Latent human cytomegalovirus enhances HIV-1 infection in CD34+ progenitor cells

Cheung, Allen Ka Loon; Huang, Yiru; Kwok, Hau Yee; Chen, Min; Chen, Zhiwei

doi:10.1182/bloodadvances.2016000638

Cited by 13 publications

(11 citation statements)

References 71 publications

(85 reference statements)

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“…A recent study of patient samples revealed that some HSPC subsets express high levels of CD4 and may harbor both CCR5-tropic and CXCR4-tropic HIV genomes (Sebastian et al, 2017). Furthermore, HSPCs latently infected with cytomegalovirus may have enhanced susceptibility to HIV-1 infection (Cheung et al, 2017). To confirm this evidence, another study using humanized BLT mice demonstrated HIV-1 infection of HPCs in vivo.…”

Section: Direct Hiv Infection Of Hspcsmentioning

confidence: 99%

Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS

Tsukamoto

2020

Front. Cell. Infect. Microbiol.

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Section: Direct Hiv Infection Of Hspcsmentioning

confidence: 99%

Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS

Tsukamoto

2020

Front. Cell. Infect. Microbiol.

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“…In some ways, it is not unsurprising that HCMV utilises aspects of the antiviral IFN response. Multiple studies of lytic infection have suggested that IFN-stimulated genes such as tetherin [ 123 ] and IFITM3 [ 124 ] could play a positive role in HCMV infection, although it is interesting to note a recent observation that long-term latent infection of CD34+ cells with HCMV results in a downregulation of multiple HIV-associated restriction factors [ 125 ]. The biological advantage of their downregulation to latent HCMV remains unclear, but it does suggest that restriction factors may be detrimental during latent carriage of HCMV genomes.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Navigating the Host Cell Response during Entry into Sites of Latent Cytomegalovirus Infection

2018

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The host cell represents a hostile environment that viruses must counter in order to establish infection. Human cytomegalovirus (HCMV) is no different and encodes a multitude of functions aimed at disabling, re-directing or hijacking cellular functions to promulgate infection. However, during the very early stages of infection the virus relies on the outcome of interactions between virion components, cell surface receptors and host signalling pathways to promote an environment that supports infection. In the context of latent infection—where the virus establishes an infection in an absence of many gene products specific for lytic infection—these initial interactions are crucial events. In this review, we will discuss key host responses triggered by viral infection and how, in turn, the virus ameliorates the impact on the establishment of non-lytic infections of cells. We will focus on strategies to evade intrinsic antiviral and innate immune responses and consider their impact on viral infection. Finally, we will consider the hypothesis that the very early events upon viral infection are important for dictating the outcome of infection and consider the possibility that events that occur during entry into non-permissive cells are unique and thus contribute to the establishment of latency.

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“…The kinase activity of UL97 influences IFN receptor signaling [134,182], vDNA replication, virion morphogenesis, nuclear egress, and more [183], making the kinase an exceptional drug target [184]. Interestingly, studies found that latent HCMV infection of CD34+ progenitor cells downregulated expression of various HIV-1 restriction factors, including SAMHD1, APOBEC3G, and Mx2, while upregulating the expression of HIV-1 coreceptors CXCR4 and CCR5 [185]. These findings begin to illuminate a mechanism behind the acceleration of HIV to AIDS in patients previously infected with HCMV [186,187].…”

Section: Samhd1 Restriction Of Dna Virusesmentioning

confidence: 99%

SAMHD1 Functions and Human Diseases

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Mahboubi

Schinazi

et al. 2020

Viruses

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Deoxynucleoside triphosphate (dNTP) molecules are essential for the replication and maintenance of genomic information in both cells and a variety of viral pathogens. While the process of dNTP biosynthesis by cellular enzymes, such as ribonucleotide reductase (RNR) and thymidine kinase (TK), has been extensively investigated, a negative regulatory mechanism of dNTP pools was recently found to involve sterile alpha motif (SAM) domain and histidine-aspartate (HD) domain-containing protein 1, SAMHD1. When active, dNTP triphosphohydrolase activity of SAMHD1 degrades dNTPs into their 2′-deoxynucleoside (dN) and triphosphate subparts, steadily depleting intercellular dNTP pools. The differential expression levels and activation states of SAMHD1 in various cell types contributes to unique dNTP pools that either aid (i.e., dividing T cells) or restrict (i.e., nondividing macrophages) viral replication that consumes cellular dNTPs. Genetic mutations in SAMHD1 induce a rare inflammatory encephalopathy called Aicardi–Goutières syndrome (AGS), which phenotypically resembles viral infection. Recent publications have identified diverse roles for SAMHD1 in double-stranded break repair, genome stability, and the replication stress response through interferon signaling. Finally, a series of SAMHD1 mutations were also reported in various cancer cell types while why SAMHD1 is mutated in these cancer cells remains to investigated. Here, we reviewed a series of studies that have begun illuminating the highly diverse roles of SAMHD1 in virology, immunology, and cancer biology.

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Latent human cytomegalovirus enhances HIV-1 infection in CD34+ progenitor cells

Abstract: Key Points HCMV latency modulates host CD34+ cells in favoring HIV-1 infection. Latent HCMV upregulates HIV entry coreceptors and downregulates HIV restriction factors in CD34+ cells.

Cited by 13 publications

References 71 publications

Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS

Hematopoietic Stem/Progenitor Cells and the Pathogenesis of HIV/AIDS

Navigating the Host Cell Response during Entry into Sites of Latent Cytomegalovirus Infection

SAMHD1 Functions and Human Diseases

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