Budding of alphaviruses

Garoff, Henrik; Sjöberg, Mathilda; Cheng, R. Holland

doi:10.1016/j.virusres.2004.08.008

Cited by 101 publications

(102 citation statements)

References 117 publications

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“…Previous studies using other mononegaviruses revealed that the M and G proteins may be critical for assembly or budding of infectious virions in concert (11,12,28). In this study, we demonstrated that the CT region of BDV G may be essential for the release of infectious particles using cells persistently infected with rBDV ⌬GLLP/M-GFP.…”

Section: Discussionmentioning

confidence: 49%

“…As a first step toward these goals, therefore, we tried to determine the region of BDV G essential for the release of infectious particles by using the ⌬GLLP/M-GFP system. Previous studies clearly revealed that the CT region of the mononegavirus G glycoprotein may play a key role in assembly of infectious virus particles in concert with M (11,12,28). We thus generated a series of alanine substitution mutants in the CT region of BDV G (Fig.…”

Section: Resultsmentioning

confidence: 99%

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A Novel Borna Disease Virus Vector System That Stably Expresses Foreign Proteins from an Intercistronic Noncoding Region

Daito

Fujino

Honda

et al. 2011

J Virol

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Borna disease virus (BDV),Borna disease virus (BDV) belongs to the Bornaviridae family within the nonsegmented, negative-strand RNA viruses and is characterized by highly neurotropic and noncytopathic infection (18,31). Previous studies revealed that BDV infects a wide variety of mammalian species, suggesting that its host range probably includes all warm-blooded animals. The most striking feature of BDV is that it readily establishes a longlasting, persistent infection in the cell nucleus (9, 31). BDV establishes a stable infection without causing apparent cell damage, even in brain cells (8), making this the only animal RNA virus capable of intranuclear parasitism. These features of BDV suggest that this virus could be a promising candidate for an efficient and stable gene delivery system to the central nervous system (CNS).Recent development of the reverse genetics system of BDV revealed that the virus has the capacity to express foreign genes from the 5Ј end of the genome (26). Recombinant BDV (rBDV) with green fluorescent protein (GFP) near the 5Ј end of the genome (rBDV 5ЈGFP) successfully infected, and was propagated in, cultured cells. This study suggested that the 5Ј

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Section: Discussionmentioning

confidence: 49%

Section: Resultsmentioning

confidence: 99%

A Novel Borna Disease Virus Vector System That Stably Expresses Foreign Proteins from an Intercistronic Noncoding Region

Daito

Fujino

Honda

et al. 2011

J Virol

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“…Budding of the highly organized alphavirus particle requires both the capsid protein and the envelope proteins (14,15) and is independent of the ESCRT machinery (16). Budding involves a one-to-one interaction of the cytoplasmic domain of E2 with a hydrophobic pocket on the capsid protein, and mutations in this critical region of E2 block E2-Cp interaction and inhibit budding (17)(18)(19)(20).…”

Section: Importancementioning

confidence: 99%

“…Budding involves a one-to-one interaction of the cytoplasmic domain of E2 with a hydrophobic pocket on the capsid protein, and mutations in this critical region of E2 block E2-Cp interaction and inhibit budding (17)(18)(19)(20). Alphavirus budding also depends on the correct formation of the E2/E1 heterodimer (21,22) and on lateral interactions between the envelope proteins that form the lattice (8,14,23,24). Unlike the case for many less-ordered enveloped viruses, structural and biochemical studies indicate that host proteins are strictly excluded from the mature alphavirus envelope (6,25).…”

Section: Importancementioning

confidence: 99%

Imaging the Alphavirus Exit Pathway

Martínez¹,

Snapp²,

Perumal

et al. 2015

Microsc Microanal

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Alphaviruses are small enveloped RNA viruses with highly organized structures that exclude host cell proteins. They contain an internal nucleocapsid and an external lattice of the viral E2 and E1 transmembrane proteins. Alphaviruses bud from the plasma membrane (PM), but the process and dynamics of alphavirus assembly and budding are poorly understood. Here we generated Sindbis viruses (SINVs) with fluorescent protein labels on the E2 envelope protein and exploited them to characterize virus assembly and budding in living cells. During virus infection, E2 became enriched in localized patches on the PM and in filopodium-like extensions. These E2-labeled patches and extensions contained all of the viral structural proteins. Correlative light and electron microscopy studies established that the patches and extensions colocalized with virus budding structures, while light microscopy showed that they excluded a freely diffusing PM marker protein. Exclusion required the interaction of the E2 protein with the capsid protein, a critical step in virus budding, and was associated with the immobilization of the envelope proteins on the cell surface. Virus infection induced two distinct types of extensions: tubulin-negative extensions that were ϳ2 to 4 m in length and excluded the PM marker, and tubulin-positive extensions that were >10 m long, contained the PM marker, and could transfer virus particles to noninfected cells. Tubulin-positive extensions were selectively reduced in cells infected with a nonbudding SINV mutant. Together, our data support a model in which alphavirus infection induces reorganization of the PM and cytoskeleton, leading to virus budding from specialized sites. IMPORTANCEAlphaviruses are important and widely distributed human pathogens for which vaccines and antiviral therapies are urgently needed. These small highly organized viruses bud from the host cell PM. Virus assembly and budding are critical but little understood steps in the alphavirus life cycle. We developed alphaviruses with fluorescent protein tags on one of the viral membrane (envelope) proteins and used a variety of microscopy techniques to follow the envelope protein and a host cell PM protein during budding. We showed that alphavirus infection induced the formation of patches and extensions on the PM where the envelope proteins accumulate. These sites excluded other PM proteins and correlated with virus budding structures. Exclusion of PM proteins required specific interactions of the viral envelope proteins with the internal capsid protein. Together, our data indicate that alphaviruses extensively reorganize the cell surface and cytoskeleton to promote their assembly and budding.

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“…It is now well established that enveloped viruses differ in their abilities to exclude host proteins from their envelope during the budding process (for a review, see reference 22). For example, host constituents are virtually excluded from alphavirus particles, while retroviruses and rhabdoviruses are less selective in the assembly of their envelope and allow the incorporation of a large number of host-cell-derived proteins.…”

mentioning

confidence: 99%

Insertion of Host-Derived Costimulatory Molecules CD80 (B7.1) and CD86 (B7.2) into Human Immunodeficiency Virus Type 1 Affects the Virus Life Cycle

Giguère

Bounou

Paquette

et al. 2004

J Virol

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Human immunodeficiency virus type 1 (HIV-1) carries virus-encoded and host-derived proteins. Recent advances in the functional characterization of host molecules inserted into mature virus particles have revealed that HIV-1 biology is influenced by the acquisition of host cell membrane components. The CD28/B7 receptor/ ligand system is considered one of the fundamental elements of the normal immune response. Two major cell types that harbor HIV-1 in vivo, i.e., monocytes/macrophages and CD4 ؉ T cells, express the costimulatory molecules CD80 (B7.1) and CD86 (B7.2). We investigated whether CD80 and CD86 are efficiently acquired by HIV-1, and if so, whether these host-encoded molecules can contribute to the virus life cycle. Here we provide the first evidence that the insertion of CD80 and CD86 into HIV-1 increases virus infectivity by facilitating the attachment and entry process due to interactions with their two natural ligands, CD28 and CTLA-4. Moreover, we demonstrate that NF-B is induced by CD80-and CD86-bearing virions when they are combined with the engagement of the T-cell receptor/CD3 complex, an event that is inhibited upon surface expression of CTLA-4. Finally, both CD80 and CD86 were found to be efficiently incorporated into R5-and X4-tropic field strains of HIV-1 expanded in cytokine-treated macrophages. Thus, besides direct interactions between the virus envelope glycoproteins and cell surface constituents, such as CD4 and some specific chemokine coreceptors, HIV-1 may attach to target cells via interactions between cell-derived molecules incorporated into virions and their natural ligands. These findings support the theory that HIV-1-associated host proteins alter virus-host dynamics.

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Budding of alphaviruses

Cited by 101 publications

References 117 publications

A Novel Borna Disease Virus Vector System That Stably Expresses Foreign Proteins from an Intercistronic Noncoding Region

A Novel Borna Disease Virus Vector System That Stably Expresses Foreign Proteins from an Intercistronic Noncoding Region

Imaging the Alphavirus Exit Pathway

Insertion of Host-Derived Costimulatory Molecules CD80 (B7.1) and CD86 (B7.2) into Human Immunodeficiency Virus Type 1 Affects the Virus Life Cycle

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