Publications by authors named "Xi-Qiu Xu"

Infections caused by coronaviruses are persistent threats to human health in recent decades, necessitating the development of innovative anti-coronaviral therapies. RNA interference (RNAi) is a conserved cell-intrinsic antiviral mechanism in diverse eukaryotic organisms, including mammals. To counteract, many viruses encode viral suppressors of RNAi (VSRs) to evade antiviral RNAi, implying that targeting VSRs could be a promising strategy to develop antiviral therapies.

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Introduction: While astrocytes participate in the CNS innate immunity against herpes simplex virus type 1 (HSV-1) infection, they are the major target for the virus. Therefore, it is of importance to understand the interplay between the astrocyte-mediated immunity and HSV-1 infection.

Methods: Both primary human astrocytes and the astrocyte line (U373) were used in this study.

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Herpes simplex virus 1 (HSV-1) is a DNA virus belonging to the family . HSV-1 infection causes severe neurological disease in the central nervous system (CNS), including encephalitis. Ferroptosis is a nonapoptotic form of programmed cell death that contributes to different neurological inflammatory diseases.

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The female reproductive tract (FRT) is a major site of HIV sexual transmission. As the outermost layer of cells in the FRT, the human cervical epithelial cells (HCEs) have direct contact with HIV or infected cells. Our early work showed that supernatant (SN) from TLR3-activated HCEs contain the antiviral factors that could potently inhibit HIV replication in macrophages.

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Chronically SHIV-infected cynomolgus monkeys were used to determine the effects of the antibody-mediated acute CD4 T cell depletion on viral load as well as on the immunological factors associated with disease progression. Compared with the control animals, CD4 T cell-depleted animals with SHIV infection showed (i) little alteration in plasma viral load over the period of 22 weeks after the depletion; (ii) increased CD4 T cell proliferation and turnover of macrophages at the early phase of the depletion, but subsequent decline to the basal levels; and (iii) little impact on the expression of the inflammatory cytokines and CC chemokines associated with disease progression. These findings indicate that the antibody-mediated acute CD4 T cell depletion had minimal impact on plasma viral load and disease progression in chronically SHIV-infected cynomolgus monkeys.

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Epithelial cells of the female reproductive tract (FRT) participate in the initial innate immunity against viral infections. Poly(dA:dT) is a synthetic analog of B form double-stranded (ds) DNA which can activate the interferon (IFN) signaling pathway-mediated antiviral immunity through DNA-dependent RNA Polymerase III. Here we investigated whether poly(dA:dT) could inhibit herpes simplex virus type 2 (HSV-2) infection of human cervical epithelial cells (End1/E6E7).

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Interleukin (IL)-22, a member of the IL-10 family, plays a role in antiviral immune responses to a number of viral infections. However, it is unclear whether IL-22 is involved in the mucosal immunity against herpes simplex virus 2 (HSV-2) infection in the female reproductive tract (FRT). In this study, we studied whether IL-22 could inhibit HSV-2 infection of human cervical epithelial cells (End1/E6E7 cells).

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The Bowman‒Birk inhibitor (BBI), a protease inhibitor derived from soybeans, has been extensively studied in anti-tumor and anti-inflammation research. We recently reported that BBI has an anti-HIV-1 property in primary human macrophages. Because HSV-2 infection plays a role in facilitating HIV-1 sexual transmission, we thus examined whether BBI has the ability to inhibit HSV-2 infection.

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Article Synopsis
  • * The study found that HCEs activate a signaling system (TLR3) which, when stimulated, produces antiviral factors like interferons that can inhibit HIV in human macrophages.
  • * HCEs also generate specific chemokines that affect HIV entry, suggesting that these cervical cells could be important targets for new strategies to prevent and control HIV transmission.
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Article Synopsis
  • The gastrointestinal (GI) tract is a key area for HIV infection due to its abundance of CD4 T cells and macrophages, highlighting the need for effective immune responses.
  • The study found that intestinal epithelial cells (IECs) can produce antiviral factors that inhibit HIV infection in macrophages by activating toll-like receptor 3 (TLR3) and triggering the release of important interferon (IFN) and chemokines.
  • Activated IECs also secrete exosomes containing anti-HIV components that prevent virus replication in macrophages, suggesting that IECs play a crucial role in protecting against HIV in the GI tract.
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