Virus-Induced Immunosuppression: Infections with Measles Virus and Human Immunodeficiency Virus

McChesney, Michael B.; Oldstone, Michael B. A.

doi:10.1016/s0065-2776(08)60696-3

Cited by 106 publications

(45 citation statements)

References 261 publications

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“…In our study, the deficit in DC activity persists over an extended period after virus clearance, as evidenced by the failure of DCs from Cl 13-infected mice at 120 days to induce the proliferation of allogeneic T cells, although virus was cleared from the host by day 60. This disassociation between LCMV clearance and prolonged immunosuppression is reminiscent of observations with measles virus (49)(50)(51). Measles virus infection impairs the host's T cell-mediated response to tuberculin and other antigens, and this impairment usually persists for a number of months after measles virus is cleared from the patient (52).…”

Section: Discussionmentioning

confidence: 78%

Viral targeting of hematopoietic progenitors and inhibition of DC maturation as a dual strategy for immune subversion

Sevilla

McGavern²,

Teng³

et al. 2004

J. Clin. Invest.

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151

148

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Section: Discussionmentioning

confidence: 78%

Viral targeting of hematopoietic progenitors and inhibition of DC maturation as a dual strategy for immune subversion

Sevilla

McGavern²,

Teng³

et al. 2004

J. Clin. Invest.

Self Cite

151

148

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“…There is extensive evidence of immunosuppression caused by morbilliviruses (Appel et al, 1982;McChesney & Oldstone, 1989). It was measles virus (MV), a member of this morbillivirus group and closely related to RPV (Sheshberadaran et al, 1986), which was the first reported virus to be associated with immunosuppression (Von Pirquet, 1908).…”

Section: Discussionmentioning

confidence: 99%

Rinderpest virus infection of bovine peripheral blood monocytes

Nores¹,

Anderson

Butcher

et al. 1995

Journal of General Virology

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The ability of rinderpest virus (RPV) to replicate in vitro in adherent peripheral blood monocytes and monocytederived macrophages under non-stimulation conditions was investigated. When flow cytometry analysis on bovine peripheral blood mononuclear cells (PBMC) was performed, monocytic cells were seen to be targets for infection by the cell culture-attenuated RBOK vaccine strain of RPV. Viral glycoprotein (H) and nucleoprotein (N) expression in adherent blood monocytes and monocyte-derived macrophages was compared with the infection in Vero cells, in which a productive infection typical of morbilliviruses is obtained. In both cell types, the infection was m.o.i.-dependent, but the rate of viral protein accumulation was slower in monocytes/ macrophages. Double-labelling experiments with monoclonal antibodies against RPV and the myeloid marker CD14 confirmed that the infected blood adherent cells were monocytes and macrophages. Productive infection of monocytes was confirmed by progeny virus titration. Permissiveness to infection was not dependent on macrophage differentiation: in vitro maturation ofmonocytes to macrophages before infection, did not increase the susceptibility of these cells to RPV infection. With the virulent Saudi RPV isolate, similar results were obtained, although the Saudi virus apparently had a higher rate of replication compared to the attenuated virus. These observations demonstrate clearly that bovine blood monocytes and monocyte-derived macrophages serve as hosts for a relatively slow but productive infection by rinderpest virus.

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“…Lethal complications of measles virus (MV) infections are a consequence of transient but severe MV-induced immunodepression (Norrby & Oxman, 1990). One of the best documented aspects of MV-dependent immunodepression is impaired ability of infected lymphocytes to respond to mitogen activation (McChesney et al, 1987(McChesney et al, , 1988Yanagi et al, 1992). The cellular and molecular mechanisms responsible for MV-related immunodepression are as yet poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Cell-to-cell contact via measles virus haemagglutinin-CD46 interaction triggers CD46 downregulation

Krantic¹,

Gimenez

Rabourdin–Combe

1995

Journal of General Virology

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CD46 downregulation by measles virus (MV) occurs after expression of virus haemagglutinin (H) protein on the surface of the infected cell and is a consequence of CD46-H interaction on the cell membrane. To assess whether CD46 downregulation also occurs after CD46-H interaction when these two molecules are expressed on distinct cells, we used human T cell line Jurkat (expressing CD46) and transfected murine fibroblast line L stably expressing MV-H protein (L.H). FACS analysis shows that cell-to-cell contact of 1 h at 37 °C triggers a reduction of CD46 cell surface labelling as detected by MCI20.6, GB24 and J4-48 monoclonal antibodies. This reduction is similar to that observed The H-mediated CD46 downregulation is reversible and restricted to CD46 since expression of other surface markers (CD3, CD14, CD47 and CD63) is unaffected. It is apparently not mediated in a protein kinase (PK) A-or PKC-dependent manner. Altogether, our results provide an unequivocal demonstration that interaction between the extracellular domains of CD46 and MV-H is sufficient to trigger CD46 downregulation.

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Virus-Induced Immunosuppression: Infections with Measles Virus and Human Immunodeficiency Virus

Cited by 106 publications

References 261 publications

Viral targeting of hematopoietic progenitors and inhibition of DC maturation as a dual strategy for immune subversion

Viral targeting of hematopoietic progenitors and inhibition of DC maturation as a dual strategy for immune subversion

Rinderpest virus infection of bovine peripheral blood monocytes

Cell-to-cell contact via measles virus haemagglutinin-CD46 interaction triggers CD46 downregulation

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