Cell-Free HIV Type 1 Infection is Restricted in the Human Trophoblast Choriocarcinoma BeWo Cell Line, Even with Expression of CD4, CXCR4 and CCR5

Dolcini, Guillermina Laura; Derrien, Muriel; Chaouat, Gérard; Barré‐Sinoussi, Françoise; Menu, Elisabeth

doi:10.1089/088922203322493021

Cited by 28 publications

(34 citation statements)

References 53 publications

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“…It is now well established that infection of primary trophoblasts or of trophoblastderived cell lines with cell-free HIV-1 is poorly or not at all productive (7,15,32). Our results showing that PSF increased viral production in these cells inoculated with HIV-1-infected PBMCs suggested that PSF could also alter the resistance of BeWo cells to cell-free virus.…”

Section: Resultsmentioning

confidence: 53%

Impact of the Placental Cytokine-Chemokine Balance on Regulation of Cell-Cell Contact-Induced Human Immunodeficiency Virus Type 1 Translocation across a Trophoblastic Barrier In Vitro

Derrien

Faye

Dolcini

et al. 2005

J Virol

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Cells constituting the placental barrier secrete soluble factors that may participate in controlling human immunodeficiency virus type 1 (HIV-1) transmission from the mother to the fetus. In this study, we asked whether placental soluble factors (PSF) could limit cell-cell contact inducing HIV-1 production that occurs after inoculation of HIV-1-infected peripheral blood mononuclear cells (HIV-1 ؉ PBMCs) onto trophoblastderived BeWo cells grown as tight and polarized barriers in a two-chamber system. The activity of recombinant chemokines and cytokines expressed by placental tissue and of factors secreted by either early or term placentae of HIV-1-negative women, was analyzed. We identified chemokines (RANTES and MIP-1␤) and cytokines (tumor necrosis factor alpha and interleukin-8) that decreased and increased, respectively, viral production in trophoblast barrier cells inoculated with HIV-1 ؉ PBMCs. Unexpectedly, factors secreted by either early or term placentae of HIV-1-negative women enhanced viral production. Nevertheless, the same PSF did not favor infection of trophoblastic barriers with cell-free HIV-1 and strongly reduced viral production in PBMCs infected with cell-free HIV-1. Moreover, PSF contained chemokines (RANTES and MIP-1␤) and a cytokine, leukemia inhibitory factor, exhibiting a strong anti-HIV-1 activity in our model of cell-to-cell infection. Together these data suggested that at the maternal interface the global activity of PSF is related to the synergistic action of several soluble factors with a balance in favor of an enhancing activity on the passage of viruses across the trophoblast barrier. This could explain the presence of viral sequences in trophoblasts in all placentae of HIV-1-infected women.

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Section: Resultsmentioning

confidence: 53%

Impact of the Placental Cytokine-Chemokine Balance on Regulation of Cell-Cell Contact-Induced Human Immunodeficiency Virus Type 1 Translocation across a Trophoblastic Barrier In Vitro

Derrien

Faye

Dolcini

et al. 2005

J Virol

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“…19 Trophoblast cells are also able to produce chemokines and their receptors. 20,21 The role of these processes in materno-foetal transmission of T. gondii is not clear. However, immunohistochemical studies in a rat model of congenital infection showed T. gondii multiplication in intact trophoblast cells.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasma gondii regulates ICAM‐1 mediated monocyte adhesion to trophoblasts

et al. 2005

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Summary Materno-foetal transmission causes one of the most serious forms of infection with the intracellular protozoan parasite Toxoplasma gondii . In the placenta, trophoblast cells constitute the barrier between maternal circulation and foetal tissue. We looked at the factors that determine the extent of cell adhesion to human BeWo trophoblast cells during T. gondii infection. BeWo monolayers stimulated with the supernatant of T. gondii -infected PBMC showed a large increase in THP-1 cell adhesion and upregulation of the intercellular adhesion molecule (ICAM)-1. Neutralization of cytokines by corresponding antibodies demonstrated that anti-IFN-γ , but not anti-TNF-α or anti-IL-1 β , led to a significant reduction of THP-1 adhesion to a BeWo monolayer. Treatment of BeWo cells with single cytokines failed to induce upregulation of adhesion. In contrast, simultaneous treatment with IFN-γ and either TNF-α or IL-1 β mimicked strongly the effect of infected cell supernatant. The results suggest that IFN-γ plays a pivotal role in the cell adhesion process through upregulation of ICAM-1 and in the process of congenital transmission of T. gondii .

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“…For cell-free virus infections of MDM, the R5 tropic primary isolate HIV-1 BaL [61] was used. The viral stock was prepared in MDM.…”

Section: Methodsmentioning

confidence: 99%

“…Luciferase reporter viruses were produced as previously described [61] by transiently cotransfecting (Lipofectamine 2000, Invitrogen, USA) 293T cells with the proviral pNL-Luc-E-R+ vector [62], which lacks the env gene and has the firefly luciferase gene inserted into the nef gene, and the expression vector pCMV harbors the gene coding for either the VSV-G envelope protein or the HIV-1 R5 (BaL) envelope protein. 293T cells were also transfected only with pNL-Luc-E-R+ (Denv pseudotype).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi

et al. 2009

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BackgroundCells of monocyte/macrophage lineage are one of the major targets of HIV-1 infection and serve as reservoirs for viral persistence in vivo. These cells are also the target of the protozoa Trypanosoma cruzi, the causative agent of Chagas disease, being one of the most important endemic protozoonoses in Latin America. It has been demonstrated in vitro that co-infection with other pathogens can modulate HIV replication. However, no studies at cellular level have suggested an interaction between T. cruzi and HIV-1 to date.Methodology/Principal FindingsBy using a fully replicative wild-type virus, our study showed that T. cruzi inhibits HIV-1 antigen production by nearly 100% (p<0.001) in monocyte-derived macrophages (MDM). In different infection schemes with luciferase-reporter VSV-G or BaL pseudotyped HIV-1 and trypomastigotes, T. cruzi induced a significant reduction of luciferase level for both pseudotypes in all the infection schemes (p<0.001), T. cruzi-HIV (>99%) being stronger than HIV-T. cruzi (∼90% for BaL and ∼85% for VSV-G) infection. In MDM with established HIV-1 infection, T. cruzi significantly inhibited luciferate activity (p<0.01). By quantifying R-U5 and U5-gag transcripts by real time PCR, our study showed the expression of both transcripts significantly diminished in the presence of trypomastigotes (p<0.05). Thus, T. cruzi inhibits viral post-integration steps, early post-entry steps and entry into MDM. Trypomastigotes also caused a ∼60-70% decrease of surface CCR5 expression on MDM. Multiplication of T. cruzi inside the MDM does not seem to be required for inhibiting HIV-1 replication since soluble factors secreted by trypomastigotes have shown similar effects. Moreover, the major parasite antigen cruzipain, which is secreted by the trypomastigote form, was able to inhibit viral production in MDM over 90% (p<0.01).Conclusions/SignificanceOur study showed that T. cruzi inhibits HIV-1 replication at several replication stages in macrophages, a major cell target for both pathogens.

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Cell-Free HIV Type 1 Infection is Restricted in the Human Trophoblast Choriocarcinoma BeWo Cell Line, Even with Expression of CD4, CXCR4 and CCR5

Cited by 28 publications

References 53 publications

Impact of the Placental Cytokine-Chemokine Balance on Regulation of Cell-Cell Contact-Induced Human Immunodeficiency Virus Type 1 Translocation across a Trophoblastic Barrier In Vitro

Impact of the Placental Cytokine-Chemokine Balance on Regulation of Cell-Cell Contact-Induced Human Immunodeficiency Virus Type 1 Translocation across a Trophoblastic Barrier In Vitro

Toxoplasma gondii regulates ICAM‐1 mediated monocyte adhesion to trophoblasts

Inhibition of HIV-1 Replication in Human Monocyte-Derived Macrophages by Parasite Trypanosoma cruzi

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