describe a new protocol to estimate previously unrecognised host-virus relationships. Host cell cultures after inoculation of natural sediment pore water samples were obtained before complete lysis. The proliferated viral genomes in the host cells were amplified using degenerate primer pairs targeting protein replication regions of single-stranded RNA (ssRNA) and single-stranded DNA (ssDNA) viruses, and then sequenced. Diverse ssRNA virus types within known diatom virus group were detected from inoculated Chaetoceros tenuissimus and C. setoensis cells. A previously unknown ssDNA virus type was detected in inoculated C. tenuissimus cells, but not in C. setoensis cells. Despite the possible protocol biases, for example non-specific adsorptions of virions onto the host cells, the present method helps to estimate the viruses infectious to a single host species. Further improvements to this protocol targeting the proliferated viral genomes might reveal unexpected diatom–virus ecological relationships.

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Li, Wanlin, and Nadia Tahiri. "Host–Virus Cophylogenetic Trajectories: Investigating Molecular Relationships between Coronaviruses and Bat Hosts." Viruses 16, no. 7 (July 15, 2024): 1133. http://dx.doi.org/10.3390/v16071133.

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Bats, with their virus tolerance, social behaviors, and mobility, are reservoirs for emerging viruses, including coronaviruses (CoVs) known for genetic flexibility. Studying the cophylogenetic link between bats and CoVs provides vital insights into transmission dynamics and host adaptation. Prior research has yielded valuable insights into phenomena such as host switching, cospeciation, and other dynamics concerning the interaction between CoVs and bats. Nonetheless, a distinct gap exists in the current literature concerning a comparative cophylogenetic analysis focused on elucidating the contributions of sequence fragments to the co-evolution between hosts and viruses. In this study, we analyzed the cophylogenetic patterns of 69 host–virus connections. Among the 69 host–virus links examined, 47 showed significant cophylogeny based on ParaFit and PACo analyses, affirming strong associations. Focusing on two proteins, ORF1ab and spike, we conducted a comparative analysis of host and CoV phylogenies. For ORF1ab, the specific window ranged in multiple sequence alignment (positions 520–680, 770–870, 2930–3070, and 4910–5080) exhibited the lowest Robinson–Foulds (RF) distance (i.e., 84.62%), emphasizing its higher contribution in the cophylogenetic association. Similarly, within the spike region, distinct window ranges (positions 0–140, 60–180, 100–410, 360–550, and 630–730) displayed the lowest RF distance at 88.46%. Our analysis identified six recombination regions within ORF1ab (positions 360–1390, 550–1610, 680–1680, 700–1710, 2060–3090, and 2130–3250), and four within the spike protein (positions 10–510, 50–560, 170–710, and 230–730). The convergence of minimal RF distance regions with combination regions robustly affirms the pivotal role of recombination in viral adaptation to host selection pressures. Furthermore, horizontal gene transfer reveals prominent instances of partial gene transfer events, occurring not only among variants within the same host species but also crossing host species boundaries. This suggests a more intricate pattern of genetic exchange. By employing a multifaceted approach, our comprehensive strategy offers a nuanced understanding of the intricate interactions that govern the co-evolutionary dynamics between bat hosts and CoVs. This deeper insight enhances our comprehension of viral evolution and adaptation mechanisms, shedding light on the broader dynamics that propel viral diversity.

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Masson, Patrick, Chantal Hulo, Edouard de Castro, Rebecca Foulger, Sylvain Poux, Alan Bridge, Jane Lomax, Lydie Bougueleret, Ioannis Xenarios, and Philippe Le Mercier. "An Integrated Ontology Resource to Explore and Study Host-Virus Relationships." PLoS ONE 9, no. 9 (September 18, 2014): e108075. http://dx.doi.org/10.1371/journal.pone.0108075.

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Happonen, Lotta Johanna, Peter Redder, Xu Peng, Laila Johanne Reigstad, David Prangishvili, and Sarah Jane Butcher. "Familial Relationships in Hyperthermo- and Acidophilic Archaeal Viruses." Journal of Virology 84, no. 9 (February 17, 2010): 4747–54. http://dx.doi.org/10.1128/jvi.02156-09.

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ABSTRACT Archaea often live in extreme, harsh environments such as acidic hot springs and hypersaline waters. To date, only two icosahedrally symmetric, membrane-containing archaeal viruses, SH1 and Sulfolobus turreted icosahedral virus (STIV), have been described in detail. We report the sequence and three-dimensional structure of a third such virus isolated from a hyperthermoacidophilic crenarchaeon, Sulfolobus strain G4ST-2. Characterization of this new isolate revealed it to be similar to STIV on the levels of genome and structural organization. The genome organization indicates that these two viruses have diverged from a common ancestor. Interestingly, the prominent surface turrets of the two viruses are strikingly different. By sequencing and mass spectrometry, we mapped several large insertions and deletions in the known structural proteins that could account for these differences and showed that both viruses can infect the same host. A combination of genomic and proteomic analyses revealed important new insights into the structural organization of these viruses and added to our limited knowledge of archaeal virus life cycles and host-cell interactions.

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Nagasaki, K., Y. Tomaru, Y. Shirai, Y. Takao, and H. Mizumoto. "Dinoflagellate-infecting viruses." Journal of the Marine Biological Association of the United Kingdom 86, no. 3 (April 10, 2006): 469–74. http://dx.doi.org/10.1017/s0025315406013361.

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Dinoflagellates (Dinophyceae) are considered to be one of the most abundant and diverse groups of phytoplankton; however, the viral impact on dinoflagellates was not studied until recently. This review shows the present information concerning the viruses infecting dinoflagellates and the ecology relationships between the host and the virus. So far, two viruses have been isolated and characterized: a large DNA virus (HcV: Heterocapsa circularisquama virus) and a small RNA virus (HcRNAV: H. circularisquama RNA virus); both of which are infectious to the harmful bloom-forming dinoflagellate H. circularisquama.In the present review, we mainly discuss the relationship between HcRNAV and H. circularisquama from the viewpoint of physiology, ecology and genetics. It will help clarify the viral impact on dinoflagellate populations in marine environments to understand the host/parasite ecology.

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Acosta-Leal, R., S. Duffy, Z. Xiong, R. W. Hammond, and S. F. Elena. "Advances in Plant Virus Evolution: Translating Evolutionary Insights into Better Disease Management." Phytopathology® 101, no. 10 (October 2011): 1136–48. http://dx.doi.org/10.1094/phyto-01-11-0017.

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Recent studies in plant virus evolution are revealing that genetic structure and behavior of virus and viroid populations can explain important pathogenic properties of these agents, such as host resistance breakdown, disease severity, and host shifting, among others. Genetic variation is essential for the survival of organisms. The exploration of how these subcellular parasites generate and maintain a certain frequency of mutations at the intra- and inter-host levels is revealing novel molecular virus–plant interactions. They emphasize the role of host environment in the dynamic genetic composition of virus populations. Functional genomics has identified host factors that are transcriptionally altered after virus infections. The analyses of these data by means of systems biology approaches are uncovering critical plant genes specifically targeted by viruses during host adaptation. Also, a next-generation resequencing approach of a whole virus genome is opening new avenues to study virus recombination and the relationships between intra-host virus composition and pathogenesis. Altogether, the analyzed data indicate that systematic disruption of some specific parameters of evolving virus populations could lead to more efficient ways of disease prevention, eradication, or tolerable virus–plant coexistence.

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Francis, Magen, Morgan King, and Alyson Kelvin. "Back to the Future for Influenza Preimmunity—Looking Back at Influenza Virus History to Infer the Outcome of Future Infections." Viruses 11, no. 2 (January 30, 2019): 122. http://dx.doi.org/10.3390/v11020122.

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The influenza virus-host interaction is a classic arms race. The recurrent and evolving nature of the influenza virus family allows a single host to be infected several times. Locked in co-evolution, recurrent influenza virus infection elicits continual refinement of the host immune system. Here we give historical context of circulating influenza viruses to understand how the individual immune history is mirrored by the history of influenza virus circulation. Original Antigenic Sin was first proposed as the negative influence of the host’s first influenza virus infection on the next and Imprinting modernizes Antigenic Sin incorporating both positive and negative outcomes. Building on imprinting, we refer to preimmunity as the continual refinement of the host immune system with each influenza virus infection. We discuss imprinting and the interplay of influenza virus homology, vaccination, and host age establishing preimmunity. We outline host signatures and outcomes of tandem infection according to the sequence of virus and classify these relationships as monosubtypic homologous, monosubtypic heterologous, heterosubtypic, or heterotypic sequential infections. Finally, the preimmunity knowledge gaps are highlighted for future investigation. Understanding the effects of antigenic variable recurrent influenza virus infection on immune refinement will advance vaccination strategies, as well as pandemic preparedness.

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Zheng, Lu-Lu, Chunyan Li, Jie Ping, Yanhong Zhou, Yixue Li, and Pei Hao. "The Domain Landscape of Virus-Host Interactomes." BioMed Research International 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/867235.

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Viral infections result in millions of deaths in the world today. A thorough analysis of virus-host interactomes may reveal insights into viral infection and pathogenic strategies. In this study, we presented a landscape of virus-host interactomes based on protein domain interaction. Compared to the analysis at protein level, this domain-domain interactome provided a unique abstraction of protein-protein interactome. Through comparisons among DNA, RNA, and retrotranscribing viruses, we identified a core of human domains, that viruses used to hijack the cellular machinery and evade the immune system, which might be promising antiviral drug targets. We showed that viruses preferentially interacted with host hub and bottleneck domains, and the degree and betweenness centrality among three categories of viruses are significantly different. Further analysis at functional level highlighted that different viruses perturbed the host cellular molecular network by common and unique strategies. Most importantly, we creatively proposed a viral disease network among viral domains, human domains and the corresponding diseases, which uncovered several unknown virus-disease relationships that needed further verification. Overall, it is expected that the findings will help to deeply understand the viral infection and contribute to the development of antiviral therapy.

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da Silva Schreiber, Maicon, and Juliana Fachinetto. "PHYLOGENETIC RELATIONSHIP BETWEEN RABIES VIRUS (RABIES LYSSAVIRUS) VARIANTS FROM TWO DIFFERENT HOST SPECIES." Veterinária e Zootecnia 31 (January 13, 2024): 1–7. http://dx.doi.org/10.35172/rvz.2024.v31.1537.

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Rabies is a fatal zoonotic disease that affects several mammals. Bats are recognized hosts of the rabies virus, and their main food source is the blood of other mammals, particularly cattle. During feeding, bats transmit the virus to cattle, which are victims of the disease, contributing to economic losses and increasing the risk of infection for humans. Based on this affinity in the rabies cycle between bats and cattle, the objective of this study was to analyze the phylogenetic relationships of rabies virus samples in cattle and bats. The G gene of the rabies virus was chosen for this study because it is directly related to the infection process. Nucleotide sequences of the viral G gene were selected from GenBank for samples obtained from infected cattle and bats. Maximum parsimony analyses were conducted using the Molecular Evolutionary Genetics Analysis software. The Maxima Parsimony tree indicated a phylogenetic relationship between the G genes of both hosts, indicating that the virus evolved from bats to cattle. Analysis of parsimoniously informative sites revealed that the viral G gene carried specific mutations in each host. Knowledge of the evolutionary relationships between the rabies virus and its hosts is critical for identifying potential new hosts and the possible routes of infection for humans.

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Rossi, Chiara, Nicola Zadra, Cristina Fevola, Frauke Ecke, Birger Hörnfeldt, René Kallies, Maria Kazimirova, et al. "Evolutionary Relationships of Ljungan Virus Variants Circulating in Multi-Host Systems across Europe." Viruses 13, no. 7 (July 7, 2021): 1317. http://dx.doi.org/10.3390/v13071317.

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The picornavirus named ‘Ljungan virus’ (LV, species Parechovirus B) has been detected in a dozen small mammal species from across Europe, but detailed information on its genetic diversity and host specificity is lacking. Here, we analyze the evolutionary relationships of LV variants circulating in free-living mammal populations by comparing the phylogenetics of the VP1 region (encoding the capsid protein and associated with LV serotype) and the 3Dpol region (encoding the RNA polymerase) from 24 LV RNA-positive animals and a fragment of the 5′ untranslated region (UTR) sequence (used for defining strains) in sympatric small mammals. We define three new VP1 genotypes: two in bank voles (Myodes glareolus) (genotype 8 from Finland, Sweden, France, and Italy, and genotype 9 from France and Italy) and one in field voles (Microtus arvalis) (genotype 7 from Finland). There are several other indications that LV variants are host-specific, at least in parts of their range. Our results suggest that LV evolution is rapid, ongoing and affected by genetic drift, purifying selection, spillover and host evolutionary history. Although recent studies suggest that LV does not have zoonotic potential, its widespread geographical and host distribution in natural populations of well-characterized small mammals could make it useful as a model for studying RNA virus evolution and transmission.

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Tangherlini, Michael, Cinzia Corinaldesi, Francesca Ape, Silvestro Greco, Teresa Romeo, Franco Andaloro, and Roberto Danovaro. "Ocean Acidification Induces Changes in Virus–Host Relationships in Mediterranean Benthic Ecosystems." Microorganisms 9, no. 4 (April 6, 2021): 769. http://dx.doi.org/10.3390/microorganisms9040769.

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Acidified marine systems represent “natural laboratories”, which provide opportunities to investigate the impacts of ocean acidification on different living components, including microbes. Here, we compared the benthic microbial response in four naturally acidified sites within the Southern Tyrrhenian Sea characterized by different acidification sources (i.e., CO2 emissions at Ischia, mixed gases at Panarea and Basiluzzo and acidified freshwater from karst rocks at Presidiana) and pH values. We investigated prokaryotic abundance, activity and biodiversity, viral abundance and prokaryotic infections, along with the biochemical composition of the sediment organic matter. We found that, despite differences in local environmental dynamics, viral life strategies change in acidified conditions from mainly lytic to temperate lifestyles (e.g., chronic infection), also resulting in a lowered impact on prokaryotic communities, which shift towards (chemo)autotrophic assemblages, with lower organic matter consumption. Taken together, these results suggest that ocean acidification exerts a deep control on microbial benthic assemblages, with important feedbacks on ecosystem functioning.

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Palmeira, Leonor, Simon Penel, Vincent Lotteau, Chantal Rabourdin-Combe, and Christian Gautier. "PhEVER: a database for the global exploration of virus–host evolutionary relationships." Nucleic Acids Research 39, suppl_1 (November 16, 2010): D569—D575. http://dx.doi.org/10.1093/nar/gkq1013.

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Torres, Andrea N., Candace K. Mathiason, and Edward A. Hoover. "Re-examination of feline leukemia virus: host relationships using real-time PCR." Virology 332, no. 1 (February 2005): 272–83. http://dx.doi.org/10.1016/j.virol.2004.10.050.

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Alkan, Cigdem, Gautier Brésard, Lise Frézal, Aurélien Richaud, Albane Ruaud, Gaotian Zhang, and Marie-Anne Félix. "Natural variation in infection specificity of Caenorhabditis briggsae isolates by two RNA viruses." PLOS Pathogens 20, no. 6 (June 11, 2024): e1012259. http://dx.doi.org/10.1371/journal.ppat.1012259.

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Antagonistic relationships such as host-virus interactions potentially lead to rapid evolution and specificity in interactions. The Orsay virus is so far the only horizontal virus naturally infecting the nematode C. elegans. In contrast, several related RNA viruses infect its congener C. briggsae, including Santeuil (SANTV) and Le Blanc (LEBV) viruses. Here we focus on the host’s intraspecific variation in sensitivity to these two intestinal viruses. Many temperate-origin C. briggsae strains, including JU1264 and JU1498, are sensitive to both, while many tropical strains, such as AF16, are resistant to both. Interestingly, some C. briggsae strains exhibit a specific resistance, such as the HK104 strain, specifically resistant to LEBV. The viral sensitivity pattern matches the strains’ geographic and genomic relationships. The heavily infected strains mount a seemingly normal small RNA response that is insufficient to suppress viral infection, while the resistant strains show no small RNA response, suggesting an early block in viral entry or replication. We use a genetic approach from the host side to map genomic regions participating in viral resistance polymorphisms. Using Advanced Intercrossed Recombinant Inbred Lines (RILs) between virus-resistant AF16 and SANTV-sensitive HK104, we detect Quantitative Trait Loci (QTLs) on chromosomes IV and III. Building RILs between virus-sensitive JU1498 and LEBV-resistant HK104 followed by bulk segregant analysis, we identify a chromosome II QTL. In both cases, further introgressions of the regions confirmed the QTLs. This diversity provides an avenue for studying virus entry, replication, and exit mechanisms, as well as host-virus specificity and the host response to a specific virus infection.

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Boromisa, Robert D., and Paul R. Grimstad. "Virus-Vector-Host Relationships of Aedes stimulans and Jamestown Canyon Virus in a Northern Indiana Enzootic Focus." American Journal of Tropical Medicine and Hygiene 35, no. 6 (November 1, 1986): 1285–95. http://dx.doi.org/10.4269/ajtmh.1986.35.1285.

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Parikka, Kaarle J., Marc Le Romancer, Nina Wauters, and Stéphan Jacquet. "Deciphering the virus-to-prokaryote ratio (VPR): insights into virus-host relationships in a variety of ecosystems." Biological Reviews 92, no. 2 (April 26, 2016): 1081–100. http://dx.doi.org/10.1111/brv.12271.

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Gaunt, Michael W., Amadou A. Sall, Xavier de Lamballerie, Andrew K. I. Falconar, Tatyana I. Dzhivanian, and Ernest A. Gould. "Phylogenetic relationships of flaviviruses correlate with their epidemiology, disease association and biogeography." Journal of General Virology 82, no. 8 (August 1, 2001): 1867–76. http://dx.doi.org/10.1099/0022-1317-82-8-1867.

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Phylogenetic analysis of the Flavivirus genus, using either partial sequences of the non-structural 5 gene or the structural envelope gene, revealed an extensive series of clades defined by their epidemiology and disease associations. These phylogenies identified mosquito-borne, tick-borne and no-known-vector (NKV) virus clades, which could be further subdivided into clades defined by their principal vertebrate host. The mosquito-borne flaviviruses revealed two distinct epidemiological groups: (i) the neurotropic viruses, often associated with encephalitic disease in humans or livestock, correlated with the Culex species vector and bird reservoirs and (ii) the non-neurotropic viruses, associated with haemorrhagic disease in humans, correlated with the Aedes species vector and primate hosts. Thus, the tree topology describing the virus–host association may reflect differences in the feeding behaviour between Aedes and Culex mosquitoes. The tick-borne viruses also formed two distinct groups: one group associated with seabirds and the other, the tick-borne encephalitis complex viruses, associated primarily with rodents. The NKV flaviviruses formed three distinct groups: one group, which was closely related to the mosquito-borne viruses, associated with bats; a second group, which was more genetically distant, also associated with bats; and a third group associated with rodents. Each epidemiological group within the phylogenies revealed distinct geographical clusters in either the Old World or the New World, which for mosquito-borne viruses may reflect an Old World origin. The correlation between epidemiology, disease correlation and biogeography begins to define the complex evolutionary relationships between the virus, vector, vertebrate host and ecological niche.

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Fulhorst, Charles F., Remi N. Charrel, Robert D. Bradley, Mary Louise Milazzo, and Darin S. Carroll. "Natural host relationships and genetic diversity of Whitewater Arroyo virus in southern Texas." American Journal of Tropical Medicine and Hygiene 67, no. 1 (July 1, 2002): 114–18. http://dx.doi.org/10.4269/ajtmh.2002.67.114.

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Ammar, E. D., S. Elnagar, A. E. Abul-Ata, and G. H. Sewify. "Vector and Host-Plant Relationships of the Leafhopper-Borne Maize Yellow Stripe Virus." Journal of Phytopathology 126, no. 3 (July 1989): 246–52. http://dx.doi.org/10.1111/j.1439-0434.1989.tb01111.x.

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Fayer, Ronald, Palmer Orlandi, and Michael L. Perdue. "Virulence factor activity relationships for hepatitis E and Cryptosporidium." Journal of Water and Health 7, S1 (August 1, 2009): S55—S63. http://dx.doi.org/10.2166/wh.2009.044.

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The hepatitis E virus and Cryptosporidium are waterborne pathogens, each consisting of distinct taxa, genotypes and isolates that infect humans, nonhuman animal species or both. Some are associated with disease, others are not. Factors contributing to disease are extremely complicated, possibly involving differences in one or more traits associated with an organism's taxon, genotype or isolate and its infectious dose, and age or condition, as well as the host's physiology and immune status. Potential virulence factors have not yet been identified for HEV. Putative virulence factors for Cryptosporidium might be found in recently recognized genes involved in processes such as excystation, adherence to host cells, invasion, intracellular maintenance and host cell destruction.

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Walsh, Sarah K., Ryan M. Imrie, Marta Matuszewska, Gavin K. Paterson, Lucy A. Weinert, Jarrod D. Hadfield, Angus Buckling, and Ben Longdon. "The host phylogeny determines viral infectivity and replication across Staphylococcus host species." PLOS Pathogens 19, no. 6 (June 8, 2023): e1011433. http://dx.doi.org/10.1371/journal.ppat.1011433.

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Virus host shifts, where a virus transmits to and infects a novel host species, are a major source of emerging infectious disease. Genetic similarity between eukaryotic host species has been shown to be an important determinant of the outcome of virus host shifts, but it is unclear if this is the case for prokaryotes where anti-virus defences can be transmitted by horizontal gene transfer and evolve rapidly. Here, we measure the susceptibility of 64 strains of Staphylococcaceae bacteria (48 strains of Staphylococcus aureus and 16 non-S. aureus species spanning 2 genera) to the bacteriophage ISP, which is currently under investigation for use in phage therapy. Using three methods–plaque assays, optical density (OD) assays, and quantitative (q)PCR–we find that the host phylogeny explains a large proportion of the variation in susceptibility to ISP across the host panel. These patterns were consistent in models of only S. aureus strains and models with a single representative from each Staphylococcaceae species, suggesting that these phylogenetic effects are conserved both within and among host species. We find positive correlations between susceptibility assessed using OD and qPCR and variable correlations between plaque assays and either OD or qPCR, suggesting that plaque assays alone may be inadequate to assess host range. Furthermore, we demonstrate that the phylogenetic relationships between bacterial hosts can generally be used to predict the susceptibility of bacterial strains to phage infection when the susceptibility of closely related hosts is known, although this approach produced large prediction errors in multiple strains where phylogeny was uninformative. Together, our results demonstrate the ability of bacterial host evolutionary relatedness to explain differences in susceptibility to phage infection, with implications for the development of ISP both as a phage therapy treatment and as an experimental system for the study of virus host shifts.

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Olson, Victoria A., Kevin L. Karem, Scott K. Smith, Christine M. Hughes, and Inger K. Damon. "Smallpox virus plaque phenotypes: genetic, geographical and case fatality relationships." Journal of General Virology 90, no. 4 (April 1, 2009): 792–98. http://dx.doi.org/10.1099/vir.0.008169-0.

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Smallpox (infection with Orthopoxvirus variola) remains a feared illness more than 25 years after its eradication. Historically, case-fatality rates (CFRs) varied between outbreaks (<1 to ∼40 %), the reasons for which are incompletely understood. The extracellular enveloped virus (EEV) form of orthopoxvirus progeny is hypothesized to disseminate infection. Investigations with the closely related Orthopoxvirus vaccinia have associated increased comet formation (EEV production) with increased mouse mortality (pathogenicity). Other vaccinia virus genetic manipulations which affect EEV production inconsistently support this association. However, antisera against vaccinia virus envelope protect mice from lethal challenge, further supporting a critical role for EEV in pathogenicity. Here, we show that the increased comet formation phenotypes of a diverse collection of variola viruses associate with strain phylogeny and geographical origin, but not with increased outbreak-related CFRs; within clades, there may be an association of plaque size with CFR. The mechanisms for variola virus pathogenicity probably involves multiple host and pathogen factors.

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Truong Nguyen, Phuoc, Santiago Garcia-Vallvé, and Pere Puigbò. "An Unsupervised Algorithm for Host Identification in Flaviviruses." Life 11, no. 5 (May 14, 2021): 442. http://dx.doi.org/10.3390/life11050442.

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Early characterization of emerging viruses is essential to control their spread, such as the Zika Virus outbreak in 2014. Among other non-viral factors, host information is essential for the surveillance and control of virus spread. Flaviviruses (genus Flavivirus), akin to other viruses, are modulated by high mutation rates and selective forces to adapt their codon usage to that of their hosts. However, a major challenge is the identification of potential hosts for novel viruses. Usually, potential hosts of emerging zoonotic viruses are identified after several confirmed cases. This is inefficient for deterring future outbreaks. In this paper, we introduce an algorithm to identify the host range of a virus from its raw genome sequences. The proposed strategy relies on comparing codon usage frequencies across viruses and hosts, by means of a normalized Codon Adaptation Index (CAI). We have tested our algorithm on 94 flaviviruses and 16 potential hosts. This novel method is able to distinguish between arthropod and vertebrate hosts for several flaviviruses with high values of accuracy (virus group 91.9% and host type 86.1%) and specificity (virus group 94.9% and host type 79.6%), in comparison to empirical observations. Overall, this algorithm may be useful as a complementary tool to current phylogenetic methods in monitoring current and future viral outbreaks by understanding host–virus relationships.

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Chatziandreou, N., N. Stock, D. Young, J. Andrejeva, K. Hagmaier, D. J. McGeoch, and R. E. Randall. "Relationships and host range of human, canine, simian and porcine isolates of simian virus 5 (parainfluenza virus 5)." Journal of General Virology 85, no. 10 (October 1, 2004): 3007–16. http://dx.doi.org/10.1099/vir.0.80200-0.

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Sequence comparison of the V/P and F genes of 13 human, canine, porcine and simian isolates of simian virus 5 (SV5) revealed a surprising lack of sequence variation at both the nucleotide and amino acid levels (0–3 %), even though the viruses were isolated over 30 years and originated from countries around the world. Furthermore, there were no clear distinguishing amino acid or nucleotide differences among the isolates that correlated completely with the species from which they were isolated. In addition, there was no evidence that the ability of the viruses to block interferon signalling by targeting STAT1 for degradation was confined to the species from which they were isolated. All isolates had an extended cytoplasmic tail in the F protein, compared with the original W3A and WR monkey isolates. Sequence analysis of viruses that were derived from human bone-marrow cells isolated in London in the 1980s revealed that, whilst they were related more closely to one another than to the other isolates, they all had identifying differences, suggesting that they were independent isolates. These results therefore support previous data suggesting that SV5 can infect humans persistently, although the relationship of SV5 to any human disease remains highly contentious. Given that SV5 has been isolated on multiple occasions from different species, it is proposed that the term simian virus 5 is inappropriate and suggested that the virus should be renamed parainfluenza virus 5.

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Rouse, Barry T., and Scott N. Mueller. "Some vexations that challenge viral immunology." F1000Research 5 (May 27, 2016): 1015. http://dx.doi.org/10.12688/f1000research.8391.1.

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The field of viral immunology seeks to understand mechanisms of virus-host interaction with a view of applying this knowledge to the design of effective vaccines and immunomodulators that control viral infections. This brief review discusses several areas of the field that hold substantial promise for translation, but where further work is critically required to find solutions. We emphasize that our fundamental understanding of virus-host relationships is moving in leaps and bounds, but we lag behind in applying this knowledge to the successful control of many viral infections.

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Smith, Daniel F. Q., and Arturo Casadevall. "On the relationship between Pathogenic Potential and Infective Inoculum." PLOS Pathogens 18, no. 6 (June 13, 2022): e1010484. http://dx.doi.org/10.1371/journal.ppat.1010484.

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Pathogenic Potential (PP) is a mathematical description of an individual microbe, virus, or parasite’s ability to cause disease in a host, given the variables of inoculum, signs of disease, mortality, and in some instances, median survival time of the host. We investigated the relationship between pathogenic potential (PP) and infective inoculum (I) using two pathogenic fungi in the wax moth Galleria mellonella with mortality as the relevant outcome. Our analysis for C. neoformans infection revealed negative exponential relationship between PP and I. Plotting the log(I) versus the Fraction of animals with signs or symptoms (Fs) over median host survival time (T) revealed a linear relationship, with a slope that varied between the different fungi studied and a y-intercept corresponding to the inoculum that produced no signs of disease. The I vs Fs/T slope provided a measure of the pathogenicity of each microbial species, which we call the pathogenicity constant or kPath. The kPath provides a new parameter to quantitatively compare the relative virulence and pathogenicity of microbial species for a given host. In addition, we investigated the PP and Fs/T from values found in preexisting literature. Overall, the relationship between Fs/T and PP versus inoculum varied among microbial species and extrapolation to zero signs of disease allowed the calculation of the lowest pathogenic inoculum (LPI) of a microbe. Microbes tended to fall into two groups: those with positive linear relationships between PP and Fs/T vs I, and those that had a negative exponential PP vs I relationship with a positive logarithmic Fs/T vs I relationship. The microbes with linear relationships tended to be bacteria, whereas the exponential-based relationships tended to be fungi or higher order eukaryotes. Differences in the type and sign of the PP vs I and Fs/T vs I relationships for pathogenic microbes suggest fundamental differences in host-microbe interactions leading to disease.

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Tscharke, David C., and Geoffrey L. Smith. "A model for vaccinia virus pathogenesis and immunity based on intradermal injection of mouse ear pinnae." Journal of General Virology 80, no. 10 (October 1, 1999): 2751–55. http://dx.doi.org/10.1099/0022-1317-80-10-2751.

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Vaccinia virus (VV) proteins that interfere with the host response to infection are of interest because they provide insight into virus–host relationships and may affect the safety and immunogenicity of recombinant VV (rVV) vaccines. Such vaccines need assessment in animal models and with this aim a model of VV infection based on intradermal injection of BALB/c ear pinnae was developed and characterized. In this model, the outcome of infection is affected by the dose of virus inoculated but virus spread is minimal and the mice suffer no signs of systemic illness. Cellular and humoral immune responses to these infections were measured readily and were independent of virus dose over a 100-fold range. Thus the model seems suitable for the analysis of the safety and immunogenicity of VV mutants lacking specific immunomodulatory proteins or bearing foreign antigens.

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Kelling, Clayton L., Jane E. Kennedy, Lisa C. Stine, Kristine K. Rump, Prem S. Paul, and James E. Partridge. "Genetic comparison of ovine and bovine pestiviruses." American Journal of Veterinary Research 51, no. 12 (December 1, 1990): 2019–24. http://dx.doi.org/10.2460/ajvr.1990.51.12.2019.

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SUMMARY Viral rna oligonucleotide fingerprinting was used to compare genetic relationships among pestiviruses originating from ovine or bovine host species. Ovine pestiviruses, including reference border disease virus and 2 border disease isolates originating from natural pestivirus infections of sheep, appeared to have a more distant genetic relationship among themselves than with certain bovine pestiviruses. A closer genetic relatedness was evident between border disease virus and 3 noncytopathic bovine pestiviruses, including Draper bovine viral diarrhea virus (bvdv), a bvdv isolate that originated from aborted bovine fetuses, and a virus that was isolated from the serum of a calf that had a chronic bvdv infection. Four noncytopathic bovine viruses, including Draper bvdv and 3 field isolates, were closely related. Reference Oregon C24V bvdv, a cytopathic virus, was closely related to only 1 of the 7 noncytopathic viruses in this study.

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Davis, Robert F. "Cucumber Mosaic Virus Isolates Seedborne inPhaseolus vulgaris: Serology, Host-Pathogen Relationships, and Seed Transmission." Phytopathology 76, no. 10 (1986): 999. http://dx.doi.org/10.1094/phyto-76-999.

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Nolt, B. L. "Indian Peanut Clump Virus Isolates: Host Range, Symptomatology, Serological Relationships, and Some Physical Properties." Phytopathology 78, no. 3 (1988): 310. http://dx.doi.org/10.1094/phyto-78-310.

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Li, You, Zhi Jiang Zeng, and Zi Long Wang. "Phylogenetic analysis of the honeybee Sacbrood virus." Journal of Apicultural Science 60, no. 1 (June 1, 2016): 31–38. http://dx.doi.org/10.1515/jas-2016-0009.

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Abstract Sacbrood virus (SBV) is one of the most common and harmful viruses to honeybees. It causes failure to pupate and death during larval stage, in adult bees it has an influence on their behavior and even shortens their life-span. In this study, we analyzed the phylogenetic relationships among the SBV isolates from all around the world, with from both Apis cerana and Apis mellifera. Phylogenetic trees were constructed based on three types of nucleotide sequences: complete genome sequence, VP1 gene and SB1-2 fragment of SBV. Moreover, genome recombination analysis was performed to assess the effect of genome recombination on the evolutionary relationship of some SBV isolates. The phylogenetic trees showed that although all the SBV isolates form two major groups, these two groups were not formed strictly according to their host specificity or geographical origin. These results indicate that both host specificity and geographic origin decide the genetic diversity of SBV strains.

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Brown, J. K. "Transmission, Host Range, and Virus-Vector Relationships of Chino del Tomate Virus, a Whitefly-Transmitted Geminivirus from Sinaloa, Mexico." Plant Disease 72, no. 10 (1988): 866. http://dx.doi.org/10.1094/pd-72-0866.

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Sidorkiewicz, Malgorzata. "Hepatitis C Virus Uses Host Lipids to Its Own Advantage." Metabolites 11, no. 5 (April 27, 2021): 273. http://dx.doi.org/10.3390/metabo11050273.

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Lipids and lipoproteins constitute indispensable components for living not only for humans. In the case of hepatitis C virus (HCV), the option of using the products of our lipid metabolism is “to be, or not to be”. On the other hand, HCV infection, which is the main cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma, exerts a profound influence on lipid and lipoprotein metabolism of the host. The consequences of this alternation are frequently observed as hypolipidemia and hepatic steatosis in chronic hepatitis C (CHC) patients. The clinical relevance of these changes reflects the fact that lipids and lipoprotein play a crucial role in all steps of the life cycle of HCV. The virus circulates in the bloodstream as a highly lipidated lipo-viral particle (LVP) that defines HCV hepatotropism. Thus, strict relationships between lipids/lipoproteins and HCV are indispensable for the mechanism of viral entry into hepatocytes, viral replication, viral particles assembly and secretion. The purpose of this review is to summarize the tricks thanks to which HCV utilizes host lipid metabolism to its own advantage.

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Lukashov, Vladimir V., and Jaap Goudsmit. "Evolutionary relationships among Astroviridae." Journal of General Virology 83, no. 6 (June 1, 2002): 1397–405. http://dx.doi.org/10.1099/0022-1317-83-6-1397.

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To study the evolutionary relationships among astroviruses, all available sequences for members of the family Astroviridae were collected. Phylogenetic analysis distinguished two deep-rooted groups: one comprising mammalian astroviruses, with ovine astrovirus being an outlier, and the other comprising avian astroviruses. All virus species as well as serotypes of human astroviruses represented individual lineages within the tree. All human viruses clustered together and separately from non-human viruses, which argue for their common evolutionary origin and against ongoing animal-to-human transmissions. The branching order of mammalian astroviruses was exactly the opposite of that of their host species, suggesting at least two cross-species transmissions involving pigs, cats and humans, possibly through intermediate hosts. Analysis of synonymous (Ds) versus non-synonymous (Da) distances revealed that negative selection is dominating in the evolution of astroviruses, with the Ds:Da ratios being up to 46 for the comparisons of the most closely related viruses. Phylogenetic analyses of all open reading frames (ORFs) based on Ds resulted in the loss of tree structures, with virus species – and in ORF2, even serotypes of human astroviruses – branching out from virtually a single node, suggesting their ancient separation. The strong selection against non-synonymous substitutions, the low number of which is, therefore, not proof of a recent separation between lineages, together with the position of the oldest available human astrovirus strain (1971) far from the common node of its serotype 4, suggest that intraserotype diversification originates from an earlier date.

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Jancovich, James K., Michel Bremont, Jeffrey W. Touchman, and Bertram L. Jacobs. "Evidence for Multiple Recent Host Species Shifts among the Ranaviruses (Family Iridoviridae)." Journal of Virology 84, no. 6 (December 30, 2009): 2636–47. http://dx.doi.org/10.1128/jvi.01991-09.

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ABSTRACT Members of the genus Ranavirus (family Iridoviridae) have been recognized as major viral pathogens of cold-blooded vertebrates. Ranaviruses have been associated with amphibians, fish, and reptiles. At this time, the relationships between ranavirus species are still unclear. Previous studies suggested that ranaviruses from salamanders are more closely related to ranaviruses from fish than they are to ranaviruses from other amphibians, such as frogs. Therefore, to gain a better understanding of the relationships among ranavirus isolates, the genome of epizootic hematopoietic necrosis virus (EHNV), an Australian fish pathogen, was sequenced. Our findings suggest that the ancestral ranavirus was a fish virus and that several recent host shifts have taken place, with subsequent speciation of viruses in their new hosts. The data suggesting several recent host shifts among ranavirus species increase concern that these pathogens of cold-blooded vertebrates may have the capacity to cross numerous poikilothermic species barriers and the potential to cause devastating disease in their new hosts.

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Calegario, Renata Faier, Sávio de Siqueira Ferreira, Eduardo Chumbinho de Andrade, and Francisco Murilo Zerbini. "Characterization of Tomato yellow spot virus, a novel tomato-infecting begomovirus in Brazil." Pesquisa Agropecuária Brasileira 42, no. 9 (September 2007): 1335–43. http://dx.doi.org/10.1590/s0100-204x2007000900016.

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The objective of this work was the biological and molecular characterization of a begomovirus detected in São Joaquim de Bicas, Minas Gerais, Brazil, named TGV-[Bi2], by determining its host range, complete nucleotide sequence and phylogenetic relationships with other begomoviruses. Biological characterization consisted of a host range study using either sap inoculation or particle bombardment as inoculation methods. The yellow spot virus can infect plants in Solanaceae and Amaranthaceae, including economically importat crops as sweet pepper, and weeds as Datura stramonium and Nicotiana silvestris. For the molecular characterization, the full-length genome (DNA-A and DNA-B) was amplified, cloned and completely sequenced. Sequence comparisons and phylogenetic analyses indicated that TGV-[Bi2] constitutes a novel begomovirus species named Tomato yellow spot virus (ToYSV), closely related to Sida mottle virus (SiMoV).

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Campagnola, Grace, Seth McDonald, Stéphanie Beaucourt, Marco Vignuzzi, and Olve B. Peersen. "Structure-Function Relationships Underlying the Replication Fidelity of Viral RNA-Dependent RNA Polymerases." Journal of Virology 89, no. 1 (October 15, 2014): 275–86. http://dx.doi.org/10.1128/jvi.01574-14.

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ABSTRACTViral RNA-dependent RNA polymerases are considered to be low-fidelity enzymes, providing high mutation rates that allow for the rapid adaptation of RNA viruses to different host cell environments. Fidelity is tuned to provide the proper balance of virus replication rates, pathogenesis, and tissue tropism needed for virus growth. Using our structures of picornaviral polymerase-RNA elongation complexes, we have previously engineered more than a dozen coxsackievirus B3 polymerase mutations that significantly altered virus replication rates andin vivofidelity and also provided a set of secondary adaptation mutations after tissue culture passage. Here we report a biochemical analysis of these mutations based on rapid stopped-flow kinetics to determine elongation rates and nucleotide discrimination factors. The data show a spatial separation of fidelity and replication rate effects within the polymerase structure. Mutations in the palm domain have the greatest effects onin vitronucleotide discrimination, and these effects are strongly correlated with elongation rates andin vivomutation frequencies, with faster polymerases having lower fidelity. Mutations located at the top of the finger domain, on the other hand, primarily affect elongation rates and have relatively minor effects on fidelity. Similar modulation effects are seen in poliovirus polymerase, an inherently lower-fidelity enzyme where analogous mutations increase nucleotide discrimination. These findings further our understanding of viral RNA-dependent RNA polymerase structure-function relationships and suggest that positive-strand RNA viruses retain a unique palm domain-based active-site closure mechanism to fine-tune replication fidelity.IMPORTANCEPositive-strand RNA viruses represent a major class of human and animal pathogens with significant health and economic impacts. These viruses replicate by using a virally encoded RNA-dependent RNA polymerase enzyme that has low fidelity, generating many mutations that allow the rapid adaptation of these viruses to different tissue types and host cells. In this work, we use a structure-based approach to engineer mutations in viral polymerases and study their effects onin vitronucleotide discrimination as well as virus growth and genome replication fidelity. These results show that mutation rates can be drastically increased or decreased as a result of single mutations at several key residues in the polymerase palm domain, and this can significantly attenuate virus growthin vivo. These findings provide a pathway for developing live attenuated virus vaccines based on engineering the polymerase to reduce virus fitness.

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Liang, Xiao-Zhen, Bernett T. K. Lee, and Sek-Man Wong. "Covariation in the Capsid Protein of Hibiscus Chlorotic Ringspot Virus Induced by Serial Passaging in a Host That Restricts Movement Leads to Avirulence in Its Systemic Host." Journal of Virology 76, no. 23 (December 1, 2002): 12320–24. http://dx.doi.org/10.1128/jvi.76.23.12320-12324.2002.

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ABSTRACT Hibiscus chlorotic ringspot virus (HCRSV) from naturally infected Hibiscus rosa-sinensis L. loses virulence in its experimental systemic host Hibiscus cannabinus L. (kenaf) after serial passages in a local lesion host Chenopodium quinoa. Here we report the genetic changes responsible for the loss of virulence at the molecular level. A remarkable covariation of eight site-specific amino acids was found in the HCRSV capsid protein (CP) after serial passages in C. quinoa: Val49→Ile, Ile95→Val, Lys270→Arg, Gly272→Asp, Tyr274→His, Ala311→Asp, Asp334→Ala, and Ala335→Thr. Covariation of at least three of the eight amino acids, Val49, Ile95, and Lys270, caused the virus to become avirulent in kenaf. Interestingly, the nature of the covariation was consistent and reproducible at each serial passage. These data indicate that the nonsynonymous substitutions of amino acids in the HCRSV CP after serial passages in C. quinoa are not likely to be random events but may be due to host-associated positive selection or accelerated genetic drift. The observed interdependence among the three amino acids leading to avirulence in kenaf may have implications for structural or functional relationships in this virus-host interaction.

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Camp, Jeremy V., Ulas Bagci, Yong-Kyu Chu, Brendan Squier, Mostafa Fraig, Silvia M. Uriarte, Haixun Guo, Daniel J. Mollura, and Colleen B. Jonsson. "Lower Respiratory Tract Infection of the Ferret by 2009 H1N1 Pandemic Influenza A Virus Triggers Biphasic, Systemic, and Local Recruitment of Neutrophils." Journal of Virology 89, no. 17 (June 10, 2015): 8733–48. http://dx.doi.org/10.1128/jvi.00817-15.

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ABSTRACTInfection of the lower respiratory tract by influenza A viruses results in increases in inflammation and immune cell infiltration in the lung. The dynamic relationships among the lung microenvironments, the lung, and systemic host responses during infection remain poorly understood. Here we used extensive systematic histological analysis coupled with live imaging to gain access to these relationships in ferrets infected with the 2009 H1N1 pandemic influenza A virus (H1N1pdm virus). Neutrophil levels rose in the lungs of H1N1pdm virus-infected ferrets 6 h postinfection and became concentrated at areas of the H1N1pdm virus-infected bronchiolar epithelium by 1 day postinfection (dpi). In addition, neutrophil levels were increased throughout the alveolar spaces during the first 3 dpi and returned to baseline by 6 dpi. Histochemical staining revealed that neutrophil infiltration in the lungs occurred in two waves, at 1 and 3 dpi, and gene expression within microenvironments suggested two types of neutrophils. Specifically, CCL3 levels, but not CXCL8/interleukin 8 (IL-8) levels, were higher within discrete lung microenvironments and coincided with increased infiltration of neutrophils into the lung. We used live imaging of ferrets to monitor host responses within the lung over time with [18F]fluorodeoxyglucose (FDG). Sites in the H1N1pdm virus-infected ferret lung with high FDG uptake had high levels of proliferative epithelium. In summary, neutrophils invaded the H1N1pdm virus-infected ferret lung globally and focally at sites of infection. Increased neutrophil levels in microenvironments did not correlate with increased FDG uptake; hence, FDG uptake may reflect prior infection and inflammation of lungs that have experienced damage, as evidenced by bronchial regeneration of tissues in the lungs at sites with high FDG levels.IMPORTANCESevere influenza disease is characterized by an acute infection of the lower airways that may progress rapidly to organ failure and death. Well-developed animal models that mimic human disease are essential to understanding the complex relationships of the microenvironment, organ, and system in controlling virus replication, inflammation, and disease progression. Employing the ferret model of H1N1pdm virus infection, we used live imaging and comprehensive histological analyses to address specific hypotheses regarding spatial and temporal relationships that occur during the progression of infection and inflammation. We show the general invasion of neutrophils at the organ level (lung) but also a distinct pattern of localized accumulation within the microenvironment at the site of infection. Moreover, we show that these responses were biphasic within the lung. Finally, live imaging revealed an early and sustained host metabolic response at sites of infection that may reflect damage and repair of tissues in the lungs.

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Murata, Takayuki. "Human Herpesvirus and the Immune Checkpoint PD-1/PD-L1 Pathway: Disorders and Strategies for Survival." Microorganisms 9, no. 4 (April 8, 2021): 778. http://dx.doi.org/10.3390/microorganisms9040778.

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The immune system has evolved as a complex and efficient means of coping with extrinsic materials, such as pathogens and toxins, as well as intrinsic abnormalities, such as cancers. Although rapid and timely activation of the immune system is obviously important, regulated downregulation of the system is almost as significant as activation to prevent runaway immunity, such as allergies and hypercytokinemia. Therefore, the immune checkpoint programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is beneficial for the host. On the other hand, pathogens have evolved to evade host immunity by taking advantage of the PD-1/PD-L1 pathway. This review is focused on human herpesviruses, such as herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein–Barr virus (EBV), which cause various types of disorders, and their relationships with the PD-1/PD-L1 pathway. Understanding such relationships will be useful for developing preventative and therapeutic methods for disorders caused by herpesviruses.

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Journal articles on the topic 'Host-virus relationships'

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