Interactions between HIV-1 and Cytomegalovirus in Human Osteosarcoma Cells Carrying Both Viruses

Miriam Margalith; Daniel J. Medina; Gueh Djen Hsiung; Benjamin R. Smith; Richard T. D'aquila; Joan C. Kaplan; Lawrence Bechtel; Monica Z. Wang; Paul R. Skolnik; Martin S. Hirsch

doi:10.1089/aid.1993.9.519

Interactions between HIV-1 and Cytomegalovirus in Human Osteosarcoma Cells Carrying Both Viruses

Miriam Margalith, Daniel J. Medina, Gueh Djen Hsiung, Benjamin R. Smith, Richard T. D'aquila, Joan C. Kaplan, Lawrence Bechtel, Monica Z. Wang, Paul R. Skolnik, Martin S. Hirsch

Virology

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Cytomegalovirus (CMV) and the human immunodeficiency virus type 1 (HIV-1) may interact in the pathogenesis of AIDS. We compared CMV replication in human osteosarcoma (HOS) cells to that in HOS cells genetically engineered to contain an envelope-deficient HIV-1 proviral construct (designated HOS-HXG). Following acute CMV infection of each cell line, HOS-HXG cells contained higher numbers of intranuclear CMV nucleocapsids than did HOS cells. Infectious CMV could be persistently detected in culture supernatant fluids of the CMV-infected HOS-HXG cells, whereas CMV was lost over several weeks from HOS cells infected with CMV in parallel. HIV-1 CMV pseudotypes were not detected in supernatant fluids from CMV-infected HOS-HXG cells. On day 119 after CMV infection, these cultures were superinfected with HIV-1. These dually infected HOS-HXG cells produced infectious HIV-1 and exhibited markedly enhanced CMV replication compared to parental CMV-infected HOS-HXG cells. Two different HIV-1 tat gene function antagonists, Ro24-7429 and chemically modified antibodies to the Tat protein, did not inhibit the replication of CMV in either acute or persistent infections of HOS-HXG cells at concentrations that inhibited HIV-1 replication.

Original language	English
Pages (from-to)	519-527
Number of pages	9
Journal	AIDS Research and Human Retroviruses
Volume	9
Issue number	6
DOIs	https://doi.org/10.1089/aid.1993.9.519
State	Published - 1 Jan 1993

ASJC Scopus subject areas

Immunology
Virology
Infectious Diseases

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10.1089/aid.1993.9.519

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title = "Interactions between HIV-1 and Cytomegalovirus in Human Osteosarcoma Cells Carrying Both Viruses",

abstract = "Cytomegalovirus (CMV) and the human immunodeficiency virus type 1 (HIV-1) may interact in the pathogenesis of AIDS. We compared CMV replication in human osteosarcoma (HOS) cells to that in HOS cells genetically engineered to contain an envelope-deficient HIV-1 proviral construct (designated HOS-HXG). Following acute CMV infection of each cell line, HOS-HXG cells contained higher numbers of intranuclear CMV nucleocapsids than did HOS cells. Infectious CMV could be persistently detected in culture supernatant fluids of the CMV-infected HOS-HXG cells, whereas CMV was lost over several weeks from HOS cells infected with CMV in parallel. HIV-1 CMV pseudotypes were not detected in supernatant fluids from CMV-infected HOS-HXG cells. On day 119 after CMV infection, these cultures were superinfected with HIV-1. These dually infected HOS-HXG cells produced infectious HIV-1 and exhibited markedly enhanced CMV replication compared to parental CMV-infected HOS-HXG cells. Two different HIV-1 tat gene function antagonists, Ro24-7429 and chemically modified antibodies to the Tat protein, did not inhibit the replication of CMV in either acute or persistent infections of HOS-HXG cells at concentrations that inhibited HIV-1 replication.",

author = "Miriam Margalith and Medina, {Daniel J.} and Hsiung, {Gueh Djen} and Smith, {Benjamin R.} and D'aquila, {Richard T.} and Kaplan, {Joan C.} and Lawrence Bechtel and Wang, {Monica Z.} and Skolnik, {Paul R.} and Hirsch, {Martin S.}",

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AU - Margalith, Miriam

AU - Medina, Daniel J.

AU - Hsiung, Gueh Djen

AU - Smith, Benjamin R.

AU - D'aquila, Richard T.

AU - Kaplan, Joan C.

AU - Bechtel, Lawrence

AU - Wang, Monica Z.

AU - Skolnik, Paul R.

AU - Hirsch, Martin S.

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N2 - Cytomegalovirus (CMV) and the human immunodeficiency virus type 1 (HIV-1) may interact in the pathogenesis of AIDS. We compared CMV replication in human osteosarcoma (HOS) cells to that in HOS cells genetically engineered to contain an envelope-deficient HIV-1 proviral construct (designated HOS-HXG). Following acute CMV infection of each cell line, HOS-HXG cells contained higher numbers of intranuclear CMV nucleocapsids than did HOS cells. Infectious CMV could be persistently detected in culture supernatant fluids of the CMV-infected HOS-HXG cells, whereas CMV was lost over several weeks from HOS cells infected with CMV in parallel. HIV-1 CMV pseudotypes were not detected in supernatant fluids from CMV-infected HOS-HXG cells. On day 119 after CMV infection, these cultures were superinfected with HIV-1. These dually infected HOS-HXG cells produced infectious HIV-1 and exhibited markedly enhanced CMV replication compared to parental CMV-infected HOS-HXG cells. Two different HIV-1 tat gene function antagonists, Ro24-7429 and chemically modified antibodies to the Tat protein, did not inhibit the replication of CMV in either acute or persistent infections of HOS-HXG cells at concentrations that inhibited HIV-1 replication.

AB - Cytomegalovirus (CMV) and the human immunodeficiency virus type 1 (HIV-1) may interact in the pathogenesis of AIDS. We compared CMV replication in human osteosarcoma (HOS) cells to that in HOS cells genetically engineered to contain an envelope-deficient HIV-1 proviral construct (designated HOS-HXG). Following acute CMV infection of each cell line, HOS-HXG cells contained higher numbers of intranuclear CMV nucleocapsids than did HOS cells. Infectious CMV could be persistently detected in culture supernatant fluids of the CMV-infected HOS-HXG cells, whereas CMV was lost over several weeks from HOS cells infected with CMV in parallel. HIV-1 CMV pseudotypes were not detected in supernatant fluids from CMV-infected HOS-HXG cells. On day 119 after CMV infection, these cultures were superinfected with HIV-1. These dually infected HOS-HXG cells produced infectious HIV-1 and exhibited markedly enhanced CMV replication compared to parental CMV-infected HOS-HXG cells. Two different HIV-1 tat gene function antagonists, Ro24-7429 and chemically modified antibodies to the Tat protein, did not inhibit the replication of CMV in either acute or persistent infections of HOS-HXG cells at concentrations that inhibited HIV-1 replication.

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Interactions between HIV-1 and Cytomegalovirus in Human Osteosarcoma Cells Carrying Both Viruses

Abstract

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