Viruses

7 pages, 83 KiB

Open AccessEditorial

Virus Dynamics and Evolution: Bridging Scales and Disciplines

by Mary Poss^1,2

¹ Department of Biology, Center for Infectious Disease Dynamics, The Pennsylvania State University, University Park, PA 16802, USA

² Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA

Viruses 2011, 3(8), 1432-1438; https://doi.org/10.3390/v3081432 - 16 Aug 2011

Cited by 1 | Viewed by 5540

Abstract

Viruses have attracted the interest of researchers from multiple disciplines and have nucleated many productive and innovative collaborations. In part, this is because viruses so intimately associate with their hosts that decoupling host and virus biology is difficult, and virus-host interactions occur at [...] Read more.

Viruses have attracted the interest of researchers from multiple disciplines and have nucleated many productive and innovative collaborations. In part, this is because viruses so intimately associate with their hosts that decoupling host and virus biology is difficult, and virus-host interactions occur at multiple scales, from within cells to populations, each of which is intrinsically complex. As a consequence, ecologists, population biologists, evolutionary biologists, and researchers from quantitative fields, including mathematics, statistics, physics and computer science, make significant contributions to the field of virology. Our understanding of virus dynamics and evolution has substantially benefited from these multidisciplinary efforts. It is now common to see advanced phylogenetic reconstruction methods used to determine the origins of emergent viruses, to estimate the effect of natural selection on virus populations, and to assess virus population dynamics. Mathematical and statistical models that elucidate complex virus and host interactions in time and space at the molecular and population level are appearing more regularly in virology and biomedical journals. Massive quantities of data now available due to technological innovation in imaging, increased disease surveillance efforts, and novel approaches to determine social contact structure are changing approaches to study the dynamics and evolution of viral infections in heterogeneous environments. The next decade presents exciting new opportunities and challenges for the expanding field of researchers investigating dynamics of viral infections that will lead to innovation and new insight on virus interactions in both individual hosts and in populations. The compilation of articles in this Special Issue on “Virus Dynamics and Evolution” is comprised of reviews and primary research, summarized below, that provide new perspectives on virus interactions with host organisms through the integration of empirical and computational analyses of virus at molecular, cellular, and population levels. [...] Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

18 pages, 3288 KiB

Open AccessArticle

Is Network Clustering Detectable in Transmission Trees?

by David Welch

Department of Statistics, Pennsylvania State University, 325 Thomas Building, University Park, PA 16802, USA

Viruses 2011, 3(6), 659-676; https://doi.org/10.3390/v3060659 - 3 Jun 2011

Cited by 13 | Viewed by 6681

Abstract

Networks are often used to model the contact processes that allow pathogens to spread between hosts but it remains unclear which models best describe these networks. One question is whether clustering in networks, roughly defined as the propensity for triangles to form, affects [...] Read more.

Networks are often used to model the contact processes that allow pathogens to spread between hosts but it remains unclear which models best describe these networks. One question is whether clustering in networks, roughly defined as the propensity for triangles to form, affects the dynamics of disease spread. We perform a simulation study to see if there is a signal in epidemic transmission trees of clustering. We simulate susceptible-exposed-infectious-removed (SEIR) epidemics (with no re-infection) over networks with fixed degree sequences but different levels of clustering and compare trees from networks with the same degree sequence and different clustering levels. We find that the variation of such trees simulated on networks with different levels of clustering is barely greater than those simulated on networks with the same level of clustering, suggesting that clustering can not be detected in transmission data when re-infection does not occur. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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19 pages, 333 KiB

Open AccessReview

An Ecological and Conservation Perspective on Advances in the Applied Virology of Zoonoses

by Kurt J. Vandegrift^1,2,*, Nina Wale² and Jonathan H. Epstein^2,*

¹ Center for Infectious Disease Dynamics, Pennsylvania State University, University Park, PA 16802, USA

² EcoHealth Alliance, 460 West 34th Street, New York, NY 10001, USA

Viruses 2011, 3(4), 379-397; https://doi.org/10.3390/v3040379 - 15 Apr 2011

Cited by 6 | Viewed by 9299

Abstract

The aim of this manuscript is to describe how modern advances in our knowledge of viruses and viral evolution can be applied to the fields of disease ecology and conservation. We review recent progress in virology and provide examples of how it is [...] Read more.

The aim of this manuscript is to describe how modern advances in our knowledge of viruses and viral evolution can be applied to the fields of disease ecology and conservation. We review recent progress in virology and provide examples of how it is informing both empirical research in field ecology and applied conservation. We include a discussion of needed breakthroughs and ways to bridge communication gaps between the field and the lab. In an effort to foster this interdisciplinary effort, we have also included a table that lists the definitions of key terms. The importance of understanding the dynamics of zoonotic pathogens in their reservoir hosts is emphasized as a tool to both assess risk factors for spillover and to test hypotheses related to treatment and/or intervention strategies. In conclusion, we highlight the need for smart surveillance, viral discovery efforts and predictive modeling. A shift towards a predictive approach is necessary in today’s globalized society because, as the 2009 H1N1 pandemic demonstrated, identification post-emergence is often too late to prevent global spread. Integrating molecular virology and ecological techniques will allow for earlier recognition of potentially dangerous pathogens, ideally before they jump from wildlife reservoirs into human or livestock populations and cause serious public health or conservation issues. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

19 pages, 221 KiB

Open AccessArticle

Genomic Analysis of Hepatitis B Virus Reveals Antigen State and Genotype as Sources of Evolutionary Rate Variation

by Abby Harrison^1,2,*, Philippe Lemey³, Matthew Hurles⁴, Chris Moyes⁵, Susanne Horn⁶, Jan Pryor², Joji Malani², Mathias Supuri⁷, Andrew Masta⁷, Burentau Teriboriki⁸, Tebuka Toatu⁸, David Penny⁹, Andrew Rambaut^10,11 and Beth Shapiro^12,*

¹ Peter Medawar Building for Pathogen Research, Nuffield Department of Medicine, University of Oxford, South Parks Road, Oxford OX1 3SY, UK

² Fiji School of Medicine, Suva, Fiji

³ Department of Microbiology and Immunology, Rega Institute, K.U. Leuven 3000, Belgium

⁴ Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA, UK

⁵ The Hepatitis Foundation of New Zealand, Ohope, Whakatane 3121, New Zealand

⁶ Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany

⁷ School of Medicine and Health Sciences, University of Papua New Guinea, P.O. Box 5623, Boroko, Port Moresby, NCD, Papua New Guinea

⁸ Nawerwere Hospital, Kiribati Ministry of Health, Tawara, Kiribati

⁹ Allan Wilson Centre for Molecular Ecology and Evolution, Massey University, Palmerston North 4442, New Zealand

¹⁰ Ashworth Laboratories, Institute of Evolutionary Biology, King’s Buildings, Edinburgh, EH8 3JT, UK

¹¹ Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA

¹² Department of Biology, The Pennsylvania State University, University Park, PA 16802, USA

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Viruses 2011, 3(2), 83-101; https://doi.org/10.3390/v3020083 - 25 Jan 2011

Cited by 46 | Viewed by 9659

Abstract

Hepatitis B virus (HBV) genomes are small, semi-double-stranded DNA circular genomes that contain alternating overlapping reading frames and replicate through an RNA intermediary phase. This complex biology has presented a challenge to estimating an evolutionary rate for HBV, leading to difficulties resolving the [...] Read more.

Hepatitis B virus (HBV) genomes are small, semi-double-stranded DNA circular genomes that contain alternating overlapping reading frames and replicate through an RNA intermediary phase. This complex biology has presented a challenge to estimating an evolutionary rate for HBV, leading to difficulties resolving the evolutionary and epidemiological history of the virus. Here, we re-examine rates of HBV evolution using a novel data set of 112 within-host, transmission history (pedigree) and among-host genomes isolated over 20 years from the indigenous peoples of the South Pacific, combined with 313 previously published HBV genomes. We employ Bayesian phylogenetic approaches to examine several potential causes and consequences of evolutionary rate variation in HBV. Our results reveal rate variation both between genotypes and across the genome, as well as strikingly slower rates when genomes are sampled in the Hepatitis B e antigen positive state, compared to the e antigen negative state. This Hepatitis B e antigen rate variation was found to be largely attributable to changes during the course of infection in the preCore and Core genes and their regulatory elements. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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8 pages, 100 KiB

Open AccessCommentary

Changes in Population Dynamics in Mutualistic versus Pathogenic Viruses

by Marilyn J. Roossinck

Plant Biology Division, The Samuel Roberts Noble Foundation, Inc., P.O. Box 2180, Ardmore, OK 73402, USA

Viruses 2011, 3(1), 12-19; https://doi.org/10.3390/v3010012 - 17 Jan 2011

Cited by 12 | Viewed by 6955

Abstract

Although generally regarded as pathogens, viruses can also be mutualists. A number of examples of extreme mutualism (i.e., symbiogenesis) have been well studied. Other examples of mutualism are less common, but this is likely because viruses have rarely been thought of [...] Read more.

Although generally regarded as pathogens, viruses can also be mutualists. A number of examples of extreme mutualism (i.e., symbiogenesis) have been well studied. Other examples of mutualism are less common, but this is likely because viruses have rarely been thought of as having any beneficial effects on their hosts. The effect of mutualism on the population dynamics of viruses is a topic that has not been addressed experimentally. However, the potential for understanding mutualism and how a virus might become a mutualist may be elucidated by understanding these dynamics. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

11 pages, 397 KiB

Open AccessReview

Rev Variation during Persistent Lentivirus Infection

by Susan Carpenter^1,*, Wei-Chen Chen² and Karin S. Dorman^2,3

¹ Department of Animal Science, Iowa State University, Ames, IA 50011, USA

² Department of Statistics, Iowa State University, Ames, IA 50011, USA

³ Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, IA 50011, USA

Viruses 2011, 3(1), 1-11; https://doi.org/10.3390/v3010001 - 11 Jan 2011

Cited by 7 | Viewed by 6340

Abstract

The ability of lentiviruses to continually evolve and escape immune control is the central impediment in developing an effective vaccine for HIV-1 and other lentiviruses. Equine infectious anemia virus (EIAV) is considered a useful model for immune control of lentivirus infection. Virus-specific cytotoxic [...] Read more.

The ability of lentiviruses to continually evolve and escape immune control is the central impediment in developing an effective vaccine for HIV-1 and other lentiviruses. Equine infectious anemia virus (EIAV) is considered a useful model for immune control of lentivirus infection. Virus-specific cytotoxic T lymphocytes (CTL) and broadly neutralizing antibody effectively control EIAV replication during inapparent stages of disease, but after years of low-level replication, the virus is still able to produce evasion genotypes that lead to late re-emergence of disease. There is a high rate of genetic variation in the EIAV surface envelope glycoprotein (SU) and in the region of the transmembrane protein (TM) overlapped by the major exon of Rev. This review examines genetic and phenotypic variation in Rev during EIAV disease and a possible role for Rev in immune evasion and virus persistence. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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21 pages, 644 KiB

Open AccessArticle

Exploratory Spatial Analysis of in vitro Respiratory Syncytial Virus Co-infections

by Ivan Simeonov^1,†, Xiaoyan Gong^2,†, Oekyung Kim², Mary Poss^2,3, Francesca Chiaromonte¹ and John Fricks^1,*

¹ Department of Statistics, Pennsylvania State University, University Park, PA 16802, USA

² Department of Biology, Pennsylvania State University, University Park, PA 16802, USA

³ Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA

^† These authors contributed equally to this paper.

Viruses 2010, 2(12), 2782-2802; https://doi.org/10.3390/v2122782 - 22 Dec 2010

Cited by 4 | Viewed by 6289

Abstract

The cell response to virus infection and virus perturbation of that response is dynamic and is reflected by changes in cell susceptibility to infection. In this study, we evaluated the response of human epithelial cells to sequential infections with human respiratory syncytial virus [...] Read more.

The cell response to virus infection and virus perturbation of that response is dynamic and is reflected by changes in cell susceptibility to infection. In this study, we evaluated the response of human epithelial cells to sequential infections with human respiratory syncytial virus strains A2 and B to determine if a primary infection with one strain will impact the ability of cells to be infected with the second as a function of virus strain and time elapsed between the two exposures. Infected cells were visualized with fluorescent markers, and location of all cells in the tissue culture well were identified using imaging software. We employed tools from spatial statistics to investigate the likelihood of a cell being infected given its proximity to a cell infected with either the homologous or heterologous virus. We used point processes, K-functions, and simulation procedures designed to account for specific features of our data when assessing spatial associations. Our results suggest that intrinsic cell properties increase susceptibility of cells to infection, more so for RSV-B than for RSV-A. Further, we provide evidence that the primary infection can decrease susceptibility of cells to the heterologous challenge virus but only at the 16 h time point evaluated in this study. Our research effort highlights the merits of integrating empirical and statistical approaches to gain greater insight on in vitro dynamics of virus-host interactions. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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18 pages, 625 KiB

Open AccessArticle

Profound Differences in Virus Population Genetics Correspond to Protection from CD4 Decline Resulting from Feline Lentivirus Coinfection

by Abinash Padhi¹, Howard Ross², Julie Terwee³, Sue VandeWoude³ and Mary Poss^1,4,5,*

¹ Department of Biology, The Pennsylvania State University, University Park, PA 16802, USA

² School of Biological Sciences, University of Auckland, Auckland, 1142, New Zealand

³ Department of Microbiology, Immunology, and Pathology, Colorado State University, Ft. Collins, CO 80523, USA

⁴ Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA

⁵ 208 Mueller Lab, Center for Infectious Disease Dynamics, The Pennsylvania State University, University Park, PA 16802, USA

Viruses 2010, 2(12), 2663-2680; https://doi.org/10.3390/v2122663 - 10 Dec 2010

Cited by 7 | Viewed by 6731

Abstract

CD4 decline is a hallmark of disease onset in individuals infected with Feline Immunodeficiency Virus (FIV) or Human Immunodeficiency Virus type 1 (HIV-1). Cats that are infected with a poorly replicating, apathogenic FIV (PLV) prior to exposure to a virulent FIV strain (FIVC) [...] Read more.

CD4 decline is a hallmark of disease onset in individuals infected with Feline Immunodeficiency Virus (FIV) or Human Immunodeficiency Virus type 1 (HIV-1). Cats that are infected with a poorly replicating, apathogenic FIV (PLV) prior to exposure to a virulent FIV strain (FIVC) maintain CD4 numbers by mechanisms that are not correlated with a measurable adaptive immune response or reduction in circulating viral load. We employed population genetic approaches based on the 3' portion of the viral genome to estimate the population structure of FIVC from single and dual infected cats. In dual infected cats, FIVC effective population size was decreased during the initial viral expansion phase, and after three weeks of infection, the population declined sharply. The FIVC population recovered to pre-bottleneck levels approximately seven weeks post-FIVC infection. However, the population emerging from the bottleneck in dual infected cats was distinct based on estimates of temporal population structure and substitution profiles. The transition to transversion rate ratio (k) increased from early to late phases in dual infected cats due primarily to a decrease in transversions whereas in single infected cats, k declined over time. Although one clone with extensive G to A substitutions, indicative of host cytidine deaminase editing, was recovered from a dual infected cat during the bottleneck, the post bottleneck population had an overall reduction in G to A substitutions. These data are consistent with a model of PLV-induced host restriction, putatively involving host DNA editing, that alters the dynamics of FIVC throughout the course of infection leading to disease attenuation. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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24 pages, 160 KiB

Open AccessReview

Insights into Arbovirus Evolution and Adaptation from Experimental Studies

by Alexander T. Ciota^1,2 and Laura D. Kramer^1,2,*

¹ The Arbovirus Laboratories, Wadsworth Center, New York State Department of Health, Slingerlands, NY 12159, USA

² University at Albany, State University of New York, Albany, NY 12222, USA

Viruses 2010, 2(12), 2594-2617; https://doi.org/10.3390/v2122594 - 2 Dec 2010

Cited by 78 | Viewed by 9620

Abstract

Arthropod-borne viruses (arboviruses) are maintained in nature by cycling between vertebrate hosts and haematophagous invertebrate vectors. These viruses are responsible for causing a significant public health burden throughout the world, with over 100 species having the capacity to cause human disease. Arbovirus outbreaks [...] Read more.

Arthropod-borne viruses (arboviruses) are maintained in nature by cycling between vertebrate hosts and haematophagous invertebrate vectors. These viruses are responsible for causing a significant public health burden throughout the world, with over 100 species having the capacity to cause human disease. Arbovirus outbreaks in previously naïve environments demonstrate the potential of these pathogens for expansion and emergence, possibly exacerbated more recently by changing climates. These recent outbreaks, together with the continued devastation caused by endemic viruses, such as Dengue virus which persists in many areas, demonstrate the need to better understand the selective pressures that shape arbovirus evolution. Specifically, a comprehensive understanding of host-virus interactions and how they shape both host-specific and virus‑specific evolutionary pressures is needed to fully evaluate the factors that govern the potential for host shifts and geographic expansions. One approach to advance our understanding of the factors influencing arbovirus evolution in nature is the use of experimental studies in the laboratory. Here, we review the contributions that laboratory passage and experimental infection studies have made to the field of arbovirus adaptation and evolution, and how these studies contribute to the overall field of arbovirus evolution. In particular, this review focuses on the areas of evolutionary constraints and mutant swarm dynamics; how experimental results compare to theoretical predictions; the importance of arbovirus ecology in shaping viral swarms; and how current knowledge should guide future questions relevant to understanding arbovirus evolution. Full article

(This article belongs to the Special Issue Virus Dynamics and Evolution)

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