Host species-specific usage of the TLR4-LPS receptor complex

2008 ◽  
Vol 14 (4) ◽  
pp. 223-231 ◽  
Author(s):  
Regina Lizundia ◽  
Kay-Sara Sauter ◽  
Geraldine Taylor ◽  
Dirk Werling
Keyword(s):  
Host Species ◽  
Receptor Complex ◽  
Species Specific

scholarly journals Predictable and host‐species specific humanization of the gut microbiota in captive primates

2021 ◽  
Author(s):  
Jennifer L. Houtz ◽  
Jon G. Sanders ◽  
Anthony Denice ◽  
Andrew H. Moeller
Keyword(s):  
Gut Microbiota ◽  
Host Species ◽  
Species Specific

scholarly journals High Natural Permissivity of Primary Rabbit Cells for HIV-1, with a Virion Infectivity Defect in Macrophages as the Final Replication Barrier

2010 ◽  
Vol 84 (23) ◽  
pp. 12300-12314 ◽  
Author(s):  
Hanna-Mari Tervo ◽  
Oliver T. Keppler
Keyword(s):  
T Cells ◽  
Late Phase ◽  
Small Animal ◽  
Receptor Complex ◽  
Restriction Factors ◽  
Cyclin T1 ◽  
Primary Rabbit ◽  
Species Specific ◽  
Hiv 1

ABSTRACT An immunocompetent, permissive, small-animal model would be valuable for the study of human immunodeficiency virus type 1 (HIV-1) pathogenesis and for the testing of drug and vaccine candidates. However, the development of such a model has been hampered by the inability of primary rodent cells to efficiently support several steps of the HIV-1 replication cycle. Although transgenesis of the HIV receptor complex and human cyclin T1 have been beneficial, additional late-phase blocks prevent robust replication of HIV-1 in rodents and limit the range of in vivo applications. In this study, we explored the HIV-1 susceptibility of rabbit primary T cells and macrophages. Envelope-specific and coreceptor-dependent entry of HIV-1 was achieved by expressing human CD4 and CCR5. A block of HIV-1 DNA synthesis, likely mediated by TRIM5, was overcome by limited changes to the HIV-1 gag gene. Unlike with mice and rats, primary cells from rabbits supported the functions of the regulatory viral proteins Tat and Rev, Gag processing, and the release of HIV-1 particles at levels comparable to those in human cells. While HIV-1 produced by rabbit T cells was highly infectious, a macrophage-specific infectivity defect became manifest by a complex pattern of mutations in the viral genome, only part of which were deamination dependent. These results demonstrate a considerable natural HIV-1 permissivity of the rabbit species and suggest that receptor complex transgenesis combined with modifications in gag and possibly vif of HIV-1 to evade species-specific restriction factors might render lagomorphs fully permissive to infection by this pathogenic human lentivirus.

scholarly journals Microbial control of host gene regulation and the evolution of host–microbiome interactions in primates

2020 ◽  
Vol 375 (1808) ◽  
pp. 20190598 ◽  
Author(s):  
Laura Grieneisen ◽  
Amanda L. Muehlbauer ◽  
Ran Blekhman
Keyword(s):  
Gene Expression ◽  
Gene Regulation ◽  
Host Species ◽  
Evolutionary Dynamics ◽  
Microbial Control ◽  
Host Gene ◽  
Primate Species ◽  
Microbiome Composition ◽  
Wide Range ◽  
Species Specific

Recent comparative studies have found evidence consistent with the action of natural selection on gene regulation across primate species. Other recent work has shown that the microbiome can regulate host gene expression in a wide range of relevant tissues, leading to downstream effects on immunity, metabolism and other biological systems in the host. In primates, even closely related host species can have large differences in microbiome composition. One potential consequence of these differences is that host species-specific microbial traits could lead to differences in gene expression that influence primate physiology and adaptation to local environments. Here, we will discuss and integrate recent findings from primate comparative genomics and microbiome research, and explore the notion that the microbiome can influence host evolutionary dynamics by affecting gene regulation across primate host species. This article is part of the theme issue ‘The role of the microbiome in host evolution’.

Immunoblotting of Creutzfeldt-Jakob disease prion proteins: Host species?specific epitopes

1987 ◽  
Vol 21 (6) ◽  
pp. 589-595 ◽  
Author(s):  
Jeffrey M. Bockman ◽  
Stanley B. Prusiner ◽  
Jun Tateishi ◽  
David T. Kingsbury
Keyword(s):  
Host Species ◽  
Prion Proteins ◽  
Jakob Disease ◽  
Species Specific

scholarly journals Host phylogeny and host ecology structure the mammalian gut microbiota at different taxonomic scales

2020 ◽  
Author(s):  
Connie A. Rojas ◽  
Santiago A. Ramírez-Barahona ◽  
Kay E. Holekamp ◽  
Kevin. R. Theis
Keyword(s):  
Gut Microbiota ◽  
Host Species ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Phylogenetic Relatedness ◽  
Host Phylogeny ◽  
Host Ecology ◽  
Herbivore Species ◽  
Rrna Gene Sequencing ◽  
Species Specific

AbstractThe gut microbiota is critical for host function. Among mammals, host phylogenetic relatedness and diet are strong drivers of gut microbiota structure, but one factor may be more influential than the other. Here, we used 16S rRNA gene sequencing to determine the relative contributions of host phylogeny and host dietary guild in structuring the gut microbiotas of 11 herbivore species from 5 families living sympatrically in southwest Kenya. Herbivore species were classified as grazers, browsers, or mixed-feeders. We found that gut microbiotas were highly species-specific, and that host family accounted for more variation in the gut microbiota (35%) than did host dietary guild (14%). Overall, similarity among gut microbiotas increased with host phylogenetic relatedness (r=0.73), yet this relationship was not apparent among seven closely related Bovid host species (r=0.21 NS). In bovids, host dietary guild explained twice as much variation in the gut microbiota as did host species. Lastly, we found that the gut microbiotas of herbivores residing in southwest Kenya closely resemble those of conspecifics from central Kenya, suggesting that regardless of variability in host local habitat, hosts consistently provide microbes with similar niches for colonization. Overall, our findings suggest that host phylogeny may structure the gut microbiota at broad taxonomic scales, but that host ecology may be more influential in shaping the gut microbiotas of closely related host species.

scholarly journals Predictable and host-species specific humanization of the gut microbiota in captive primates

2021 ◽  
Author(s):  
Jennifer Houtz ◽  
Jon Sanders ◽  
Anthony Denice ◽  
Andrew Moeller
Keyword(s):  
Gut Microbiota ◽  
Host Species ◽  
Rrna Gene ◽  
Gene Variants ◽  
Gastrointestinal Dysfunction ◽  
Human Gut ◽  
Captive Populations ◽  
In Captivity ◽  
Species Specific ◽  
Bacterial 16S Rrna Gene

Humans and non-human primates (NHPs) harbor complex gut microbial communities that affect phenotypes and fitness. The gut microbiotas of wild NHPs reflect their hosts’ phylogenetic histories and are compositionally distinct from those of humans, but in captivity the endogenous gut microbial lineages of NHPs can be lost or replaced by lineages found in humans. Despite its potential contributions to gastrointestinal dysfunction, this humanization of the gut microbiota has not been investigated systematically across captive NHP species. Here we show through comparisons of well-sampled wild and captive populations of apes and monkeys that the fraction of the gut microbiota humanized by captivity varies significantly between NHP species but is remarkably reproducible between captive populations of the same NHP species. Conspecific captive populations displayed significantly greater than expected overlap in the sets of bacterial 16S rRNA gene variants that were differentially abundant between captivity and the wild. This overlap was evident even between captive populations residing on different continents but was never observed between heterospecific captive populations. In addition, we developed an approach incorporating human gut microbiota data to rank NHPs’ gut microbial clades based on the propensity of their lineages to be lost or replaced by lineages found in humans in captivity. Relatively few microbial genera displayed reproducible degrees of humanization in different captive host species, but most microbial genera were reproducibly humanized or retained from the wild in conspecific pairs of captive populations. These results demonstrate that the gut microbiotas of captive NHPs display predictable, host-species specific responses to captivity.

scholarly journals Lentiviral Vif Degrades the APOBEC3Z3/APOBEC3H Protein of Its Mammalian Host and Is Capable of Cross-Species Activity

2010 ◽  
Vol 84 (16) ◽  
pp. 8193-8201 ◽  
Author(s):  
Rebecca S. LaRue ◽  
Joy Lengyel ◽  
Stefán R. Jónsson ◽  
Valgerdur Andrésdóttir ◽  
Reuben S. Harris
Keyword(s):  
Host Species ◽  
Equine Infectious Anemia Virus ◽  
Bovine Immunodeficiency Virus ◽  
Mammalian Host ◽  
Neutralization Capacity ◽  
Type Protein ◽  
Immunodeficiency Virus ◽  
Species Activity ◽  
Species Specific ◽  
Anemia Virus

ABSTRACT All lentiviruses except equine infectious anemia virus (EIAV) use the small accessory protein Vif to counteract the restriction activity of the relevant APOBEC3 (A3) proteins of their host species. Prior studies have suggested that the Vif-A3 interaction is species specific. Here, using the APOBEC3H (Z3)-type proteins from five distinct mammals, we report that this is generally not the case: some lentiviral Vif proteins are capable of triggering the degradation of both the A3Z3-type protein of their normal host species and those of several other mammals. For instance, SIVmac Vif can mediate the degradation of the human, macaque, and cow A3Z3-type proteins but not of the sheep or cat A3Z3-type proteins. Maedi-visna virus (MVV) Vif is similarly promiscuous, degrading not only sheep A3Z3 but also the A3Z3-type proteins of humans, macaques, cows, and cats. In contrast to the neutralization capacity of these Vif proteins, human immunodeficiency virus (HIV), bovine immunodeficiency virus (BIV), and feline immunodeficiency virus (FIV) Vif appear specific to the A3Z3-type protein of their hosts. We conclude, first, that the Vif-A3Z3 interaction can be promiscuous and, second, despite this tendency, that each lentiviral Vif protein is optimized to degrade the A3Z3 protein of its mammalian host. Our results thereby suggest that the Vif-A3Z3 interaction is relevant to lentivirus biology.

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