Global phylogeography and evolution of chelonid fibropapilloma-associated herpesvirus

Abstract

6Lisbon Oceanarium, 1999-005 Lisbon, Portugal A global phylogeny for chelonid fibropapilloma-associated herpesvirus (CFPHV), the most likely aetiological agent of fibropapillomatosis (FP) in sea turtles, was inferred, using dated sequences, through Bayesian Markov chain Monte Carlo analysis and used to estimate the virus evolutionary rate independent of the evolution of the host, and to resolve the phylogenetic positions of new haplotypes from Puerto Rico and the Gulf of Guinea. Four phylogeographical groups were identified: eastern Pacific, western Atlantic/eastern Caribbean, mid-west Pacific and Atlantic. The latter comprises the Gulf of Guinea and Puerto Rico, suggesting recent virus gene flow between these two regions. One virus haplotype from Florida remained elusive, representing either an independent lineage sharing a common ancestor with all other identified virus variants or an Atlantic representative of the lineage giving rise to the eastern Pacific group. The virus evolutionary rate ranged from 1.62¾10 "4 to 2.22¾10 "4 substitutions per site per year, which is much faster than what is expected for a herpesvirus. The mean time for the most recent common ancestor of the modern virus variants was estimated at 192.90-429.71 years ago, which, although more recent than previous estimates, still supports an interpretation that the global FP pandemic is not the result of a recent acquisition of a virulence mutation(s). The phylogeographical pattern obtained seems partially to reflect sea turtle movements, whereas altered environments appear to be implicated in current FP outbreaks and in the modern evolutionary history of CFPHV. INTRODUCTIONChelonid fibropapilloma-associated herpesvirus (CFPHV) is the most likely aetiological agent of fibropapillomatosis (FP) (Arthur et al., 2008a;Greenblatt et al., 2005;Lackovich et al., 1999;Quackenbush et al., 1998), a neoplastic disease of sea turtles, characterized by recent outbreaks (Diez et al., 2010;Foley et al., 2005;Work & Balazs, 1999). The tumours can be both external and internal and, although benign, depending on location and size, they may obstruct crucial functions such as swimming, feeding and sight, or may impede organ function (Herbst, 1994;Herbst & Klein, 1995). Severe FP also leads to bacteraemia (Work et al., 2003). The most susceptible life stages appear to be neritic juveniles and subadults, whereas in adults the disease is rare (Ene et al., 2005;Herbst & Klein, 1995;Work et al., 2004). A high prevalence of FP is common in anthropogenically altered environments (Aguirre & Lutz, 2004;Herbst, 1994;Van Houtan et al., 2010), suggesting that factors in these environments promote disease outbreaks, for example, through the enhancement of virus transmissibility and/or the enhancement of disease expression via substances thatThe GenBank/EMBL/DDBJ accession numbers for the CFPHV sequences determined in this study are JN580279-JN580296 and JN625251-JN625262.Further details about samples are available with the online version of this paper. Phylogenies of herpesv...

Detection and characterization of fibropapilloma associated herpesvirus of marine turtles in Rio Grande do Sul, Brazil

“…The same pattern of variants was maintained within the 483-bp sequence of the DNA polymerase (Herbst et al, 2004;Patricio et al 2012) that was analyzed in the present study. Sequencing of the ϐibropapilloma specimens collected in RS was introduced into phylogeographic groups described (Patricio et al, 2012), and was allocated in Atlantic group (Fig.3). There is no record of turtle migration between Brazil and Puerto Rico, but telemetry (Hays et al 2001) Histopathology showed the presence of epithelial hyperplasia and nuclear halos as described by Matushima et al (2001) in ϐibropapillomas from São Paulo state.…”

“…Variant D, which was isolated from the loggerhead turtle (Caretta caretta), differs by 5.6% from the other variants, whereas the HA variant differs from the Florida variants A, B and C by only 2.2% (Herbst et al 2004). The same pattern of variants was maintained within the 483-bp sequence of the DNA polymerase (Herbst et al, 2004;Patricio et al 2012) that was analyzed in the present study. Sequencing of the ϐibropapilloma specimens collected in RS was introduced into phylogeographic groups described (Patricio et al, 2012), and was allocated in Atlantic group (Fig.3).…”

“…Kimura 2-parameter pairwise distances (Kimura 1980), calculated for the different nucleotide sequences detected in Brazil, were used to construct a phylogenetic unrooted tree by using the neighbor joining distance methods in the Molecular Evolutionary Genetics Analysis software MEGA 4 (Tamura et al 2007). The following parameters were used for multiple alignment: gap opening penalty = 3, gap extension penalty = 1.8, and keeping the default parameters (Patricio et al 2012). The statistical conϐidence of the tree topologies was performed by 1000 bootstrap replications using the same software.…”

“…Analyzing glycoprotein B (Greenblatt et al, 2005), four groups of variants were described: the Atlantic (formed by sequences from Florida and Barbados), the Middle Paciϐic (Hawaii), the Western Paciϐic (Australia) and the Eastern Paciϐic (Costa Rica and California). Four phylogeographic groups were described: the Eastern Paciϐic (consisting of the samples from San Diego, Costa Rica and Mexico), the Western Atlantic/Eastern Caribbean (Florida samples and Barbados), the Mid-west Paciϐic (Australia and Hawaii samples) and Atlantic (Gulf of Guinea and Puerto Rico samples) (Patricio et al 2012). …”

Global distribution of Chelonid fibropapilloma-associated herpesvirus among clinically healthy sea turtles

“…Consequently the role of CFPHV as the causative agent for FP tumours remains inconclusive. Given CFPHV's putative causal role in FP, to date most studies into the epidemiology, pathology, DNA detection, prevalence and phylogeography of CFPHV have been performed using DNA extracted from tumour tissue [8,19,24,25], thus cannot be used to estimate the prevalence of latent CFPHV infections. While a small number of studies have attempted to detect and quantify viral DNA from tumour free tissue [12,[26][27][28], the samples used were either from known FP infected animals, or from localized populations known to be infected by the virus.…”