Lipid rafts play an important role in the early stage of severe acute respiratory syndrome-coronavirus life cycle

Li, Guimei; Li, Yonggang; Yamate, Masanobu; Li, Shu-Ming; Ikuta, Kazuyoshi

doi:10.1016/j.micinf.2006.10.015

Cited by 160 publications

(202 citation statements)

References 30 publications

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“…3A). This finding is compatible with reports that lipid rafts are required for virus entry but not for virus release in MHV (48) and SARS-CoV (49). Although the presence of RNA is necessary for efficient N-N interaction, we found that M-M or M-N interaction does not require RNA (Fig.…”

Section: Discussionsupporting

confidence: 93%

Self-assembly of Severe Acute Respiratory Syndrome Coronavirus Membrane Protein

Tseng

Wang²,

Huang

et al. 2010

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 93%

Self-assembly of Severe Acute Respiratory Syndrome Coronavirus Membrane Protein

Tseng

Wang²,

Huang

et al. 2010

Journal of Biological Chemistry

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“…Moreover, upon M␤CD treatment, membrane cholesterol levels remain low for 9 to 12 h (25,43). Cells were treated with M␤CD (10 mM) for 1 h either 1 h prior to or 1 h after infection with BDV (MOI, 0.1), and at 48 h p.i., we examined the number of BDV-infected cells based on expression of BDV N as determined by IFA (Fig.…”

Section: Effect Of M␤cd On Bdv Infectionmentioning

confidence: 99%

Borna Disease Virus Requires Cholesterol in both Cellular Membrane and Viral Envelope for Efficient Cell Entry

Clemente

Parseval²,

Perez

et al. 2009

J Virol

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Borna disease virus (BDV), the prototypic member of the family Bornaviridae within the order Mononegavirales, provides an important model for the investigation of viral persistence within the central nervous system (CNS) and of associated brain disorders. BDV is highly neurotropic and enters its target cell via receptor-mediated endocytosis, a process mediated by the virus surface glycoprotein (G), but the cellular factors and pathways determining BDV cell tropism within the CNS remain mostly unknown. Cholesterol has been shown to influence viral infections via its effects on different viral processes, including replication, budding, and cell entry. In this work, we show that cell entry, but not replication and gene expression, of BDV was drastically inhibited by depletion of cellular cholesterol levels. BDV G-mediated attachment to BDV-susceptible cells was cholesterol independent, but G localized to lipid rafts (LR) at the plasma membrane. LR structure and function critically depend on cholesterol, and hence, compromised structural integrity and function of LR caused by cholesterol depletion likely inhibited the initial stages of BDV cell internalization. Furthermore, we also show that viral-envelope cholesterol is required for BDV infectivity.Borna disease virus (BDV) is an enveloped virus with a nonsegmented negative-strand RNA genome whose organization (3Ј-N-p10/P-M-G-L-5Ј) is characteristic of mononegaviruses (6, 28, 46, 48). However, based on its unique genetics and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales (8,28,46,49).BDV can infect a variety of cell types in cell culture but in vivo exhibits exquisite neurotropism and causes central nervous system (CNS) disease in different vertebrate species, which is frequently manifested in behavioral abnormalities (19,33,44,53). Both host and viral factors contribute to a variable period of incubation and heterogeneity in the symptoms and pathology associated with BDV infection (14,16,29,42,44). BDV provides an important model for the investigation of both immune-mediated pathological events associated with virus-induced neurological disease and mechanisms whereby noncytolytic viruses induce neurodevelopmental and behavioral disturbances in the absence of inflammation (15,18,41). Moreover, serological data and molecular epidemiological studies suggest that BDV, or a BDV-like virus, can infect humans and that it might be associated with certain neuropsychiatric disorders (17, 24), which further underscores the interest in understanding the mechanisms underlying BDV persistence in the CNS and its effect on brain cell functions. The achievement of these goals will require the elucidation of the determinants of BDV cell tropism within the CNS.

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“…Human immunodeficiency virus type-1 infection requires cholesterol, both in the target cell membrane and the viral envelope (Guyader et al, 2002;Liao et al, 2001Liao et al, , 2003. Many viruses require cholesterol in the target cell membrane, such as Semliki Forest virus (Phalen and Kielian, 1991;Ahn et al, 2002), severe acute respiratory syndrome-coronavirus (Li et al, 2007) and SV40 virus (Anderson et al, 1996). For influenza virus and duck hepatitis B virus, the presence of cholesterol in its viral envelope is critical, but it is not essential in the target cell (Sun and Whittaker, 2003;Funk et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Critical role of cholesterol in bovine herpesvirus type 1 infection of MDBK cells

Zhu

Ding

Tao

et al. 2010

Veterinary Microbiology

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Cholesterol is involved in the life cycle of many viruses. Here, we examined the role of cholesterol for both viral envelope and target cell membrane for bovine herpesvirus type 1 (BoHV-1) infection. Cholesterol depletion by pretreatment of Madin-Darby bovine kidney (MDBK) cells with a cholesterol-sequestering drug methyl-beta-cyclodextrin (MbetaCD), inhibited the production of BoHV-1 in a dose-dependent manner. This inhibitory effect was partially reversed by cholesterol replenishment, indicating that the reduction was caused by cholesterol depletion. Cholesterol depletion at the post-entry stage only had a mild effect on the virus production. However, cell membrane cholesterol depletion did not reduce the virus attachment. In addition, treatment of BoHV-1 particles with MbetaCD also reduced the virus infectivity significantly and the effect was partially reversed by addition of exogenous cholesterol. Taken together, these data implicated that cell membrane cholesterol mainly contributed to BoHV-1 entry into MDBK cells and the viral envelope cholesterol was also essential for the virus infectivity.

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Lipid rafts play an important role in the early stage of severe acute respiratory syndrome-coronavirus life cycle

Cited by 160 publications

References 30 publications

Self-assembly of Severe Acute Respiratory Syndrome Coronavirus Membrane Protein

Self-assembly of Severe Acute Respiratory Syndrome Coronavirus Membrane Protein

Borna Disease Virus Requires Cholesterol in both Cellular Membrane and Viral Envelope for Efficient Cell Entry

Critical role of cholesterol in bovine herpesvirus type 1 infection of MDBK cells

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