Growth of Measles Virus in the Lymphoid Tissues of Monkeys

Yamanouchi, Kazuya; Chino, Fumitoshi; Kobune, Fumio; Kodama, Hideo; Tsuruhara, Takashi

doi:10.1093/infdis/128.6.795

Cited by 36 publications

(30 citation statements)

References 5 publications

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“…This MV binding activity is destroyed by proteases, and its reexpression is inhibited by cycloheximide and tunicamycin. This strongly supports the hypothesis that MV binds to a surface glycoprotein component as has been suggested previously (Krah, 1989;Valdimarsson et al, 1975 (Yamanouchi et al, 1973). We can thus propose that the MV receptor has a wide if not ubiquitous distribution on human tissue types.…”

Section: Discussionsupporting

confidence: 91%

A Monoclonal Antibody Recognizes a Human Cell Surface Glycoprotein Involved In Measles Virus Binding

Naniche

Rabourdin-Combe

et al. 1992

Journal of General Virology

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Measles virus (MV) has a very limited host range, humans being the only natural reservoir of the virus. This restriction may be due to the absence of an MV receptor on the surface of non-primate cells. We have studied the MV-binding ability of several cell lines and attempted to characterize the receptor by studying the binding of 35S-labelled MV and by a rosette formation technique. We confirmed that all the human cell lines examined (HeLa, Raji and Jurkat) bound MV and that the murine cell lines (BW and L) did not. The glycoprotein nature of the receptor activity was demonstrated by the fact that it could be removed from the cell membrane using proteolytic enzymes and by its failure to be re-expressed in the presence of a protein synthesis inhibitor or an N-glycosylation inhibitor. A monoclonal antibody isolated after immunization of mice with Raji cells specifically inhibited MV binding and infection of human cells, and recognized human and simian but not murine cells. Depending on the cell line (HeLa, Raji, Jurkat or Vero), this antibody immunoprecipitated one or two glycoproteins with apparent MrS of 57K and/or 67K from human and simian cells, but not from murine cells.

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Section: Discussionsupporting

confidence: 91%

A Monoclonal Antibody Recognizes a Human Cell Surface Glycoprotein Involved In Measles Virus Binding

Naniche

Rabourdin-Combe

et al. 1992

Journal of General Virology

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“…This second viremia allows the spreading of the virus to other lymphoid organs, including the thymus, where a profound thymic injury, characterized by degenerative and/or necrotic lesions, occurs (8,62). Human thymic stromal cells, particularly TEC, have been described as targets for MV during the acute phase of infection (35,64). In a SCID-hu thymic implant model, MV infection of TEC cause apoptosis of uninfected thymocytes (1).…”

Section: Discussionmentioning

confidence: 99%

Measles Virus (MV) Nucleoprotein Binds to a Novel Cell Surface Receptor Distinct from FcγRII via Its C-Terminal Domain: Role in MV-Induced Immunosuppression

Laine

Trescol-Biémont

Longhi

et al. 2003

J Virol

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“…Both viruses replicate in lymphoid tissue, providing extensive opportunities for interaction (Kilby, 2001;Yamanouchi et al, 1973). In an ex vivo model using human lymphoid tissues, MV inhibited the replication of both CXCR4-tropic and CCR5-tropic HIV-1, but the inhibitory effect was greater for CCR5-tropic HIV-1 (Grivel et al, 2005).…”

Section: Introductionmentioning

confidence: 97%

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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Growth of Measles Virus in the Lymphoid Tissues of Monkeys

Cited by 36 publications

References 5 publications

A Monoclonal Antibody Recognizes a Human Cell Surface Glycoprotein Involved In Measles Virus Binding

A Monoclonal Antibody Recognizes a Human Cell Surface Glycoprotein Involved In Measles Virus Binding

Measles Virus (MV) Nucleoprotein Binds to a Novel Cell Surface Receptor Distinct from FcγRII via Its C-Terminal Domain: Role in MV-Induced Immunosuppression

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

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