Cellular immune responses during complicated and uncomplicated measles virus infections of man

Hirsch, Robert; Griffin, Diane E.; Johnson, Richard T.; Cooper, Stephen R.; Soriano, Imelda Lindo de; Roedenbeck, Susi; Vaisberg, Abraham

doi:10.1016/0090-1229(84)90184-3

Cited by 138 publications

(64 citation statements)

References 35 publications

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“…PBMCs isolated from people with measles have suppressed lymphoproliferative responses to mitogens (Hirsch et al, 1984;Ward et al, 1991). Coexpression of MV haemagglutinin and fusion glycoproteins on non-lymphoid cells inhibits the proliferation of lymphocytes through a mechanism that requires cleavage of the fusion protein (Weidmann et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

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Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Garcia

Griffin

et al. 2008

Journal of General Virology

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Acute measles virus (MV) infection results in a decrease in plasma human immunodeficiency virus type 1 (HIV-1) RNA levels in co-infected children. An in vitro peripheral blood mononuclear cell (PBMC) culture system was used to assess the mechanisms by which MV blocks HIV-1 replication. MV inhibited proliferation of CD4 + T lymphocytes, the target cell for HIV-1 replication. In the presence of MV, cells did not progress to G 1b and S phases, steps critical for the completion of HIV-1 reverse transcription and productive replication. This block in cell-cycle progression was characterized by an increased proportion of CD4 + and HIV-1-infected cells retained in the parental generation in PBMCs co-cultured with MV and HIV-1, and decreased levels of cyclins and RNA synthesis. Early HIV-1 replication was also inhibited in the presence of MV, as measured by reduced expression of a luciferase reporter gene and lower levels of both early (LTR) and late (LTR-gag) DNA intermediates of HIV-1 reverse transcription in the presence of CCR5-tropic HIV-1. The effects of MV on lymphoproliferation and p24 antigen production were reproduced by n-butyrate and hydroxyurea, drugs that block the cell cycle in G 1a and G 1 /S, respectively. It was concluded that MV inhibits HIV-1 productive replication in part by blocking the proliferation of CD4 + T lymphocytes.

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Section: Discussionmentioning

confidence: 99%

“…MV blocks the proliferation of lymphocytes (Hirsch et al, 1984;Ward et al, 1991). To determine whether MV inhibited proliferation of CD4 + T lymphocytes in the presence of HIV-1, PBMCs were labelled with CFSE and co-stained for CD4 or HIV-1 core antigens.…”

Section: Co-infects Hiv-1-infected Cd4 + T Lymphocytes and Blocks mentioning

confidence: 99%

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Garcia

Griffin

et al. 2008

Journal of General Virology

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“…MV-infected lymphocytes die due to apoptosis (Addae et al, 1995 ;Auwaerter et al, 1996 ;Esolen et al, 1995). Peripheral blood lymphocytes (PBLs) isolated from measles patients show a reduced proliferation capacity in response to polyclonal stimulation (Hirsch et al, 1984 ;Whittle et al, 1978) possibly due to a cell cycle arrest in the end of the G1 phase (McChesney et al, 1987(McChesney et al, , 1988. Even uninfected PBLs were shown to exhibit decreased proliferation in presence of cells that express measles glycoproteins (Niewiesk et al, 1997 ;Schlender et al, 1996).…”

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confidence: 99%

A recombinant measles virus expressing biologically active human interleukin-12.

Singh

Billeter

1999

Journal of General Virology

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Suppression of cell-mediated immunity (CMI) iswell-documented during and after measles. This immunosuppression is suggested to result from decreased production of interleukin-12 (IL-12), a key interleukin for CMI. In an attempt to clearly discern the role of IL-12 in measles-induced immunosuppression, a measles virus (MV) that expresses biologically active human IL-12 was generated. This was achieved by inserting the coding sequences of the two subunits (p35 and p40) of human IL-12 separated by an internal ribosome entry site in an additional transcription unit between the H and the L genes of MV. Although the IL-12-expressing MV grew slightly slower than the normal MV, it stably maintained the inserted sequences (3n2 kb) and uniformly expressed the foreign genes after 10 passages in cell culture. These findings suggest that MV is a well-suited vector for delivery of proteins of immunogenic and therapeutic importance.

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“…Since p38 MAPK is considered as the major positive regulator of DC phenotypic maturation and IL-12 cytokine production 54 , it is possible that this signaling pathway is involved in the phenotypic and functional changes in DCs, following MV-H contact. Several studies have shown decreased lymphocyte proliferation in measles patients 55,56 , or hSLAM 1 transgenic mice 57 , as well as abrogation of DC allostimulatory capacities upon interaction with both wt MV 4,45 and vaccine MV strains 4,6 . Our results indicate that MV-H interaction with CD150 expressing DC could play an important role in these immunosuppressive consequences of MV infection.…”

Section: Discussionmentioning

confidence: 99%

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

et al. 2015

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Measles virus (MV) is highly contagious pathogen, which causes a profound immunosuppression, resulting in high infant mortality. This virus infects dendritic cells (DCs) following the binding of MV hemagglutinin (MV-H) to CD150 receptor and alters DC functions by a mechanism that is not completely understood. We have analyzed the effect of MV-H interaction with CD150-expressing DCs on the DC signaling pathways and consequent phenotypic and functional changes in the absence of infectious context. We demonstrated that contact between CD150 on human DCs and MV-H expressed on membrane of transfected CHO cells was sufficient to modulate the activity of two major regulatory pathways of DC differentiation and function: to stimulate Akt and inhibit p38 MAPK phosphorylation, without concomitant ERK1/2 activation. Furthermore, interaction with MV-H decreased the expression level of DC activation markers CD80, CD83, CD86, and HLA-DR and strongly downregulated IL-12 production but did not modulate IL-10 secretion. Moreover, contact with MV-H suppressed DC-mediated T-cell alloproliferation, demonstrating profound alteration of DC maturation and functions. Finally, engagement of CD150 by MV-H in mice transgenic for human CD150 decreased inflammatory responses, showing the immunosuppressive effect of CD150-MV-H interaction in vivo. Altogether, these results uncover novel mechanism of MV-induced immunosuppression, implicating modulation of cell signaling pathways following MV-H interaction with CD150-expressing DCs and reveal anti-inflammatory effects of CD150 stimulation.

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Cellular immune responses during complicated and uncomplicated measles virus infections of man

Cited by 138 publications

References 35 publications

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

A recombinant measles virus expressing biologically active human interleukin-12.

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

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