Paralysis caused by dinotefuran at environmental concentration via interfering the Ca-ROS-mitochondria pathway in .

Introduction: Dinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.

Methods: In this study, the mitochondria damage and oxidative stress of dinotefuran on were investigated at environmental concentrations by long-term exposure.

The SARS-unique domain (SUD) of SARS-CoV-2 nsp3 protein inhibits the antiviral immune responses through the NF-κB pathway.

Nuclear factor κB (NF-κB) plays a crucial role in various cellular processes, including inflammatory and immune responses. Its activation is tightly regulated by the IKK (IκB kinase) complex. Upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the virus is initially recognized by the innate immune system and typically activates the NF-κB pathway, leading to a severe inflammatory response.

Long-term exposure to environmental concentration of dinotefuran disrupts ecdysis and sex ratio by dysregulating related gene expressions in .

Introduction: Currently, although there have been a few reports on the endocrine-disrupting effects of neonicotinoids, the effect on Chironomidae during long-term exposure remains unknown.

Methods: Ecdysis and sex ratio, along with ecdysone-relevant gene expressions of representative neonicotinoid dinotefuran on were investigated at different environmental concentrations by long-term exposure.

Results: A low dose of dinotefuran delayed pupation and emergence via inhibiting ecdysis.

Necroptosis takes place in human immunodeficiency virus type-1 (HIV-1)-infected CD4+ T lymphocytes.

Human immunodeficiency virus type 1 (HIV-1) infection is characterized by progressive depletion of CD4+ T lymphocytes and dysfunction of the immune system. The numbers of CD4+ T lymphocytes in the human body are maintained constantly by homeostatic mechanisms that failed during HIV-1 infection, resulting in progressive loss of CD4+ T cells mainly via apoptosis. Recently, a non-apoptotic form of necrotic programmed cell death, named necroptosis, has been investigated in many biological and pathological processes.

DDX5 facilitates HIV-1 replication as a cellular co-factor of Rev.

HIV-1 Rev plays an important role in the late phase of HIV-1 replication, which facilitates export of unspliced viral mRNAs from the nucleus to cytoplasm in infected cells. Recent studies have shown that DDX1 and DDX3 are co-factors of Rev for the export of HIV-1 transcripts. In this report, we have demonstrated that DDX5 (p68), which is a multifunctional DEAD-box RNA helicase, functions as a new cellular co-factor of HIV-1 Rev.