scholarly journals Blockade of HIV-1 Infection of New World Monkey Cells Occurs Primarily at the Stage of Virus Entry

2002 ◽  
Vol 196 (4) ◽  
pp. 431-445 ◽  
Author(s):  
Jason A. LaBonte ◽  
Gregory J. Babcock ◽  
Trushar Patel ◽  
Joseph Sodroski
Keyword(s):  
New World ◽  
Virus Entry ◽  
World Monkey ◽  
Squirrel Monkeys ◽  
Viral Envelope ◽  
Envelope Glycoproteins ◽  
New World Monkeys ◽  
Common Marmosets ◽  
New World Monkey ◽  
Hiv 1

HIV-1 naturally infects chimpanzees and humans, but does not infect Old World monkeys because of replication blocks that occur after virus entry into the cell. To understand the species-specific restrictions operating on HIV-1 infection, the ability of HIV-1 to infect the cells of New World monkeys was examined. Primary cells derived from common marmosets and squirrel monkeys support every phase of HIV-1 replication with the exception of virus entry. Efficient HIV-1 entry typically requires binding of the viral envelope glycoproteins and host cell receptors, CD4 and either CCR5 or CXCR4 chemokine receptors. HIV-1 did not detectably bind or utilize squirrel monkey CD4 for entry, and marmoset CD4 was also very inefficient compared with human CD4. A marmoset CD4 variant, in which residues 48 and 59 were altered to the amino acids found in human CD4, supported HIV-1 entry efficiently. The CXCR4 molecules of both marmosets and squirrel monkeys supported HIV-1 infection, but the CCR5 proteins of both species were only marginally functional. These results demonstrate that the CD4 and CCR5 proteins of New World monkeys represent the major restriction against HIV-1 replication in these primates. Directed adaptation of the HIV-1 envelope glycoproteins to common marmoset receptors might allow the development of New World monkey models of HIV-1 infection.

scholarly journals Adaptation of the Human Immunodeficiency Virus Type 1 Envelope Glycoproteins to New World Monkey Receptors

2007 ◽  
Vol 82 (1) ◽  
pp. 346-357 ◽  
Author(s):  
Beatriz Pacheco ◽  
Stephane Basmaciogullari ◽  
Jason A. LaBonte ◽  
Shi-Hua Xiang ◽  
Joseph Sodroski
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
New World ◽  
World Monkey ◽  
Envelope Glycoproteins ◽  
New World Monkey ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) infection encounters an early block in the cells of New World monkeys because the CD4 receptor does not efficiently support HIV-1 entry. We adapted HIV-1(NL4-3) and HIV-1(KB9), two HIV-1 variants with different envelope glycoproteins, to replicate efficiently in cells expressing the CD4 and CXCR4 proteins of the common marmoset, a New World monkey. The HIV-1(NL4-3) adaptation involves three gp120 changes that result in a specific increase in affinity for the marmoset CD4 glycoprotein. The already high affinity of the HIV-1(KB9) envelope glycoproteins for marmoset CD4 did not significantly change as a result of the adaptation. Instead, changes in the gp120 variable loops and gp41 ectodomain resulted in improved replication in cells expressing the marmoset receptors. HIV-1(KB9) became relatively sensitive to neutralization by soluble CD4 and antibodies as a result of the adaptation. These results demonstrate the distinct mechanistic pathways by which the HIV-1 envelope glycoproteins can adapt to less-than-optimal CD4 molecules and provide HIV-1 variants that can overcome some of the early blocks in New World monkey cells.

scholarly journals Species-Specific Inhibition of Foamy Viruses from South American Monkeys by New World Monkey TRIM5α Proteins

2010 ◽  
Vol 84 (8) ◽  
pp. 4095-4099 ◽  
Author(s):  
Beatriz Pacheco ◽  
Andrés Finzi ◽  
Kathleen McGee-Estrada ◽  
Joseph Sodroski
Keyword(s):  
New World ◽  
World Monkey ◽  
Foamy Virus ◽  
South American ◽  
New World Primates ◽  
Common Marmosets ◽  
Geographic Ranges ◽  
New World Monkey ◽  
Foamy Viruses ◽  
Species Specific

ABSTRACT Foamy virus evolution closely parallels that of the host species, indicating virus-host coadaptation. We studied simian foamy viruses (SFVs) from common marmosets, spider monkeys, and squirrel monkeys, New World monkey (NWM) species that share geographic ranges. The TRIM5α protein from each of these NWM species inhibited the replication of at least one of the SFVs associated with the other two species but did not affect the replication of its own SFV. Thus, TRIM5α has potentially shaped the evolution of SFVs in NWM hosts. Conversely, SFVs may have influenced the evolution of TRIM5 variants in New World primates.

scholarly journals Identification of Postentry Restrictions to Mason-Pfizer Monkey Virus Infection in New World Monkey Cells

2008 ◽  
Vol 82 (22) ◽  
pp. 11140-11151 ◽  
Author(s):  
William E. Diehl ◽  
Elizabeth Stansell ◽  
Shari M. Kaiser ◽  
Michael Emerman ◽  
Eric Hunter
Keyword(s):  
Cell Lines ◽  
New World ◽  
Rhesus Macaques ◽  
World Monkey ◽  
Resistant Cell Line ◽  
Spider Monkey ◽  
Primate Species ◽  
New World Monkeys ◽  
Old World ◽  
New World Monkey

ABSTRACT TRIM5α has been shown to be a major postentry determinant of the host range for gammaretroviruses and lentiviruses and, more recently, spumaviruses. However, the restrictive potential of TRIM5α against other retroviruses has been largely unexplored. We sought to determine whether or not Mason-Pfizer monkey virus (M-PMV), a prototype betaretrovirus isolated from rhesus macaques, was sensitive to restriction by TRIM5α. Cell lines from both Old World and New World primate species were screened for their susceptibility to infection by vesicular stomatitis virus G protein pseudotyped M-PMV. All of the cell lines tested that were established from Old World primates were found to be susceptible to M-PMV infection. However, fibroblasts established from three New World monkey species specifically resisted infection by this virus. Exogenously expressing TRIM5α from either tamarin or squirrel monkeys in permissive cell lines resulted in a block to M-PMV infection. Restriction in the resistant cell line of spider monkey origin was determined to occur at a postentry stage. However, spider monkey TRIM5α expression in permissive cells failed to restrict M-PMV infection, and interference with endogenous TRIM5α in the spider monkey fibroblasts failed to relieve the block to infectivity. Our results demonstrate that TRIM5α specificity extends to betaretroviruses and suggest that New World monkeys have evolved additional mechanisms to restrict the infection of at least one primate betaretrovirus.

scholarly journals Apparent effect of rabbit endogenous lentivirus type K acquisition on retrovirus restriction by lagomorph Trim5αs

2013 ◽  
Vol 368 (1626) ◽  
pp. 20120498 ◽  
Author(s):  
Melvyn W. Yap ◽  
Jonathan P. Stoye
Keyword(s):  
New World ◽  
Selective Pressure ◽  
World Monkey ◽  
Old World Monkeys ◽  
Apparent Effect ◽  
New World Monkey ◽  
Cottontail Rabbit ◽  
Type K ◽  
Hiv 1 ◽  
B30.2 Domain

To test the hypothesis that rabbit endogenous lentivirus type K (RELIK) could play a role in shaping the evolution of TRIM5α, the susceptibility of viruses containing the RELIK capsid (CA) to TRIM5 restriction was evaluated. RELIK CA-containing viruses were susceptible to the TRIM5αs from Old World monkeys but were unaffected by most ape or New World monkey factors. TRIM5αs from various lagomorph species were also isolated and tested for anti-retroviral activity. The TRIM5αs from both cottontail rabbit and pika restrict a range of retroviruses, including HIV-1, HIV-2, FIV, EIAV and N-MLV. TRIM5αs from the European and cottontail rabbit, which have previously been found to contain RELIK, also restricted RELIK CA-containing viruses, whereas a weaker restriction was observed with chimeric TRIM5α containing the B30.2 domain from the pika, which lacks RELIK. Taken together, these results could suggest that the pika had not been exposed to exogenous RELIK and that endogenized RELIK might exert a selective pressure on lagomorph TRIM5α.

scholarly journals Functional and Genetic Analysis of Viral Receptor ACE2 Orthologs Reveals a Broad Potential Host Range of SARS-CoV-2

2020 ◽  
Author(s):  
Yinghui Liu ◽  
Gaowei Hu ◽  
Yuyan Wang ◽  
Xiaomin Zhao ◽  
Fansen Ji ◽  
...  
Keyword(s):  
Host Range ◽  
Viral Entry ◽  
New World ◽  
Virus Entry ◽  
World Monkey ◽  
Spike Protein ◽  
Dependent Manner ◽  
Genetic Determinant ◽  
New World Monkey ◽  
Palm Civet

AbstractThe pandemic of Coronavirus Disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a major global health threat. Epidemiological studies suggest that bats are the natural zoonotic reservoir for SARS-CoV-2. However, the host range of SARS-CoV-2 and intermediate hosts that facilitate its transmission to humans remain unknown. The interaction of coronavirus with its host receptor is a key genetic determinant of host range and cross-species transmission. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as the receptor to enter host cells in a species-dependent manner. It has been shown that human, palm civet, pig and bat ACE2 can support virus entry, while the murine ortholog cannot. In this study, we characterized the ability of ACE2 from diverse species to support viral entry. We found that ACE2 is expressed in a wide range of species, with especially high conservation in mammals. By analyzing amino acid residues of ACE2 critical for virus entry, based on structure of SARS-CoV spike protein interaction with human, bat, palm civet, pig and ferret ACE2, we identified approximately eighty ACE2 proteins from mammals that could potentially mediate SARS-CoV-2 entry. Functional assays showed that 44 of these mammalian ACE2 orthologs, including those of domestic animals, pets, livestock, and animals commonly found in zoos and aquaria, could bind SARS-CoV-2 spike protein and support viral entry. In contrast, New World monkey ACE2 orthologs could not bind SARS-CoV-2 spike protein and support viral entry. We further identified the genetic determinant of New World monkey ACE2 that restricts viral entry using genetic and functional analyses. In summary, our study demonstrates that ACE2 from a remarkably broad range of species can facilitate SARS-CoV-2 entry. These findings highlight a potentially broad host tropism of SARS-CoV-2 and suggest that SARS-CoV-2 might be distributed much more widely than previously recognized, underscoring the necessity to monitor susceptible hosts to prevent future outbreaks.

scholarly journals Retrovirus Restriction by TRIM5α Variants from Old World and New World Primates

2005 ◽  
Vol 79 (7) ◽  
pp. 3930-3937 ◽  
Author(s):  
Byeongwoon Song ◽  
Hassan Javanbakht ◽  
Michel Perron ◽  
Do Hyun Park ◽  
Matthew Stremlau ◽  
...  
Keyword(s):  
New World ◽  
World Monkey ◽  
Old World Monkeys ◽  
Old World ◽  
New World Monkey ◽  
Monkey Species ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
B30.2 Domain ◽  
Antiretroviral Activity

ABSTRACT The TRIM5α proteins of humans and some Old World monkeys have been shown to block infection of particular retroviruses following virus entry into the host cell. Infection of most New World monkey cells by the simian immunodeficiency virus of macaques (SIVmac) is restricted at a similar point. Here we examine the antiretroviral activity of TRIM5α orthologs from humans, apes, Old World monkeys, and New World monkeys. Chimpanzee and orangutan TRIM5α proteins functionally resembled human TRIM5α, potently restricting infection by N-tropic murine leukemia virus (N-MLV) and moderately restricting human immunodeficiency virus type 1 (HIV-1) infection. Notably, TRIM5α proteins from several New World monkey species restricted infection by SIVmac and the SIV of African green monkeys, SIVagm. Spider monkey TRIM5α, which has an expanded B30.2 domain v3 region due to a tandem triplication, potently blocked infection by a range of retroviruses, including SIVmac, SIVagm, HIV-1, and N-MLV. Tandem duplications in the TRIM5α B30.2 domain v1 region of African green monkeys are also associated with broader antiretroviral activity. Thus, variation in TRIM5α proteins among primate species accounts for the observed patterns of postentry restrictions in cells from these animals. The TRIM5α proteins of some monkey species exhibit dramatic lengthening of particular B30.2 variable regions and an expanded range of susceptible retroviruses.

scholarly journals Signaling Lymphocytic Activation Molecule Family Receptor Homologs in New World Monkey Cytomegaloviruses

2015 ◽  
Vol 89 (22) ◽  
pp. 11323-11336 ◽  
Author(s):  
Natàlia Pérez-Carmona ◽  
Domènec Farré ◽  
Pablo Martínez-Vicente ◽  
Cox Terhorst ◽  
Pablo Engel ◽  
...  
Keyword(s):  
Ligand Binding ◽  
New World ◽  
World Monkey ◽  
Host Immune System ◽  
New World Monkeys ◽  
Dna Viruses ◽  
Cell Surface Glycoprotein ◽  
New World Monkey ◽  
Slam Family ◽  
Signaling Lymphocytic Activation Molecule

ABSTRACTThroughout evolution, large DNA viruses have been usurping genes from their hosts to equip themselves with proteins that restrain host immune defenses. Signaling lymphocytic activation molecule (SLAM) family (SLAMF) receptors are involved in the regulation of both innate and adaptive immunity, which occurs upon engagement with their ligands via homotypic or heterotypic interactions. Here we report a total of seven SLAMF genes encoded by the genomes of two cytomegalovirus (CMV) species, squirrel monkey CMV (SMCMV) and owl monkey CMV (OMCMV), that infect New World monkeys. Our results indicate that host genes were captured by retrotranscription at different stages of the CMV-host coevolution. The most recent acquisition led to S1 in SMCMV. S1 is a SLAMF6 homolog with an amino acid sequence identity of 97% to SLAMF6 in its ligand-binding N-terminal Ig domain. We demonstrate that S1 is a cell surface glycoprotein capable of binding to host SLAMF6. Furthermore, the OMCMV genome encodes A33, an LY9 (SLAMF3) homolog, and A43, a CD48 (SLAMF2) homolog, two soluble glycoproteins which recognize their respective cellular counterreceptors and thus are likely to be viral SLAMF decoy receptors. In addition, distinct copies of further divergent CD48 homologs were found to be encoded by both CMV genomes. Remarkably, all these molecules display a number of unique features, including cytoplasmic tails lacking characteristic SLAMF signaling motifs. Taken together, our findings indicate a novel immune evasion mechanism in which incorporation of host SLAMF receptors that retain their ligand-binding properties enables viruses to interfere with SLAMF functions and to supply themselves with convenient structural molds for expanding their immunomodulatory repertoires.IMPORTANCEThe way in which viruses shape their genomes under the continual selective pressure exerted by the host immune system is central for their survival. Here, we report that New World monkey cytomegaloviruses have broadly captured and duplicated immune cell receptors of the signaling lymphocyte activation molecule (SLAM) family during host-virus coevolution. Notably, we demonstrate that several of these viral SLAMs exhibit exceptional preservation of their N-terminal immunoglobulin domains, which results in maintenance of their ligand-binding capacities. At the same time, these molecules present distinctive structural properties which include soluble forms and the absence of typical SLAM signaling motifs in their cytoplasmic domains, likely reflecting the evolutionary adaptation undergone to efficiently interfere with host SLAM family activities. The observation that the genomes of other large DNA viruses might bear SLAM family homologs further underscores the importance of these molecules as a novel class of immune regulators and as convenient scaffolds for viral evolution.

scholarly journals Pulmonary granuloma is not always the tuberculosis hallmark: pathological findings of different tuberculosis stages in New and Old World Nonhuman Primates naturally infected with the Mycobacterium tuberculosis Complex

2021 ◽  
Author(s):  
Asheley H. B. Pereira ◽  
Claudia A. A. Lopes ◽  
Thalita A. Pissinatti ◽  
Ana C. A. Pinto ◽  
Daniel R. A. Oliveira ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
New World ◽  
Nonhuman Primates ◽  
World Monkey ◽  
Histological Evaluation ◽  
New World Monkeys ◽  
Old World Monkeys ◽  
Pathological Findings ◽  
Old World ◽  
Pulmonary Granuloma

Abstract Herein we present the pathological findings of different tuberculosis stages in Old and New World monkeys kept under human care in Rio de Janeiro, Brazil and naturally infected with Mycobacterium tuberculosis Complex. Fifteen nonhuman primates from five different colonies were incorporated into the study. There are 60% (9/15) Old World Monkeys and 40% (6/15) New World Monkeys. According to the gross and histopathologic findings, the lesions in nonhuman primates of this study are classified into the chronic-active, extrapulmonary, early-activation or latent-reactivation tuberculosis stage. Among the Old World Monkey, 66.7% (6/9) of nonhuman primates, all rhesus monkeys (Macaca mulatta), showed severe granulomatous pneumonia. In all Old World Monkeys cases, typical granulomas were seen in at least one organ regardless of the stage of the disease. In the New World Monkeys, the typical pulmonary granulomas were seen in 16.7% (1/6) of the cases, just in the latent-reactivation stage in Uta Hick’s Bearded Saki (Chiropotes utahickae). In this study, 66.7% (6/9) of Old World Monkeys (OWM) and 83.3% (5/6) of New World Monkeys (NWM) showed pulmonary changes at the histological evaluation. The tuberculosis diagnosis in the nonhuman primates in this study was based on pathological, immunohistochemical, molecular, and bacteriological culture. Although the typical presentation was observed in some cases, the absence of pulmonary granuloma did not exclude the tuberculosis occurrence in nonhuman primates of the Old and New World. Tuberculosis should be included as a cause of interstitial pneumonia with foamy macrophages infiltration in the New World nonhuman primates. Due to the high sensitivity of immunohistochemistry with Anti-Mycobacterium tuberculosis, we suggest the addition of this technique as a diagnostic tool of tuberculosis in the nonhuman primates even when the typical changes are not seen.

scholarly journals CENP-B box, a nucleotide motif involved in centromere formation, occurs in a New World monkey

2016 ◽  
Vol 12 (3) ◽  
pp. 20150817 ◽  
Author(s):  
Aorarat Suntronpong ◽  
Kazuto Kugou ◽  
Hiroshi Masumoto ◽  
Kornsorn Srikulnath ◽  
Kazuhiko Ohshima ◽  
...  
Keyword(s):  
Repetitive Dna ◽  
New World ◽  
World Monkey ◽  
Common Marmoset ◽  
Alpha Satellite ◽  
Satellite Repeat ◽  
New World Monkey ◽  
Alpha Satellite Dna ◽  
Negative Results ◽  
Contig Sequence

Centromere protein B (CENP-B) is one of the major proteins involved in centromere formation, binding to centromeric repetitive DNA by recognizing a 17 bp motif called the CENP-B box. Hominids (humans and great apes) carry large numbers of CENP-B boxes in alpha satellite DNA (AS, the major centromeric repetitive DNA of simian primates). Only negative results have been reported regarding the presence of the CENP-B box in other primate taxa. Consequently, it is widely believed that the CENP-B box is confined, within primates, to the hominids. We report here that the common marmoset, a New World monkey, contains an abundance of CENP-B boxes in its AS. First, in a long contig sequence we constructed and analysed, we identified the motif in 17 of the 38 alpha satellite repeat units. We then sequenced terminal regions of additional clones and found the motif in many of them. Immunostaining of marmoset cells demonstrated that CENP-B binds to DNA in the centromeric regions of chromosomes. Therefore, functional CENP-B boxes are not confined to hominids. Our results indicate that the efficiency of identification of the CENP-B box may depend largely on the sequencing methods used, and that the CENP-B box in centromeric repetitive DNA may be more common than researchers previously thought.

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