Caveolin-1 limits human influenza A virus (H1N1) propagation in mouse embryo-derived fibroblasts

Bohm, Katrin; Sun, Lina; Thakor, Divyeshsinh T.; Wirth, Manfred

doi:10.1016/j.virol.2014.05.028

Cited by 9 publications

(7 citation statements)

References 84 publications

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“…For example, overexpression of CAV-1 significantly decreases the transcription level of HIV-1, and the decrease of CAV-1 expression leads to an enhancement of HIV-1 replication. As well known, HIV actually benefits from the activation of host inflammatory responses [104,105]. Further investigations suggested that CAV-1 suppresses the NF-κB p65 acetylation, a requirement for signaling activation [106,107].…”

Section: The Role Of Caveolae/cav-1 In Virus Replicationmentioning

confidence: 90%

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Multifaceted Functions of Host Cell Caveolae/Caveolin-1 in Virus Infections

Xing

Wen

Wei

et al. 2020

Viruses

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Virus infection has drawn extensive attention since it causes serious or even deadly diseases, consequently inducing a series of social and public health problems. Caveolin-1 is the most important structural protein of caveolae, a membrane invagination widely known for its role in endocytosis and subsequent cytoplasmic transportation. Caveolae/caveolin-1 is tightly associated with a wide range of biological processes, including cholesterol homeostasis, cell mechano-sensing, tumorigenesis, and signal transduction. Intriguingly, the versatile roles of caveolae/caveolin-1 in virus infections have increasingly been appreciated. Over the past few decades, more and more viruses have been identified to invade host cells via caveolae-mediated endocytosis, although other known pathways have been explored. The subsequent post-entry events, including trafficking, replication, assembly, and egress of a large number of viruses, are caveolae/caveolin-1-dependent. Deprivation of caveolae/caveolin-1 by drug application or gene editing leads to abnormalities in viral uptake, viral protein expression, or virion release, whereas the underlying mechanisms remain elusive and must be explored holistically to provide potential novel antiviral targets and strategies. This review recapitulates our current knowledge on how caveolae/caveolin-1 functions in every step of the viral infection cycle and various relevant signaling pathways, hoping to provide a new perspective for future viral cell biology research.

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Section: The Role Of Caveolae/cav-1 In Virus Replicationmentioning

confidence: 90%

“…Strikingly, the elevated levels of ROS and apoptosis cause the increase of IVA virion yield. In other words, CAV-1 plays a role in limiting IVA infection [105].…”

Section: The Role Of Caveolae/cav-1 In Other Viruses Infection-related Signal Transductionmentioning

confidence: 99%

Multifaceted Functions of Host Cell Caveolae/Caveolin-1 in Virus Infections

Xing

Wen

Wei

et al. 2020

Viruses

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“…Although the combined data suggest a function of caveolae in viral biogenesis, an association with caveolin-1 alone does not directly demonstrate the involvement of caveolae in virus morphogenesis. In addition, siRNA-mediated knockdown of caveolin-1 was shown to have no effect on RSV morphogenesis and infection in cultured cells (Kipper et al, 2015), and there is some evidence that caveolin-1 might have an anti-viral role during virus infection (Gabor et al, 2013; Bohm et al, 2014; He et al, 2016). Thus, the role of caveolin-1 and caveolae in virus-infected cells remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly

Ludwig

Nguyen

Leong

et al. 2017

Journal of Cell Science

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Respiratory syncytial virus (RSV) is an enveloped virus that assembles into filamentous virus particles on the surface of infected cells. Morphogenesis of RSV is dependent upon cholesterol-rich (lipid raft) membrane microdomains, but the specific role of individual raft molecules in RSV assembly is not well defined. Here, we show that RSV morphogenesis occurs within caveolar membranes and that both caveolin-1 and cavin-1 (also known as PTRF), the two major structural and functional components of caveolae, are actively recruited to and incorporated into the RSV envelope. The recruitment of caveolae occurred just prior to the initiation of RSV filament assembly, and was dependent upon an intact actin network as well as a direct physical interaction between caveolin-1 and the viral G protein. Moreover, cavin-1 protein levels were significantly increased in RSV-infected cells, leading to a virus-induced change in the stoichiometry and biophysical properties of the caveolar coat complex. Our data indicate that RSV exploits caveolae for its assembly, and we propose that the incorporation of caveolae into the virus contributes to defining the biological properties of the RSV envelope.

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“…For instance, both RAB7A and CD63 are required for the HIV-1 replication cycle 25 26 . In addition, LSD1, HSPA5, and CAV-1 have been reported to influence the efficiency of viral infection and replication 27 28 29 30 31 ; NPC1 is the key influencer for Ebola virus to enter cells 32 ; SEC22b can inhibit the release of infectious viral progeny 33 ; and the down-regulation of CD59 is associated with the development of hepatitis B cytotoxicity 34 .…”

Section: Resultsmentioning

confidence: 99%

Profiling of Host Cell Response to Successive Canine Parvovirus Infection Based on Kinetic Proteomic Change Identification

Zhao

Cheng

Wang

et al. 2016

Sci Rep

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Canine parvovirus (CPV) reproduces by co-opting the resources of host cells, inevitably causing cytotoxic effects to the host cells. Feline kidney F81 cells are sensitive to CPV infection and show disparate growing statuses at different time points post-infection. This study analysed the response of F81 cells to CPV infection at successive infection time points by iTRAQ-based quantitative proteomics. Differentially expressed proteins (DEPs) during 60 h of infection and at selected time points post-infection were identified by an analysis of variance test and a two-tailed unpaired t test, respectively. DEPs with similar quantitative changes were clustered by hierarchical clustering and analysed by gene ontology enrichment, revealing that 12 h and 60 h post-infection were the optimal times to analyse the autonomous parvovirus replication and apoptosis processes, respectively. Using the MetacoreTM database, 29 DEPs were enriched in a network involved in p53 regulation. Besides, a significantly enriched pathway suggests that the CPV-induced cytopathic effect was probably due to the deficiency of functional CFTR caused by CPV infection. This study uncovered the systemic changes in key cellular factors involved in CPV infection and help to understand the molecular mechanisms of the anti-cancer activity of CPV and the cytopathic effects induced by CPV infection.

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Caveolin-1 limits human influenza A virus (H1N1) propagation in mouse embryo-derived fibroblasts

Cited by 9 publications

References 84 publications

Multifaceted Functions of Host Cell Caveolae/Caveolin-1 in Virus Infections

Multifaceted Functions of Host Cell Caveolae/Caveolin-1 in Virus Infections

Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly

Profiling of Host Cell Response to Successive Canine Parvovirus Infection Based on Kinetic Proteomic Change Identification

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