AIDS-associated retroviruses (ARV) can productively infect other cells besides human T helper cells

Levy, Jay A.; Shimabukuro, Joni; McHugh, Thomas M.; Casavant, Conrad H.; Stites, Daniel P.; Oshiro, Lyndon S.

doi:10.1016/0042-6822(85)90146-1

Cited by 235 publications

(100 citation statements)

References 21 publications

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“…A lthough HIV-1 was introduced into the human population from a nonhuman primate reservoir in the chimpanzee fairly recently (1), it does not infect nonhuman primates and replicates poorly or not at all on activated nonhuman primate lymphocytes in vitro (2,3). HIV-1 can replicate at detectable levels in experimentally infected chimpanzees (4-7), but virus loads remain low, and chimpanzee T cells in culture are largely refractory to infection (8).…”

mentioning

confidence: 99%

A dominant block to HIV-1 replication at reverse transcription in simian cells

Münk

Brandt

Lucero

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

212

225

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mentioning

confidence: 99%

A dominant block to HIV-1 replication at reverse transcription in simian cells

Münk

Brandt

Lucero

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

212

225

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“…Whether these are due to actual infection of the monocytes by HIV (11,12) or are secondary to its effects on other cells (1,3,6) needs clarification. Additional studies on mononuclear phagocyte function in relation to HIV infection are clearly indicated to define further the immunopathology of AIDS.…”

Section: Resultsmentioning

confidence: 99%

“…In a preliminary communication, we reported studies on RES Fc-receptor-specific clearance in patients with AIDS (a study of splenic macrophage function) (20). In this previous study, 11 of (20). These in vivo RES defects led us to study the function ofperipheral blood monocytes in an in vitro antibody-dependent cell-mediated cytotoxicity assay with chicken erythrocytes as target cells.…”

Section: Resultsmentioning

confidence: 99%

Demonstration of defective C3-receptor-mediated clearance by the reticuloendothelial system in patients with acquired immunodeficiency syndrome.

Bender¹,

Bohnsack²,

Sourlis³

et al. 1987

J. Clin. Invest.

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“…Moreover, the relationship between the level of CD4 expression and susceptibility to infection by HIV is complex. For example, Levy et al (6) found that the level of Leu-3 expression did not always correlate with production of HIV in a study of unrelated cell lines. Independently isolated clones of the Molt-4 T cell line varied in their susceptibility to infection by HIV while expressing similar levels of the CD4 antigen (7).…”

Section: Discussionmentioning

confidence: 99%

“…CD4 expression is also necessary for HIV-induced cell fusion (29)(30)(31)(32)(33). Although HIV preferentially infects CD4+ T cells, it also infects cells of different lineages, including monocytes and macrophages (6,(34)(35)(36)(37)(38)(39), B lymphocytes (6,8,39,40), promyelocytes (6), and cells of neural origin (41)(42)(43). CD4 can be expressed by these cell lines (4,6,35,44,45), but whether HIV only infects cells of these lineages that express CD4, or whether other receptors, or other modes of cell entry, are involved is unclear.…”

Section: Discussionmentioning

confidence: 99%

Phenotypic variation in the response to the human immunodeficiency virus among derivatives of the CEM T and WIL-2 B cell lines.

Chaffee

Leeds

Matthews

et al. 1988

The Journal of Experimental Medicine

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Expression of the CD4 glycoprotein, the surface receptor for the human immunodeficiency virus (HIV) (1-4), and of specific transcription factors that promote the expression of HIV genes (5) are characteristics that target a subset of lymphocytes for the pathological consequences of HIV infection. Additional properties of CD4+ lymphocytes and other HIV host cells could affect the efficiency of replication or the cytopathic effects of the virus, and thereby determine whether the outcome of infection is cell death; the establishment of a latent, nonproductive state; or the evolution of a chronic, virus-producing reservoir. The existence and potential importance of such host cell-specific factors is suggested by the variable response to HIV infection among cultured human lymphoid cell lines in vitro (6-8). The basis for this variability is poorly understood, and the spectrum of responses to HIV infection in vitro has not been well characterized.The regulation of deoxyribonucleotide pool size and turnover in host cells could affect the reverse transcription of the HIV genome and subsequent replication of double-stranded circular viral DNA, and could strongly influence the therapeutic activity or cytotoxicity of antiretroviral nucleoside analogs. In view of these possibilities, we initiated studies of the ability of HIV to infect mutant lymphoblastoid cell lines with altered nucleoside metabolism . We chose the CEM human T cell line (9) and the WIL-2 human B cell line (10) because they have been shown to differ strikingly in their regulation of deoxynucleotide metabolism (11,12), and because of the availability of mutants of each that are deficient in specific nucleoside kinase activities, which could be useful for studies of antiretroviral nucleoside analog metabolism. Here we report a systematic characterization ofthe responses ofthese mutants and other derivatives of CEM and WIL-2 to infection with the HTLV IIIB strain of HIV.

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AIDS-associated retroviruses (ARV) can productively infect other cells besides human T helper cells

Cited by 235 publications

References 21 publications

A dominant block to HIV-1 replication at reverse transcription in simian cells

A dominant block to HIV-1 replication at reverse transcription in simian cells

Demonstration of defective C3-receptor-mediated clearance by the reticuloendothelial system in patients with acquired immunodeficiency syndrome.

Phenotypic variation in the response to the human immunodeficiency virus among derivatives of the CEM T and WIL-2 B cell lines.

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