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Poliovirus
Published in Patricia G. Melloy, Viruses and Society, 2023
Scientists have also started manipulating poliovirus to develop a type of oncolytic virus that can kill cancerous cells. Some scientists are developing attenuated poliovirus strains that can actually kill tumors like neuroblastoma in mouse models (Toyoda et al. 2007). Other scientists have found that many solid tumors express the CD155 receptor, the receptor for poliovirus, and are trying to use attenuated poliovirus as a type of cancer immunotherapy, stimulating the immune system to go after CD155-expressing cells (Gromeier and Nair 2018). Hopefully, a virus like poliovirus, which has caused so much human suffering, can now be used, through genetic engineering, to help cure diseases like cancer.
Polio
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
The poliovirus was shown to infect human cells by binding to a specific receptor on the cell surface – a glycoprotein in the immunoglubulin superfamily of proteins. Labelled CD155, it was identified in 1989 and its recognition finally made it clear why the virus causes disease in such a small number of species – this receptor is found only on the cells of humans, higher primates and Old World monkeys.72After the poliovirus binds to CD155, it is taken up by endocytosis and viral replication begins. Within 4–6 hours, up to 10,000 polio virions are released by cell lysis, the primary viremia of polio infection.73
Neuropathogenesis of viral infections
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Avindra Nath, Joseph R. Berger
Infected leukocytes infect resident brain cells via cell to cell contact resulting in localized areas of brain infection. Viral replication may be restricted at the level of viral entry, such that the virus may infect only those cells that have specific receptors. For example, polio virus infection is dependent upon expression of its receptor, CD155, in the gut [14] and neurons [15]. Other viruses may easily enter cells, but replication may be determined availability of certain host proteins. For example, JCV enters a wide variety of cell types but it replicates in those brain derived cells such as astrocytes that have NF-1D protein [16] while, JCV does not replicate in neurons even if the viral genome is microinjected into the nucleus due to the lack of NF-1D [17]. However, JCV may rarely infect cerebellar granule cells [18] and cortical pyramidal neurons [19]. Similarly, herpes and adenoviruses are capable of entering a large number of cell types but infection gets established only in a few cell types. The ability of viruses to infect multiple cell types and use multiple receptor and non-receptor mediated mechanisms for invading an organism aids their survival in nature.
Oncolytic virus therapy for malignant gliomas: entering the new era
Published in Expert Opinion on Biological Therapy, 2023
Hirotaka Fudaba, Hiroaki Wakimoto
Poliovirus is a single-stranded RNA virus of the Piconaviridae family. CD155, a type 1 transmembrane glycoprotein and a member of the nectin-like family, serves as the cellular receptor for poliovirus. Reovirus is a double-stranded RNA virus of the Reoviridae family. Reolysin is a Dearing type 3 strain virus, which replicates in Ras mutant cells. Measles virus (MV) is a single-stranded, a negative-sense RNA virus of the Paramyxoviridae family. MV-CEA is an attenuated strain of measles virus (MV), derived from the Edmonston vaccine lineage, genetically engineered to produce carcinoembryonic antigen (CEA), which has demonstrated efficacy against GBM in preclinical studies [8–10]. Newcastle disease virus, a negative-sense, single-stranded RNA virus, was previously studied clinically in GBM, sarcoma, and neuroblastoma, but no clinical trial has been active since 2015.
Immune targeting of three independent suppressive pathways (TIGIT, PD-L1, TGFβ) provides significant antitumor efficacy in immune checkpoint resistant models
Published in OncoImmunology, 2022
S. Elizabeth Franks, Kellsye P. Fabian, Ginette Santiago-Sánchez, Benjamin Wolfson, James W. Hodge
TIGIT is an inhibitory receptor with expression restricted to T cells and natural killer (NK) cells, with highest expression found on regulatory T cells (Tregs).10 CD155 is the dominant cognate receptor that interacts with the immunosuppressive receptor TIGIT, and the immunoactivating receptor CD226.11 CD226 is to CD28 as TIGIT is to CTLA-4, with TIGIT binding to CD155 in an inhibitory fashion, at much greater affinity (1–3 nM), in comparison to the positive signaling moiety CD226 (115 nM).12,13 TIGIT, while constitutively expressed on Tregs, is found in low abundance on naïve cells and is significantly upregulated following antigenic stimulation of T cells. TIGIT can deliver inhibitory signals in a paracrine and autocrine fashion, through binding with CD155 and direct disruption of homodimerization of CD226, respectively.14
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
These three neurotropic viruses utilize different receptors. CD155, also known as PV receptor (PVR), serves as the receptor for PV infection [145]. For EV-D68, both sialic acid and ICAM-5 were shown to be responsible for virus attachment and entry [146,147]. Interestingly, both EV-A71 and PV share similar target cells for primary replication including oropharyngeal mucosa, alimentary mucosa, the tonsils and Peyer’s patches of small intestine [141,145]. Similar to EV-A71, PV can also access the host CNS through retrograde axonal transport [148–150] and crossing the BBB [91]. The distribution of inflammation in autopsy cases of EV-A71 resembled those of PV [86]. Unlike the common enteroviruses such as EV-A71 and PV, EV-D68 behaves more like human rhinovirus and is transmitted through the respiratory rather than the fecal-oral route [151]. For EV-D68, the pathogenesis and neuroinvasion are poorly understood. A recent study has shown that EV-D68 can infect motor neurons and utilize retrograde axonal transport to reach CNS [152]. Taken together, these three neurotropic viruses use retrograde axonal transport for trafficking of viruses to CNS and blocking this pathway could block CNS infection.