Abstract:Papillomaviruses (PVs) are widespread pathogens. However, the extent of PV infections in bats remains largely unknown. This work represents the first comprehensive study of PVs in Iberian bats. We identified four novel PVs in the mucosa of free-ranging Eptesicus serotinus (EserPV1, EserPV2, and EserPV3) and Rhinolophus ferrumequinum (RferPV1) individuals and analyzed their phylogenetic relationships within the viral family. We further assessed their prevalence in different populations of E. serotinus and its c… Show more
“…5). This genomic locus has been implicated in at least five independent integration events during the evolution of the Papillomaviridae [2, 89], either involving additional coding regions, such as E5 ORFs in DeltaPVs or in TauPVs , or long non-coding regions of unknown function in different members of the Lambda-MuPV crowngroup and of the Beta-XiPV crowngroup. Figure 5.Global scenario of PV evolution.…”
Papillomaviruses (PVs) are a numerous family of small dsDNA viruses infecting virtually all mammals. PVs cause infections without triggering a strong immune response, and natural infection provides only limited protection against reinfection. Most PVs are part and parcel of the skin microbiota. In some cases, infections by certain PVs take diverse clinical presentations from highly productive self-limited warts to invasive cancers. We propose PVs as an excellent model system to study the evolutionary interactions between the immune system and pathogens causing chronic infections: genotypically, PVs are very diverse, with hundreds of different genotypes infecting skin and mucosa; phenotypically, they display extremely broad gradients and trade-offs between key phenotypic traits, namely productivity, immunogenicity, prevalence, oncogenicity and clinical presentation. Public health interventions have been launched to decrease the burden of PV-associated cancers, including massive vaccination against the most oncogenic human PVs, as well as systematic screening for PV chronic anogenital infections. Anti-PVs vaccines elicit protection against infection, induce cross-protection against closely related viruses and result in herd immunity. However, our knowledge on the ecological and intrapatient dynamics of PV infections remains fragmentary. We still need to understand how the novel anthropogenic selection pressures posed by vaccination and screening will affect viral circulation and epidemiology. We present here an overview of PV evolution and the connection between PV genotypes and the phenotypic, clinical manifestations of the diseases they cause. This differential link between viral evolution and the gradient cancer-warts-asymptomatic infections makes PVs a privileged playground for evolutionary medicine research.
“…5). This genomic locus has been implicated in at least five independent integration events during the evolution of the Papillomaviridae [2, 89], either involving additional coding regions, such as E5 ORFs in DeltaPVs or in TauPVs , or long non-coding regions of unknown function in different members of the Lambda-MuPV crowngroup and of the Beta-XiPV crowngroup. Figure 5.Global scenario of PV evolution.…”
Papillomaviruses (PVs) are a numerous family of small dsDNA viruses infecting virtually all mammals. PVs cause infections without triggering a strong immune response, and natural infection provides only limited protection against reinfection. Most PVs are part and parcel of the skin microbiota. In some cases, infections by certain PVs take diverse clinical presentations from highly productive self-limited warts to invasive cancers. We propose PVs as an excellent model system to study the evolutionary interactions between the immune system and pathogens causing chronic infections: genotypically, PVs are very diverse, with hundreds of different genotypes infecting skin and mucosa; phenotypically, they display extremely broad gradients and trade-offs between key phenotypic traits, namely productivity, immunogenicity, prevalence, oncogenicity and clinical presentation. Public health interventions have been launched to decrease the burden of PV-associated cancers, including massive vaccination against the most oncogenic human PVs, as well as systematic screening for PV chronic anogenital infections. Anti-PVs vaccines elicit protection against infection, induce cross-protection against closely related viruses and result in herd immunity. However, our knowledge on the ecological and intrapatient dynamics of PV infections remains fragmentary. We still need to understand how the novel anthropogenic selection pressures posed by vaccination and screening will affect viral circulation and epidemiology. We present here an overview of PV evolution and the connection between PV genotypes and the phenotypic, clinical manifestations of the diseases they cause. This differential link between viral evolution and the gradient cancer-warts-asymptomatic infections makes PVs a privileged playground for evolutionary medicine research.
“…Recently, various viruses have been reported to be harbored by M. nattereri [15], including herpes- [16], lyssa- [17] and astroviruses (e.g. [18]).…”
BackgroundAs bats have recently been described to harbor many different viruses, several studies have investigated the genetic co-variation between viruses and different bat species. However, little is known about the genetic co-variation of viruses and different populations of the same bat species, although such information is needed for an understanding of virus transmission dynamics within a given host species. We hypothesized that if virus transmission between host populations depends on events linked to gene flow in the bats, genetic co-variation should exist between host populations and astroviruses.ResultsWe used 19 nuclear and one mitochondrial microsatellite loci to analyze the genetic population structure of the Natterer’s bat (Myotis nattereri) within and among populations at different geographical scales in Germany. Further, we correlated the observed bat population structure to that of partial astrovirus sequences (323–394 nt fragments of the RNA-dependent RNA polymerase gene) obtained from the same bat populations. Our analyses revealed that the studied bat colonies can be grouped into three distinct genetic clusters, corresponding to the three geographic regions sampled. Furthermore, we observed an overall isolation-by-distance pattern, while no significant pattern was observed within a geographic region. Moreover, we found no correlation between the genetic distances among the bat populations and the astrovirus sequences they harbored. Even though high genetic similarity of some of the astrovirus haplotypes found in several different regions was detected, identical astrovirus haplotypes were not shared between different sampled regions.ConclusionsThe genetic population structure of the bat host suggests that mating sites where several local breeding colonies meet act as stepping-stones for gene flow. Identical astrovirus haplotypes were not shared between different sampled regions suggesting that astroviruses are mostly transmitted among host colonies at the local scale. Nevertheless, high genetic similarity of some of the astrovirus haplotypes found in several different regions implies that occasional transmission across regions with subsequent mutations of the virus haplotypes does occur.Electronic supplementary materialThe online version of this article (doi:10.1186/s12862-016-0856-0) contains supplementary material, which is available to authorized users.
“…For example, it was proposed that herpes simplex virus 2 (HSV-2) arose as a consequence of the transmission of a chimpanzee simplex virus to the human lineage (50). Similarly, host switches as well as lineage duplications have been documented in papillomaviruses (2,3). It seems clear that processes other than codivergence were also at play during PyV evolution, as notably illustrated by the 13 human PyV identified thus far and Estimates that are incompatible with those determined in Prado-Martinez et al (43) appear in bold.…”
It has long been hypothesized that polyomaviruses (PyV; family Polyomaviridae) codiverged with their animal hosts. In contrast, recent analyses suggested that codivergence may only marginally influence the evolution of PyV. We reassess this question by focusing on a single lineage of PyV infecting hominine hosts, the Merkel cell polyomavirus (MCPyV) lineage. By characterizing the genetic diversity of these viruses in seven African great ape taxa, we show that they exhibit very strong host specificity. Reconciliation analyses identify more codivergence than noncodivergence events. In addition, we find that a number of host and PyV divergence events are synchronous. Collectively, our results support codivergence as the dominant process at play during the evolution of the MCPyV lineage. More generally, our results add to the growing body of evidence suggesting an ancient and stable association of PyV and their animal hosts.
IMPORTANCEThe processes involved in viral evolution and the interaction of viruses with their hosts are of great scientific interest and public health relevance. It has long been thought that the genetic diversity of double-stranded DNA viruses was generated over long periods of time, similar to typical host evolutionary timescales. This was also hypothesized for polyomaviruses (family Polyomaviridae), a group comprising several human pathogens, but this remains a point of controversy. Here, we investigate this question by focusing on a single lineage of polyomaviruses that infect both humans and their closest relatives, the African great apes. We show that these viruses exhibit considerable host specificity and that their evolution largely mirrors that of their hosts, suggesting that codivergence with their hosts played a major role in their diversification. Our results provide statistical evidence in favor of an association of polyomaviruses and their hosts over millions of years.
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