Population dynamics of rhesus macaques and associated foamy virus in Bangladesh.

Foamy viruses are complex retroviruses that have been shown to be transmitted from nonhuman primates to humans. In Bangladesh, infection with simian foamy virus (SFV) is ubiquitous among rhesus macaques, which come into contact with humans in diverse locations and contexts throughout the country. We analyzed microsatellite DNA from 126 macaques at six sites in Bangladesh in order to characterize geographic patterns of macaque population structure. We also included in this study 38 macaques owned by nomadic people who train them to perform for audiences. PCR was used to analyze a portion of the proviral gag gene from all SFV-positive macaques, and multiple clones were sequenced. Phylogenetic analysis was used to infer long-term patterns of viral transmission. Analyses of SFV gag gene sequences indicated that macaque populations from different areas harbor genetically distinct strains of SFV, suggesting that geographic features such as forest cover play a role in determining the dispersal of macaques and SFV. We also found evidence suggesting that humans traveling the region with performing macaques likely play a role in the translocation of macaques and SFV. Our studies found that individual animals can harbor more than one strain of SFV and that presence of more than one SFV strain is more common among older animals. Some macaques are infected with SFV that appears to be recombinant. These findings paint a more detailed picture of how geographic and sociocultural factors influence the spectrum of simian-borne retroviruses

Population Status and Conservation of Hoolock Gibbons Hylobates Hoolock Harlan 1834 in Bangladesh

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A Novel Bayesian Method for Detection of APOBEC3-Mediated Hypermutation and Its Application to Zoonotic Transmission of Simian Foamy Viruses

<div><p>Simian Foamy Virus (SFV) can be transmitted from non-human primates (NHP) to humans. However, there are no documented cases of human to human transmission, and significant differences exist between infection in NHP and human hosts. The mechanism for these between-host differences is not completely understood. In this paper we develop a new Bayesian approach to the detection of APOBEC3-mediated hypermutation, and use it to compare SFV sequences from human and NHP hosts living in close proximity in Bangladesh. We find that human APOBEC3G can induce genetic changes that may prevent SFV replication in infected humans in vivo.</p></div

Comparison of MAP to mid-P and RR effect size estimates based on mutation count simulations of 600 bp (A) and 1200 bp (B) length sequences.

<p>The ratio of the mean squared error (MSE) of the RR estimate to that of the MAP estimator is plotted for each simulation parameter set. Points are grouped into lines and colored by control context mutation probability. The x-axis shows the relative probability ratio used for simulation. MSE ratio values greater than one indicate parameter regimes where MAP estimator does better than the RR or the mid-P estimator. Note that because RR isn't necessarily well-defined when one of the counts is zero, pseudocounts were added (see <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1003493#s4" target="_blank">Materials and Methods</a>). Arrows label simulations in the parameter regime of the indicated study.</p

Hypermutation activity by strain, presented on both a sequence by sequence and host by host basis.

<p>These counts are only for core strains. Additionally, since both monkeys and humans are frequently infected with more than one strain, the host counts for a given strain represent the total number of animals infected with that strain, even if infected with other strains as well.</p

The positive rate of Fisher test (before/), mid-P test (between/), and our methodology (after/) under various simulated relative probability ratios.

<p>The rows show a variety of different statistical cutoffs, and columns show a variety of relative probability ratios. The rejection frequency of our method is closer to the cutoff under the null hypothesis, and is more frequently able to find a difference when one exists. These simulations were based on simulated sequences of 1200 bp, with 1/16 of sequence positions in the focus context, and 3/16 in a control context, and with a background (control context) G to A mutation probability of 0.008.</p

Overview of sequences found to be hypermutated.

<p>Every sequence found to be hypermutated in our data set has a column (51 of 77 human sequences, and 105 of 1097 monkey blood sequences and 8 of 152 monkey buccal sequences). The top plot represents hypermutation intensity, where the dot shows the Maximum A Posteori (MAP) value for the relative probability ratio and the lower limit of the line shows the 0.05 quantile. Sequences colored by species and sample type (whole blood (WB) or buccal swab (BS)). The call pattern is the context in which the strongest dinucleotide hypermutation signal was found (using IUPAC degenerate nucleotide notation). “Stops” signifies the presence of in frame stop codons.</p

Viral sequences show distinct hypermutation profiles in the two host species, congruent with activity observed in other studies.

<p>Box and whisker plots on the same data are overlaid, where the thick horizontal bar shows the median value of the observations and the rectangle spans the first and third quartiles; points are randomly “jittered” horizontally within a species to avoid superimposed points. Panels labeled by target context using IUPAC degenerate notation, thus “R” designates A or G, and “M” designates A or C.</p