Transactivation induced by human T-lymphotropic virus type III (HTLV III) maps to a viral sequence encoding 58 amino acids and lacks tissue specificity

Seigel, Leonard J.; Ratner, Lee; Josephs, Steven F.; Dersefi, David; Feinberg, Mark B.; Reyes, Gregory R.; O’Brien, Stephen J.; Wong‐Staal, Flossie

doi:10.1016/0042-6822(86)90419-8

Cited by 118 publications

(78 citation statements)

References 22 publications

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“…In addition to the entry block, Tat transactivation of the HIV-1 long terminal repeat (LTR) is inefficient in murine cells, resulting in low-level provirus expression (2,14,17,34,41). The defect in Tat function was complemented in human-rodent somatic cell lines containing human chromosome 12 (2,17,34), a finding that suggested the presence of a speciesspecific Tat cofactor.…”

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confidence: 80%

Mouse-Human Heterokaryons Support Efficient Human Immunodeficiency Virus Type 1 Assembly

Mariani

Rasala

Rütter

et al. 2001

J Virol

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Murine cells do not support human immunodeficiency virus type 1 (HIV-1) replication because of blocks to virus entry, proviral expression, and virion assembly. In murine 3T3 fibroblasts, the block to HIV-1 entry is relieved by the introduction of human CD4 and CCR5 or CXCR4, and proviral expression is increased by the introduction of the Tat cofactor, human cyclin T1; however, because of the assembly block, virus fails to spread. A panel of rodent cell lines expressing human CD4, CCR5, and cyclin T1 was established and studied for the ability to support virus replication. Mus musculus lymphoid cell lines EL4 and L1-2 and Mus dunni fibroblasts supported only low levels of virus assembly and released small amounts of infectious virus. CHO and Rat2 cell lines produced more infectious virus, but this production was still 40-fold lower than production in human cells. Only CHO cells expressing the three human cofactors were partially permissive for HIV-1 replication. To investigate the basis of the block to HIV-1 assembly, mouse-human heterokaryons were tested for ability to assemble and release virus. Fusion of human cells to HIV-1-infected mouse cells expressing CD4, CCR5, and cyclin T1 caused a 12-fold increase in virion release and a 700-fold increase in infectious virus production. Fusion of HIV-1-infected M. dunni tail fibroblasts to uninfected human cells caused a similar increase in virus release. More efficient virus release was not caused by increased proviral transcription or increased synthesis of virion components. Analysis of reciprocal heterokaryons suggested the absence of an inhibitor of virus assembly. Taken together, the results suggested that murine fibroblasts lack a cofactor that is required for efficient virus assembly and release.

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confidence: 80%

Mouse-Human Heterokaryons Support Efficient Human Immunodeficiency Virus Type 1 Assembly

Mariani

Rasala

Rütter

et al. 2001

J Virol

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“…The human immunodeficiency virus type 1 (HIV-1) replication cycle is blocked at several stages in murine cells, including at binding and entry (11), postentry (1,6), transcription (14,21), late gene expression (2,9,25), and assembly (2,12). Expression of required human cofactors can overcome some defects (4,11,26), and certain murine cells can be engineered to support a partial HIV-1 replication cycle, up to and including early gene expression (2,5,12).…”

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confidence: 99%

Matrix-Induced Inhibition of Membrane Binding Contributes to Human Immunodeficiency Virus Type 1 Particle Assembly Defects in Murine Cells

Hatziioannou

Martín-Serrano

Zang

et al. 2005

J Virol

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Defective human immunodeficiency virus type 1 (HIV-1) assembly in murine cells is accompanied by poor plasma membrane binding and proteolytic processing of the HIV-1 Gag precursor. Here, we show that such defects are induced by the propensity of the HIV-1 MA globular head to inhibit membrane binding and particle assembly, particularly at the low expression levels observed in murine cells. Simple additions to or deletion of the MA globular head can improve the yield of infectious virions from murine cells by >50-fold. Expression level and autoinhibition can be important confounding variables in studies of HIV-1 assembly and contribute to defects encountered in murine cells.

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“…Functions of the TAT gene have been analyzed in HIVinfected cells (13,19,21) and in transfected cells in which TAT gene expression is directed by a transfected plasmid (13,21) or by a stably integrated plasmid (22). TAR has been mapped to nucleotides -17 to +80 with respect to the transcription initiation site in the HIV LTR (19); thus, the cap site is located within TAR.…”

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confidence: 99%

Elevated levels of mRNA can account for the trans-activation of human immunodeficiency virus.

Peterlin

Luciw²,

Barr

et al. 1986

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

281

185

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The genome of human immunodeficiency virus encodes a protein that dramatically elevates amounts of viral proteins. The precise mechanism of this trans-activation remains to be established. It has been reported that transactivation can occur without major changes in the levels of mRNA. We constructed recombinant plasmids containing those viral sequences required in cis for trans-activation linked to the chloramphenicol acetyltransferase gene. These plasmids were introduced into cultured cells in either the presence or absence ofa second plasmid that directed expression ofthe viral trans-activator protein. Expression of the chloramphenicol acetyltransferase gene was measured at the level of protein (by enzymatic assay) and RNA (by ribonuclease protection and primer extension). Our results demonstrate that trans-activation is accompanied by large increases in mRNA levels; these increases may be sufficient to explain the elevated levels of trans-activated protein.

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Transactivation induced by human T-lymphotropic virus type III (HTLV III) maps to a viral sequence encoding 58 amino acids and lacks tissue specificity

Cited by 118 publications

References 22 publications

Mouse-Human Heterokaryons Support Efficient Human Immunodeficiency Virus Type 1 Assembly

Mouse-Human Heterokaryons Support Efficient Human Immunodeficiency Virus Type 1 Assembly

Matrix-Induced Inhibition of Membrane Binding Contributes to Human Immunodeficiency Virus Type 1 Particle Assembly Defects in Murine Cells

Elevated levels of mRNA can account for the trans-activation of human immunodeficiency virus.

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