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Hypothesis: RNA and DNA Viral Sequence Integration into the Mammalian Host Genome Supports Long-Term B Cell and T Cell Adaptive Immunity
Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Max Planck Institute for Infection Biology, Berlin, Germany; Humboldt University, Berlin, Germany.
2017 (engelsk)Inngår i: Viral immunology, ISSN 0882-8245, E-ISSN 1557-8976, Vol. 30, nr 9, s. 628-632Artikkel i tidsskrift, Editorial material (Annet vitenskapelig) Published
Abstract [en]

Viral sequence integration into the mammalian genome has long been perceived as a health risk. In some cases, integration translates to chronic viral infection, and in other instances, oncogenic gene mutations occur. However, research also shows that animal cells can benefit from integrated viral sequences (e.g., to support host cell development or to silence foreign invaders). Here we propose that, comparable with the clustered regularly interspaced short palindromic repeats that provide bacteria with adaptive immunity against invasive bacteriophages, animal cells may co-opt integrated viral sequences to support immune memory. We hypothesize that host cells express viral peptides from open reading frames in integrated sequences to boost adaptive B cell and T cell responses long after replicating viruses are cleared. In support of this hypothesis, we examine previous literature describing (1) viruses that infect acutely (e.g., vaccinia viruses and orthomyxoviruses) followed by unexplained, long-term persistence of viral nucleotide sequences, viral peptides, and virus-specific adaptive immunity, (2) the high frequency of endogenous viral genetic elements found in animal genomes, and (3) mechanisms with which animal host machinery supports foreign sequence integration.

sted, utgiver, år, opplag, sider
MARY ANN LIEBERT, INC , 2017. Vol. 30, nr 9, s. 628-632
Emneord [en]
viral sequence integration, CRISPR, hypothesis
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-142262DOI: 10.1089/vim.2017.0099ISI: 000414394200002PubMedID: 29028182OAI: oai:DiVA.org:umu-142262DiVA, id: diva2:1163200
Tilgjengelig fra: 2017-12-06 Laget: 2017-12-06 Sist oppdatert: 2018-06-09bibliografisk kontrollert

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