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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Some wasps, including the ichneumonid Venturia canescens, instead of releasing into their host polydnaviruses containing viral DNA, release “virus-like particles” that contain no viral DNA but only parasitoid-produced protein virulence factors. It is as if the viral symbiont has been hijacked in such a way to take advantage of its packaging abilities but the packages delivered into the host contain parasitoid proteins rather than viral DNA. This process has been termed symbiotic endogenous virus replacement.
Adenovirus
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Jennifer McGuire, Joseph R. Berger
Adenoviruses can cause persistent infection with prolonged viral shedding in the feces that may last months to years after the initial acute infection [58]. Serological evidence that adenoviruses can be transmitted from kidney and liver transplants also suggests that these organs can occasionally harbor adenoviruses in a latent form [59]. Reactivation of endogenous virus may play a role in adenoviral diseases in immunocompromised patients. The major reservoirs for persistent adenoviral infection and the mechanisms of viral persistence are unknown.
Endogenous Proviruses
Published in Pimentel Enrique, Oncogenes, 2020
Another human endogenous virus, ERV3, consists also of a single copy and is located on chromosome 7.21 Monosomy or partial deletion of human chromosome 7 is frequently observed in ANLL. The proto-oncogene c-erb-B is located on the same chromosome but at a position (7p 11-13) outside the usual site of breakage in ANLL (7q32-34). It remains to be determined whether ERV3 is located near this chromosomal breakpoint and whether it plays a role in the fragility of this site.22 Although ERV3 retains the typical full-length gene order of retroviruses (5′LTR-gag-pol-env-3′LTR), it is apparently also a defective provirus due to the presence of terminator codons in the open reading frames of both its gag and pol gene sequences. ERV3 cannot function as an infectious virus but some of its genes may be capable of expression. The 5′ and 3′ LTRs of ERV3 resemble those of functional mammalian type-C retroviruses but have diverged from one another by 8.8%.22
CAR-T cell therapy for triple-negative breast cancer and other solid tumors: preclinical and clinical progress
Published in Expert Opinion on Investigational Drugs, 2022
Chiara Corti, Konstantinos Venetis, Elham Sajjadi, Lorenzo Zattoni, Giuseppe Curigliano, Nicola Fusco
CAR-T cell therapies encompass several classes of drugs characterized by engineered T cells targeting cancer-specific proteins. In the recent past, these drugs led to relevant changes in the clinical management of refractory hematologic malignancies [43]. To combine the T cell effector function with antibody specificity, T cells are collected from the patient and activation through the introduction of CARs either by viral vectors (i.e. lentivirus, retrovirus, or adenovirus) or non-viral vectors (i.e. synthetic DNA, mRNA transposons, CRISPR-Cas9, or plasmids) [44]. Then, the CAR-modified patient T cells are expanded in vitro and finally reinfused into the patient after lymphodepleting chemotherapy [44]. Most of the clinical studies take advantage of the viral transfer method, consisting of the CAR-encoding gene transferring by the virus into the T cell, and subsequently integrated into the genomic DNA. The CAR gene will be carried by the offspring of these transduced cells, expressing the receptor on their surface [26,45]. For the CAR introduction phase, virus-specific T-cell populations are employed, such as those specific for varicella-zoster virus, Epstein-Barr virus, adenovirus, cytomegalovirus, or multivirus-specific T cells. Thus, these T cells can proliferate and therefore increase their persistence and number through their endogenous virus-specific TCR [45]. Other strategies to enhance T-cell proliferation could be considered as virus vaccination (e.g. varicella-zoster virus vaccination, or oncolytic adenovirus injected intratumorally). Memory T cells could be alternatively used for increasing the persistence of the CAR-T cells [26,45].
Immunopathology of Virus-Induced Anterior Uveitis
Published in Ocular Immunology and Inflammation, 2018
Jolanda D. F. De Groot-Mijnes, Anita S. Y. Chan, Soon-Phaik Chee, Georges M. G. M. Verjans
While the majority of adults are latently infected with HSV-1 and VZV, only a limited number of latently infected individuals will develop HAU. Various factors that determine the incidence and spectrum of ocular herpetic diseases are immune status, age, genetic predisposition, time and route of infection, and potentially the virus strain.6–8,13 HSV-1 and VZV are endemic worldwide infecting about 70% and >90% of individuals, respectively.14 Upon primary infection, commonly during early childhood, both viruses establish a lifelong latent infection in sensory and autonomic neurons from which they reactivate leading to regular asymptomatic virus shedding and incidentally recurrent disease of variable clinical severity ranging from cold sores and shingles to potentially sight- (keratitis and uveitis: both viruses) or even life-threatening neurological diseases (HSV-1 encephalitis).14,15 Intra-ganglionic innate (neuron-interacting satellite glial cells) and adaptive immunity (T cells) are essential to control herpesvirus latency in neurons. Whereas innate immunity is most likely sufficient to prevent VZV to escape from latency, HSV-1-specific CD8 T cells are of additional importance to prevent HSV-1 reactivation.14,16–18 Because most if not all HAU patients have already antibodies to the triggering herpesvirus and latency has not been detected in ocular tissues,11,19 the disease is not initiate by a primary infection but most likely due to reactivation of endogenous virus that entered the eye via trans-axonal transport from the innervating sensory or autonomic ganglia.7,10 The independent distribution of latent HSV-1 and VZV in these ganglia, particularly the dissimilarity in latent virus between paired left and right ganglia of the human head and neck, may explain the clinical observation that HAU usually occurs unilaterally.20,21