Compartmentalization of Human Immunodeficiency Virus Type 1 between Blood Monocytes and CD4<sup>+</sup>T Cells during Infection

Fulcher, Jennifer A.; Hwangbo, Yon; Zioni, Rafael; Nickle, David C.; Lin, Xudong; Heath, Laura; Mullins, James I.; Corey, Lawrence; Zhu, Tuofu

doi:10.1128/jvi.78.15.7883-7893.2004

Cited by 81 publications

(110 citation statements)

References 113 publications

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“…Despite the relatively high CXCR4 expression on all monocyte subsets, HIV-1 appears to preferentially use CCR5 for entry into monocytes as we (13) and others (58,59) have shown previously. However, one recent study has identified HIV-1 genotypes that predict a CXCR4-using virus as a minor variant in monocytes from some patients (59).…”

Section: Discussionmentioning

confidence: 88%

“…However, one recent study has identified HIV-1 genotypes that predict a CXCR4-using virus as a minor variant in monocytes from some patients (59). Although CD14 high CD16 Ϫ monocytes expressed more CXCR4 than CD14 high CD16 ϩ or CD14 low CD16 ϩ monocytes, both CD14 high CD16 Ϫ and CD16 ϩ monocytes were relatively refractory to a virus using the CXCR4-tropic envelope of HIV-1 HXB2 .…”

Section: Discussionmentioning

confidence: 99%

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The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

Ellery

Tippett

Chiu

et al. 2007

The Journal of Immunology

299

276

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HIV-1 persists in peripheral blood monocytes in individuals receiving highly active antiretroviral therapy (HAART) with viral suppression, despite these cells being poorly susceptible to infection in vitro. Because very few monocytes harbor HIV-1 in vivo, we considered whether a subset of monocytes might be more permissive to infection. We show that a minor CD16+ monocyte subset preferentially harbors HIV-1 in infected individuals on HAART when compared with the majority of monocytes (CD14highCD16−). We confirmed this by in vitro experiments showing that CD16+ monocytes were more susceptible to CCR5-using strains of HIV-1, a finding that is associated with higher CCR5 expression on these cells. CD16+ monocytes were also more permissive to infection with a vesicular stomatitis virus G protein-pseudotyped reporter strain of HIV-1 than the majority of monocytes, suggesting that they are better able to support HIV-1 replication after entry. Consistent with this observation, high molecular mass complexes of apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G) were observed in CD16+ monocytes that were similar to those observed in highly permissive T cells. In contrast, CD14highCD16− monocytes contained low molecular mass active APOBEC3G, suggesting this is a mechanism of resistance to HIV-1 infection in these cells. Collectively, these data show that CD16+ monocytes are preferentially susceptible to HIV-1 entry, more permissive for replication, and constitute a continuing source of viral persistence during HAART.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

Ellery

Tippett

Chiu

et al. 2007

The Journal of Immunology

299

276

View full text Add to dashboard Cite

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“…The role these cells play in patients on suppressive cART is not fully understood (43)(44)(45). We sorted myeloid cells from both peripheral blood and GALT from all of the eight patients and found HIV-1 DNA in myeloid cells from peripheral blood and GALT in three and four of the eight patient samples, respectively.…”

Section: Discussionmentioning

confidence: 99%

The HIV-1 reservoir in eight patients on long-term suppressive antiretroviral therapy is stable with few genetic changes over time

Josefsson

Stockenström

Faria

et al. 2013

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

249

296

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Significance Identifying the source and dynamics of persistent HIV-1 during combinational antiretroviral therapy (cART) is crucial for understanding the barriers to curing HIV infection. Through genetic characterization of HIV-1 DNA in infected cells from peripheral blood and gut-associated lymphoid tissue from patients after long-term suppressive cART, our study reveals that the primary barrier to a cure is a remarkably stable pool of infected memory CD4 + T cells. Through in-depth phylogenetic analyses, we determined that the HIV-1 reservoir in these cells from eight patients is kept stable during long-term cART and, with little evidence of viral replication, this population could be maintained by homeostatic cell proliferation or other processes.

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“…Infected monocytes can seed HIV in down-stream lineage cells, namely macrophages, which can then serve as a virus source in multiple tissue sites (Fulcher et al, 2004). Despite whether HIV-1 can replicate in monocytes themselves, once the cell has entered a tissue site and differentiated into either a macrophage or dendritic cell, then the virus can start replicating and infecting the tissue.…”

Section: Expression Of Toll-like Receptors (Tlrs)mentioning

confidence: 99%

Monocytes and their Role in Human Immunodeficiency Virus Pathogenesis

Sassé

Zhou

et al. 2012

American Journal of Infectious Diseases

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Monocytes play several significant immunological roles during HIV infection. The phenotypic pliability and the cellular differentiation ability monocytes possess are crucial to the ways they combat infections and control inflammatory processes. The purpose of this review is to provide a comprehensive snapshot of the importance of monocytes in HIV-1 infection and pathogenesis. Moreover, this review also provides newly emerging data on how HIV leads to the subversion and manipulation of monocyte transcriptome and proteome, which may have implications in understanding the genomic and proteomic basis of monocyte function and its interaction with HIV.

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Compartmentalization of Human Immunodeficiency Virus Type 1 between Blood Monocytes and CD4⁺T Cells during Infection

Cited by 81 publications

References 113 publications

The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

The HIV-1 reservoir in eight patients on long-term suppressive antiretroviral therapy is stable with few genetic changes over time

Monocytes and their Role in Human Immunodeficiency Virus Pathogenesis

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Compartmentalization of Human Immunodeficiency Virus Type 1 between Blood Monocytes and CD4+T Cells during Infection

Cited by 81 publications

References 113 publications

The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

The CD16+ Monocyte Subset Is More Permissive to Infection and Preferentially Harbors HIV-1 In Vivo

The HIV-1 reservoir in eight patients on long-term suppressive antiretroviral therapy is stable with few genetic changes over time

Monocytes and their Role in Human Immunodeficiency Virus Pathogenesis

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Product

Resources

About

Compartmentalization of Human Immunodeficiency Virus Type 1 between Blood Monocytes and CD4⁺T Cells during Infection