IFN-λ inhibits HIV-1 integration and post-transcriptional events in vitro, but there is only limited in vivo repression of viral production

Tian, Ren‐Rong; Guo, Hongxiong; Wei, Ji‐Fu; Yang, Chuankun; He, Shaoheng; Wang, Jianhua

doi:10.1016/j.antiviral.2012.04.011

Cited by 31 publications

(27 citation statements)

References 45 publications

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“…In spite of this, several studies have analyzed the association between the IFNL4 genetic markers and HIV-1 infection susceptibility and/or disease progression obtaining contradictory results [7][8][9][10][11]. For that reason, it is necessary to perform additional association studies using the functional polymorphism in order to clarify the role of this gene in the HIV-1 infection susceptibility.…”

mentioning

confidence: 88%

“…Although IFNL family members can inhibit HIV-1 infection of macrophages and T-cells in vitro, their effect on the viral replication is limited in vivo [6,7]. In spite of this, several studies have analyzed the association between the IFNL4 genetic markers and HIV-1 infection susceptibility and/or disease progression obtaining contradictory results [7][8][9][10][11].…”

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confidence: 94%

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IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

Real

Herrero

Rivero‐Juárez

et al. 2015

Aids

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The interferon (IFN)L4 polymorphism rs368234815 is associated with hepatitis C virus (HCV) spontaneous clearance and response to IFN-based treatments. The role of this polymorphism in HIV-1 infection is controversial. We investigated whether genetic variation at IFNL4 is associated to HIV-1 acquisition. The HCV protective allele TT was associated with decreased likelihood of HIV-1 infection in male intravenous drug users [odds ratio (OR): 0.3; P = 0.006], and this association was not modified by the genotype of CCR5. These results suggest that genetic susceptibility to HCV and HIV-1 infection shares common molecular pathways.

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confidence: 88%

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confidence: 94%

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

Real

Herrero

Rivero‐Juárez

et al. 2015

Aids

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“…Monocyte-derived dendritic cells (MDDCs) and PHA-P-activated autologous PBLs were used as controls. Viral replication was assessed by quantitative real-time PCR-based methods at the indicated culture times (36). HIV-1 AD8 and NL4-3 exhibited integrants and late reverse transcriptase products in mast cells 2 days after viral exposure (Fig.…”

Section: Human Gut Mucosal Mast Cells Support Hiv-1 Infectionmentioning

confidence: 99%

Human Mucosal Mast Cells Capture HIV-1 and Mediate Viral trans -Infection of CD4 ⁺ T Cells

Jiang

Wei

et al. 2016

J Virol

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Despite great advances in antiretroviral therapies, human immunodeficiency virus type 1 (HIV-1) infection still remains a major global epidemic. Sexual transmission is the principal route of HIV-1 acquisition, making the genital and rectal mucosae the major sites of viral transmission. The intestinal mucosa is also the primary site where HIV-1 amplifies to disseminate virus throughout the host and is critical in the early events in the establishment of infection and evasion of immune defenses. However, the mechanisms contributing to the establishment of HIV-1 primary infection remain largely unexplored. Cell-associated viral dissemination has been proposed to play pivotal roles in HIV-1 primary infection, and multiple cell types, such as dendritic cells (DCs) and macrophages, have been reported to be hijacked by HIV-1 for local and systemic viral spread (1-4). DCs provide one of the best-described cell models for understanding cell-mediated HIV-1 capture and dissemination (1,(5)(6)(7)(8).Mast cells are derived from hematopoietic progenitor cells and undergo final maturation in vascularized tissues. Mast cells are strategically in close contact with the host-environment interface, such as the skin, airway, gastrointestinal tract, and urinary tract. They express numerous pathogen-associated molecular patterns and play an important role in the early immunosurveillance for many pathogens (9, 10). Mast cells can interact with various immune cells in complex ways, including release of soluble factors and direct contact (11), and are important immune effector and modulatory cells that help to link innate and adaptive immunity in the fight against pathogens (9,(12)(13)(14). They have been shown to be important for host defense against various viruses, such as vesicular stomatitis virus, Sendai virus, hantavirus, reovirus, dengue virus, influenza virus, herpes simplex virus, and murine cytomegalovirus (15-23). Additionally, mast cells can serve as antigenpresenting cells and participate in traditional immunologic synapse formation with T cells to mediate antigen-specific T cell activation (24).

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“…27 Furthermore, the recently described type III IFN-k (IL-28/29), which has similar antiviral properties to Type I IFN, has been shown to block HIV-1 infection in macrophages in vitro 28,29 by inhibiting HIV-1 integration and post-transcriptional events. 30 Interestingly, IFN-k receptors are largely restricted to cells of epithelial origin. Together these results suggest that IFN-e and IFN-k may play a unique role in protecting the genital mucosa and future explorations of their potential role in protecting the FGT against HIV may prove valuable in the context of vaccine or microbicide development.…”

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confidence: 99%

Influence of Common Mucosal Co‐Factors on HIV Infection in the Female Genital Tract

Ferreira

Kafka

Kaushic

2014

American J Rep Immunol

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IFN-λ inhibits HIV-1 integration and post-transcriptional events in vitro, but there is only limited in vivo repression of viral production

Cited by 31 publications

References 45 publications

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

Human Mucosal Mast Cells Capture HIV-1 and Mediate Viral trans -Infection of CD4 ⁺ T Cells

Influence of Common Mucosal Co‐Factors on HIV Infection in the Female Genital Tract

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IFN-λ inhibits HIV-1 integration and post-transcriptional events in vitro, but there is only limited in vivo repression of viral production

Cited by 31 publications

References 45 publications

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

IFNL4 rs368234815 polymorphism is associated with innate resistance to HIV-1 infection

Human Mucosal Mast Cells Capture HIV-1 and Mediate Viral trans -Infection of CD4 + T Cells

Influence of Common Mucosal Co‐Factors on HIV Infection in the Female Genital Tract

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Human Mucosal Mast Cells Capture HIV-1 and Mediate Viral trans -Infection of CD4 ⁺ T Cells