Modulation of Immune System Function by Measles Virus Infection: Role of Soluble Factor and Direct Infection

Fujinami, Robert S.; Sun, Xinmin; Howell, Joseph M.; Jenkin, James C.; Burns, James

doi:10.1128/jvi.72.12.9421-9427.1998

Cited by 55 publications

(17 citation statements)

References 42 publications

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“…It is tempting to speculate that MV N translocates to the plasma membrane using a non-classical transport mechanism, as reported for some other virus proteins [94]. The existence of a soluble factor produced by infected PBLs or B-cell lines, capable of inhibiting lymphocyte proliferation has been proposed [95,96]. Whether N or its fragments may have some of the immunosuppressive effects seen in these studies, remains to be analysed.…”

Section: Role Of the MV Nucleoproteinmentioning

confidence: 83%

Immunosuppression caused by measles virus: role of viral proteins

Kerdiles

Sellin

Druelle

et al. 2005

Reviews in Medical Virology

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Measles virus (MV) causes transient but profound immunosuppression resulting in increased susceptibility to secondary bacterial and viral infections. Due to the development of these opportunistic infections, measles remains the leading vaccine-preventable cause of child death worldwide. Different immune abnormalities have been associated with measles, including disappearance of delayed-type hypersensitivity reactions, impaired lymphocyte and antigen-presenting cell functions, down-regulation of pro-inflammatory interleukin 12 production and altered interferon alpha/beta signalling pathways. Several MV proteins have been suggested to hinder immune functions: hemagglutinin, fusion protein, nucleoprotein and the non-structural V and C proteins. This review will focus on the novel functions attributed to MV proteins in the immunosuppression associated with measles. Here, we highlight new advances in the field, emphasising the interaction between MV proteins and their cellular targets, in particular the cell membrane receptors, CD46, CD150, TLR2 and FcgammaRII in the induction of immunological abnormalities associated with measles.

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Section: Role Of the MV Nucleoproteinmentioning

confidence: 83%

Immunosuppression caused by measles virus: role of viral proteins

Kerdiles

Sellin

Druelle

et al. 2005

Reviews in Medical Virology

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“…Cell membrane-associated MV components inhibit antigen processing (Marttila et al, 2001). It has been speculated that the production of a soluble factor can inhibit antigen-specific T cell proliferation and the proliferation of uninfected B cells (Fujinami et al, 1998). However, the mechanism of MV induced lymphopenia is unknown.…”

Section: Discussionmentioning

confidence: 99%

Canine distemper virus-induced depletion of uninfected lymphocytes is associated with apoptosis

Schobesberger

Summerfield²,

Doherr

et al. 2005

Veterinary Immunology and Immunopathology

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Canine distemper virus (CDV), a negative stranded RNA morbillivirus, causes a multisystemic disease in dogs, which is associated with a severe immune suppression. The aim of the study was to examine the influence of early CDV infection on leukocyte depletion, lymphopenia and virus-induced cell death in dogs infected with a virulent CDV strain. From 10 infected dogs, peripheral blood leukocytes were harvested periodically, phenotyped and analyzed for CDV antigen content and apoptosis using Annexin V-FITC and propidium iodide labeling. CDV infection induced a severe CD3+ T cell and CD21+ B cell depletion in all animals at 3 days post-infection (d.p.i.). For dogs with severe distemper, developing virus persistence in the lymphoid tissue and central nervous system, this lymphopenia lasted until the end of the experiment. Increased levels of lymphocyte apoptosis were found at 3 d.p.i., and monocyte apoptosis at 6 d.p.i. This was more prominent in the group of animals with severe distemper. At 3 d.p.i. no leukocyte infection was detectable indicating that the early lymphocyte depletion and apoptosis was not a direct consequence of virus infection. Taken together, our results demonstrate that CDV-induced lymphopenia is an early event and that the degree of lymphocyte depletion correlates with the severity of disease and virus persistence in the lymphoid tissue and central nervous system.

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“…Since the frequency of infected PBMC in vivo is low, mechanisms independent of infectioninduced arrest of proliferation or cell lysis are likely to cause MV-induced immunosuppression. These include the production of inhibitory soluble mediators by infected T or B cells [4,5], or cell-cell surface contact mediated signals that can result in down-regulation of immunostimulatory cytokines such as IL-12, induction of apoptosis or proliferative arrest [6][7][8]. Our previous studies revealed that the expression of proteolytically activated MV F and MV H proteins on the surface of infected cells, MV F-and H-transfected cells and viral particles is necessary and sufficient to induce a state of proliferative unresponsiveness in an excess amount of uninfected PBMC in vitro and in vivo [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Measles virus-induced promotion of dendritic cell maturation by soluble mediators does not overcome the immunosuppressive activity of viral glycoproteins on the cell surface

2000

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Measles virus (MV) infection promotes maturation of dendritic cells (DC), but also interferes with DC functions, and MV renders the DC inhibitory for T cell proliferation. We now describe that MV infection triggers the release of type I IFN from monocyte‐derived DC (Mo‐DC) which contributes to DC maturation. There is no evidence that soluble mediators are released interfering with the stimulatory activity of uninfected DC. Since inhibition of allogeneic T cell proliferation was unaffected by a fusion inhibitory peptide (Z‐fFG), MV infection of T cells did not contribute to inhibition. Allogeneic T cell proliferation depended on the percentage of DC expressing MV F/H glycoproteins within the DC population and their surface expression levels, was induced upon addition of UV‐inactivated MV to a mixed lymphocyte reaction stimulated by lipopolysaccharide‐matured DC, and was not induced by DC infected with a recombinant MV encoding the ectodomain of vesicular stomatitis virus G protein (MG/FV) instead of the MV glycoproteins. Similarly, DC infected with MV, but not with MG/FV inhibited mitogen‐induced proliferation of T cells. Thus, a dominant inhibitory signal is delivered to T cells by the MV glycoproteins on the surface of DC overcoming positive signals by co‐stimulatory molecules promoted by maturation factors released from infected DC.

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Modulation of Immune System Function by Measles Virus Infection: Role of Soluble Factor and Direct Infection

Cited by 55 publications

References 42 publications

Immunosuppression caused by measles virus: role of viral proteins

Immunosuppression caused by measles virus: role of viral proteins

Canine distemper virus-induced depletion of uninfected lymphocytes is associated with apoptosis

Measles virus-induced promotion of dendritic cell maturation by soluble mediators does not overcome the immunosuppressive activity of viral glycoproteins on the cell surface

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