Human cytomegalovirus infection-induced autophagy was associated with the biological behavioral changes of human umbilical vein endothelial cell (HUVEC)

Zhao, Jun; Zhong, Feng; Yu, Haiyang; Chen, Zhiwu; Wang, Ming-Li; Chen, Jason

doi:10.1016/j.biopha.2018.03.156

Cited by 11 publications

(3 citation statements)

References 23 publications

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“…Autophagy triggered during viral infections can either enhance or inhibit virus proliferation depending on the kind of virus and the related host cell [ 98 , 99 ]. Autophagy is inhibited by some viruses, including human cytomegalovirus, coxsackievirus B3, and herpes simplex virus type 1 [ 100 , 101 , 102 ]. Other viruses, such as the hepatitis B virus, the human immunodeficiency virus, the dengue virus, and the influenza virus, however, promote their replication and maturation by increasing autophagy [ 103 , 104 , 105 , 106 ].…”

Section: Strategies Of Immune Evasion By Sars-cov-2mentioning

confidence: 99%

SARS-CoV-2: A Master of Immune Evasion

2022

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Viruses and their hosts have coevolved for a long time. This coevolution places both the pathogen and the human immune system under selective pressure; on the one hand, the immune system has evolved to combat viruses and virally infected cells, while viruses have developed sophisticated mechanisms to escape recognition and destruction by the immune system. SARS-CoV-2, the pathogen that is causing the current COVID-19 pandemic, has shown a remarkable ability to escape antibody neutralization, putting vaccine efficacy at risk. One of the virus’s immune evasion strategies is mitochondrial sabotage: by causing reactive oxygen species (ROS) production, mitochondrial physiology is impaired, and the interferon antiviral response is suppressed. Seminal studies have identified an intra-cytoplasmatic pathway for viral infection, which occurs through the construction of tunneling nanotubes (TNTs), hence enhancing infection and avoiding immune surveillance. Another method of evading immune monitoring is the disruption of the antigen presentation. In this scenario, SARS-CoV-2 infection reduces MHC-I molecule expression: SARS-CoV-2’s open reading frames (ORF 6 and ORF 8) produce viral proteins that specifically downregulate MHC-I molecules. All of these strategies are also exploited by other viruses to elude immune detection and should be studied in depth to improve the effectiveness of future antiviral treatments. Compared to the Wuhan strain or the Delta variant, Omicron has developed mutations that have impaired its ability to generate syncytia, thus reducing its pathogenicity. Conversely, other mutations have allowed it to escape antibody neutralization and preventing cellular immune recognition, making it the most contagious and evasive variant to date.

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Section: Strategies Of Immune Evasion By Sars-cov-2mentioning

confidence: 99%

SARS-CoV-2: A Master of Immune Evasion

2022

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“…Depending on the type of virus and the corresponding host cell, autophagy activated during viral infections can either benefit or impede virus replication. Some viruses, such as human cytomegalovirus, coxsackievirus B3, and herpes simplex virus type 1, inhibit autophagy [27][28][29]. Conversely, other viruses, such as hepatitis B virus, human immunodeficiency virus, dengue virus, and influenza virus, facilitate their replication and maturation by enhancing the autophagy [30][31][32][33][34].…”

Section: Autophagymentioning

confidence: 99%

The interplay between emerging human coronavirus infections and autophagy

Zhao

Mao

et al. 2021

Emerging Microbes & Infections

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Following outbreaks of severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) in 2002 and 2012, respectively, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third highly pathogenic emerging human coronavirus (hCoV). SARS-CoV-2 is currently causing the global coronavirus disease 2019 (COVID-19) pandemic. CoV infections in target cells may stimulate the formation of numerous double-membrane autophagosomes and induce autophagy. Several studies provided evidence that hCoV infections are closely related to various cellular aspects associated with autophagy. Autophagy may even promote hCoV infection and replication. However, so far it is unclear how hCoV infections induce autophagy and whether the autophagic machinery is necessary for viral propagation. Here, we summarize the most recent advances concerning the mutual interplay between the autophagic machinery and the three emerging hCoVs, SARS-CoV, MERS-CoV, and SARS-CoV-2 and the model system mouse hepatitis virus. We also discuss the applicability of approved and well-tolerated drugs targeting autophagy as a potential treatment against COVID-19.

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“…VCAM1 rarely expresses in endothelial cells under physiological conditions. However, it could be quickly induced/activated directly or indirectly by various stimuli, such as pro-inflammatory factors [e.g., tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and interferon-gamma (IFN-γ)] ( Carlos et al, 1990 ; Neish et al, 1992 ; Paleolog et al, 1992 ), oxidative stresses [e.g., reactive oxygen species (ROS) and oxidative modification of low-density lipoprotein (ox-LDL)] ( Yoshida et al, 2000 ; Lee et al, 2007 ; Zhu et al, 2008 ), and infections (e.g., coronavirus disease 2019, human immunodeficiency virus, and human cytomegalovirus) ( Liu et al, 2005 ; Zhao et al, 2018 ; Robles et al, 2022 ). Endothelial dysfunction and ongoing cardiovascular inflammation are caused by immune cells penetrating the arterial wall as a result of activated VCAM1 on endothelial cells, which attracts leukocytes, monocytes, and neutrophils ( Goswami et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Nuciferine induces autophagy to relieve vascular cell adhesion molecule 1 activation via repressing the Akt/mTOR/AP1 signal pathway in the vascular endothelium

Wei,

Yin,

Yang

et al. 2023

Front. Pharmacol.

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Pro-inflammatory factor-associated vascular cell adhesion molecule 1 (VCAM1) activation initiates cardiovascular events. This study aimed to explore the protective role of nuciferine on TNFα-induced VCAM1 activation. Nuciferine was administrated to both high-fat diet (HFD)-fed mice and the TNFα-exposed human vascular endothelial cell line. VCAM1 expression and further potential mechanism(s) were explored. Our data revealed that nuciferine intervention alleviated VCAM1 activation in response to both high-fat diet and TNFα exposure, and this protective effect was closely associated with autophagy activation since inhibiting autophagy by either genetic or pharmaceutical approaches blocked the beneficial role of nuciferine. Mechanistical studies revealed that Akt/mTOR inhibition, rather than AMPK, SIRT1, and p38 signal pathways, contributed to nuciferine-activated autophagy, which further ameliorated TNFα-induced VCAM1 via repressing AP1 activation, independent of transcriptional regulation by IRF1, p65, SP1, and GATA6. Collectively, our data uncovered a novel biological function for nuciferine in protecting VCAM1 activation, implying its potential application in improving cardiovascular events.

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Human cytomegalovirus infection-induced autophagy was associated with the biological behavioral changes of human umbilical vein endothelial cell (HUVEC)

Cited by 11 publications

References 23 publications

SARS-CoV-2: A Master of Immune Evasion

SARS-CoV-2: A Master of Immune Evasion

The interplay between emerging human coronavirus infections and autophagy

Nuciferine induces autophagy to relieve vascular cell adhesion molecule 1 activation via repressing the Akt/mTOR/AP1 signal pathway in the vascular endothelium

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