HSV-1 Cytoplasmic Envelopment and Egress

Ahmad, Imran; Wilson, Duncan W.

doi:10.3390/ijms21175969

Cited by 54 publications

(63 citation statements)

References 263 publications

(644 reference statements)

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“…The inhibitory effect of Vps35 on HSV-1 propagation might also arise from its regulation on the trafficking of HSV-1 envelope proteins required for the assembly and release of HSV-1 virions and or on the trafficking of other host virus-restricting factor(s). Based on a model summarized by Ahmad and Wilson [ 56 ], envelopment of naïve HSV-1 capsids at trans-Golgi networks requires at least the core fusion machinery gB, gD, and gH/gL, which are endocytosed from plasma membranes of host cells and delivered to trans-Golgi networks. While gB is known to contain signals for endocytosis and retrieval to trans-Golgi networks, gD and gH/gL do not contain a recognizable endocytic signal and rely on other viral proteins, e.g., gK/UL20 and gM, for endocytosis and delivery to trans-Golgi networks [ 56 , 57 ].…”

Section: Discussionmentioning

confidence: 99%

“…Based on a model summarized by Ahmad and Wilson [ 56 ], envelopment of naïve HSV-1 capsids at trans-Golgi networks requires at least the core fusion machinery gB, gD, and gH/gL, which are endocytosed from plasma membranes of host cells and delivered to trans-Golgi networks. While gB is known to contain signals for endocytosis and retrieval to trans-Golgi networks, gD and gH/gL do not contain a recognizable endocytic signal and rely on other viral proteins, e.g., gK/UL20 and gM, for endocytosis and delivery to trans-Golgi networks [ 56 , 57 ]. We analyzed the cytoplasmic sequences and found retrieval signals for recognition by retromer, e.g., FDV (aa336-338) in gK and multiple [F/Y/W]X[L/M/V] motifs in gM.…”

Section: Discussionmentioning

confidence: 99%

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Parkinson’s Disease Causative Mutation in Vps35 Disturbs Tetherin Trafficking to Cell Surfaces and Facilitates Virus Spread

Ding

Chhetri

et al. 2021

Cells

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Parkinson’s disease (PD) is the most common neurodegenerative movement disorder, characterized by progressive loss of dopaminergic neurons in the substantia nigra, intraneuronal deposition of misfolded proteins known as Lewy bodies, and chronic neuroinflammation. PD can arise from monogenic mutations, but in most cases, the etiology is unclear. Viral infection is gaining increasing attentions as a trigger of PD. In this study, we investigated whether the PD-causative 620 aspartate (D) to asparagine (N) mutation in the vacuolar protein sorting 35 ortholog (Vps35) precipitated herpes simplex virus (HSV) infection. We observed that ectopic expression of Vps35 significantly reduced the proliferation and release of HSV-1 virions; the D620N mutation rendered Vps35 a partial loss of such inhibitory effects. Tetherin is a host cell protein capable of restricting the spread of encapsulated viruses including HSV-1 and SARS-Cov-2, both of which are implicated in the development of parkinsonism. Compared with cells overexpressing wildtype Vps35, cells expressing mutant Vps35 with D620N had less Tetherin on cell surfaces. Real-time and static cell imaging revealed that Tetherin recycled through Vps35-positive endosomes. Expression of Vps35 with D620N reduced endosomal dynamics and frequency of motile Tetherin-containing vesicles, a sign of defective production of recycling carriers. Our study suggests that the D620N mutation in Vps35 hinders Tetherin trafficking to cell surfaces and facilitates virus spread.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Parkinson’s Disease Causative Mutation in Vps35 Disturbs Tetherin Trafficking to Cell Surfaces and Facilitates Virus Spread

Ding

Chhetri

et al. 2021

Cells

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“…Herpes simplex viral vectors used for gene therapy were mainly modified from Herpes Simplex virus type 1 (HSV-1), an enveloped double-stranded DNA virus ( 73 ). Due to the neurotropic nature, HSV vectors are attractive for gene transduction in central nervous system tumors.…”

Section: Viral Vectorsmentioning

confidence: 99%

Viral Gene Therapy for Glioblastoma Multiforme: A Promising Hope for the Current Dilemma

Wang

Jia

et al. 2021

Front. Oncol.

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Glioblastoma multiforme (GBM), as one of the most common malignant brain tumors, was limited in its treatment effectiveness with current options. Its invasive and infiltrative features led to tumor recurrence and poor prognosis. Effective treatment and survival improvement have always been a challenge. With the exploration of genetic mutations and molecular pathways in neuro-oncology, gene therapy is becoming a promising therapeutic approach. Therapeutic genes are delivered into target cells with viral vectors to act specific antitumor effects, which can be used in gene delivery, play an oncolysis effect, and induce host immune response. The application of engineering technology makes the virus vector used in genetics a more prospective future. Recent advances in viral gene therapy offer hope for treating brain tumors. In this review, we discuss the types and designs of viruses as well as their study progress and potential applications in the treatment of GBM. Although still under research, viral gene therapy is promising to be a new therapeutic approach for GBM treatment in the future.

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“…These genes will allow the virus to escape immediate cellular antiviral responses, replicate the viral genome, and assemble new viral particles ( 11 , 12 ). New copies of the viral DNA will be packaged into new capsids in the nucleus and traverse the nuclear membranes to access the cytoplasm, where they are complemented with additional tegument proteins and acquire an envelope with viral glycoproteins before exiting the cell in exocytic vesicles ( Figure 1 ) ( 13 ). The new infectious viral particles released by skin epithelial cells can then gain access to type-C fibers of sensory neurons that innervate the skin and reach the cell body of neurons by retrograde axonal transport ( 14 , 15 ).…”

Section: Introductionmentioning

confidence: 99%

Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection

et al. 2021

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Herpes simplex virus type 1 (HSV-1) infection is highly prevalent in humans, with approximately two-thirds of the world population living with this virus. However, only a fraction of those carrying HSV-1, which elicits lifelong infections, are symptomatic. HSV-1 mainly causes lesions in the skin and mucosae but reaches the termini of sensory neurons innervating these tissues and travels in a retrograde manner to the neuron cell body where it establishes persistent infection and remains in a latent state until reactivated by different stimuli. When productive reactivations occur, the virus travels back along axons to the primary infection site, where new rounds of replication are initiated in the skin, in recurrent or secondary infections. During this process, new neuron infections occur. Noteworthy, the mechanisms underlying viral reactivations and the exit of latency are somewhat poorly understood and may be regulated by a crosstalk between the infected neurons and components of the immune system. Here, we review and discuss the immune responses that occur at the skin during primary and recurrent infections by HSV-1, as well as at the interphase of latently-infected neurons. Moreover, we discuss the implications of neuronal signals over the priming and migration of immune cells in the context of HSV-1 infection.

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HSV-1 Cytoplasmic Envelopment and Egress

Cited by 54 publications

References 263 publications

Parkinson’s Disease Causative Mutation in Vps35 Disturbs Tetherin Trafficking to Cell Surfaces and Facilitates Virus Spread

Parkinson’s Disease Causative Mutation in Vps35 Disturbs Tetherin Trafficking to Cell Surfaces and Facilitates Virus Spread

Viral Gene Therapy for Glioblastoma Multiforme: A Promising Hope for the Current Dilemma

Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection

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