Restriction of lentivirus in monkeys

Besnier, Caroline; Takeuchi, Yasuhiro; Towers, Greg J.

doi:10.1073/pnas.172384599

Cited by 264 publications

(284 citation statements)

References 27 publications

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“…Similar restrictions for some murine leukemia viruses have been observed with human cells (44). By examining the infection of heterokaryons and by performing infections in the presence of competitor viruses, the cellular factors responsible for retroviral restriction have been demonstrated to be dominant and saturable (2,3,15,28,37). A chimeric HIV-1 reporter virus in which the HIV-1 CA protein was largely replaced with the SIV mac CA sequence escaped the monkey cell restrictions, demonstrating that the CA protein of HIV-1 is an important viral determinant for susceptibility to postentry restriction (39).…”

mentioning

confidence: 53%

“…Uncoating events are likely to be relevant to HIV-1 tropism restrictions in cells of some nonhuman primate species, given the substantial reduction in reverse transcription products detected in newly infected cells (2,15,29). Thus, although HIV-1 entry into cells of several Old World monkey species is efficiently supported by simian CD4 and chemokine coreceptors (14,35), HIV-1 infection of these cells is restricted at a postentry step (2,3,15,28,31,45). Old World monkeys are natural hosts for SIV mac , which is not susceptible to postentry restrictions in these cells (16,30,31).…”

mentioning

confidence: 99%

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Binding and Susceptibility to Postentry Restriction Factors in Monkey Cells Are Specified by Distinct Regions of the Human Immunodeficiency Virus Type 1 Capsid

Owens

Song

Perron

et al. 2004

J Virol

115

118

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In cells of Old World and some New World monkeys, dominant factors restrict human immunodeficiency virus type 1 (HIV-1) infections after virus entry. The simian immunodeficiency virus SIV mac is less susceptible to these restrictions, a property that is determined largely by the viral capsid protein. For this study, we altered exposed amino acid residues on the surface of the HIV-1 capsid, changing them to the corresponding residues found on the SIV mac capsid. We identified two distinct pathways of escape from early, postentry restriction in monkey cells. One set of mutants that were altered near the base of the cyclophilin A-binding loop of the N-terminal capsid domain or in the interdomain linker exhibited a decreased ability to bind the restricting factor(s). Consistent with the location of this putative factor-binding site, cyclophilin A and the restricting factor(s) cooperated to achieve the postentry block. A second set of mutants that were altered in the ridge formed by helices 3 and 6 of the N-terminal capsid domain efficiently bound the restricting factor(s) but were resistant to the consequences of factor binding. These results imply that binding of the simian restricting factor(s) is not sufficient to mediate the postentry block to HIV-1 and that SIV mac capsids escape the block by decreases in both factor binding and susceptibility to the effects of the factor(s).

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mentioning

confidence: 53%

mentioning

confidence: 99%

Binding and Susceptibility to Postentry Restriction Factors in Monkey Cells Are Specified by Distinct Regions of the Human Immunodeficiency Virus Type 1 Capsid

Owens

Song

Perron

et al. 2004

J Virol

115

118

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“…This interaction, involving amino acid 332 of TRIM5␣ in humans (15) and 334 in monkeys, may explain the high relative rates of nonsynonymous changes of the primate TRIM5␣ gene (13). TRIM5␣ has been described in primates and several mammals (3,6,30,33,41) but not in sheep or goats, both of which are infected by SRLV, their own lentivirus. This study aimed to identify and characterize the ovine and caprine TRIM5␣ proteins and explore the possible restrictive role of ovine TRIM5␣ on VMV infection.…”

mentioning

confidence: 99%

“…The vector contains the LTR of Moloney murine leukemia virus (MLV), driving expression of an N-terminal hemagglutinin (HA)-tagged OvT5␣ protein and the gene for the red fluorescent protein (RFP). The resulting vector (pCTCR-HAOvT5) was packaged into vesicular stomatitis virus G envelope protein (VSV-G)-pseudotyped MLV cores by cotransfection of 293T cells as described previously (3). Culture supernatants containing MLV virions encoding OvT5 were used to transduce the Mus dunni tail fibroblast (MDTF) cell line, and HA-tagged OvT5 stably expressing cells were obtained.…”

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confidence: 99%

Ovine TRIM5α Can Restrict Visna/Maedi Virus

Jáuregui

Crespo

Glaria

et al. 2012

J Virol

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The restrictive properties of tripartite motif-containing 5 alpha (TRIM5␣) from small ruminant species have not been explored. Here, we identify highly similar TRIM5␣ sequences in sheep and goats. Cells transduced with ovine TRIM5␣ effectively restricted the lentivirus visna/maedi virus DNA synthesis. Proteasome inhibition in cells transduced with ovine TRIM5␣ restored restricted viral DNA synthesis, suggesting a conserved mechanism of restriction. Identification of TRIM5␣ active molecular species may open new prophylactic strategies against lentiviral infections.S mall ruminant lentiviruses (SRLV), including visna/maedi virus (VMV) and caprine encephalitis virus (CAEV), are widespread in sheep and goats, causing a slow progressive disease. Since neither treatment nor efficient vaccines are available, infection is commonly controlled by early diagnosis and culling (23). Recently, the study of host cell restriction factors interfering with the retroviral life cycle, such as the tripartite motif-containing 5 (TRIM5) protein, has gained interest (10, 37). TRIM5 family members bear a RING-B-box-coiled-coil structure consisting of an N-terminal RING domain (with E3 ubiquitin ligase activity), a B-box domain, and a coiled-coil domain (19). The TRIM5␣ isoform, which is active against retroviruses, contains a C-terminal PRYSPRY domain that binds retroviral capsid CA (12,20,35). This interaction, involving amino acid 332 of TRIM5␣ in humans (15) and 334 in monkeys, may explain the high relative rates of nonsynonymous changes of the primate TRIM5␣ gene (13). TRIM5␣ has been described in primates and several mammals (3, 6, 30, 33, 41) but not in sheep or goats, both of which are infected by SRLV, their own lentivirus. This study aimed to identify and characterize the ovine and caprine TRIM5␣ proteins and explore the possible restrictive role of ovine TRIM5␣ on VMV infection.First, we cloned and sequenced ovine and caprine TRIM5␣ cDNA sequences. For this, total RNA from ovine skin fibroblasts (SF), bronchoalveolar lavage (BAL) fluid, or lung tissue obtained from domestic sheep of the Assaf (n ϭ 3), Churra (n ϭ 2), and Rasa Aragonesa (n ϭ 4) breeds was purified using TRIzol (Invitrogen) passed through RNeasy minikit columns (Qiagen), before being reverse transcribed with SuperScript II (Invitrogen) using an oligo(dT) primer according to the manufacturer's instructions. To clone the caprine counterpart, cDNA from peripheral blood mononuclear cells (PBMC) from goats of the Roccaverano (n ϭ 1) and Murciano-Granadina (n ϭ 2) breeds was used. These cDNAs were employed as the PCR template using Phusion high-fidelity DNA polymerase (Finnzymes) with the forward primer TrimEXNFw (5=-TGCA CCTCGAGATGGCTTCAGGAATCCTG-3=, XhoI site underlined) and the reverse primer PJ2 (5=-GATCCGGGCCCTCAAC AGCTTGGTGAGC-3=, ApaI site underlined) following standard thermal profiles. Amplified products were cloned into the TOPO Blunt vector (Invitrogen) as a shuttle/sequencing vector, yielding a total of 12 ovine and 5 caprine independent sequences. Four ov...

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“…12 One mg of lentiviral plasmids p8.91 and pMD.G (both gifts from D. Trono) and pSIN or pHR plasmids (1.5 mg) were co-transfected into HEK293t cells seeded at 8Â10 6 cells in a 10-cm dish 24 h before transfection. Media was changed on the 293t cells 1 h before transfection.…”

Section: Lentiviral Vector Productionmentioning

confidence: 99%

Lentiviral Manipulation of Gene Expression in Human Adult and Embryonic Stem Cells

Clements¹,

Godfrey²,

Crossley³

et al. 2006

Tissue Engineering

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Human stem cells could revolutionize the field of medicine by providing a diverse range of cell types for tissue replacement therapies and drug discovery. To achieve this goal, genetic tools need to be optimized and developed for controlling and manipulating stem cells ex vivo. Here we describe a lentiviral delivery system capable of high infection rates in human mesenchymal and embryonic stem cells. The lentiviral backbone was modified to express mono-and bi-cistronic transgenes and was also used to deliver short hairpin ribonucleic acid for specific silencing of gene expression in human stem cells. We show that lentiviral transduction can be used to alter gene expression without altering the genes' ability to differentiate in vitro. These vectors will enable rapid analysis of gene function in stem cells and permit the generation of knock-in / knock-out models of human disease in the rapidly developing field of gene therapy.

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Restriction of lentivirus in monkeys

Cited by 264 publications

References 27 publications

Binding and Susceptibility to Postentry Restriction Factors in Monkey Cells Are Specified by Distinct Regions of the Human Immunodeficiency Virus Type 1 Capsid

Binding and Susceptibility to Postentry Restriction Factors in Monkey Cells Are Specified by Distinct Regions of the Human Immunodeficiency Virus Type 1 Capsid

Ovine TRIM5α Can Restrict Visna/Maedi Virus

Lentiviral Manipulation of Gene Expression in Human Adult and Embryonic Stem Cells

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