Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Jan 30;11(2):124.
doi: 10.3390/v11020124.

Modeling Host-Virus Interactions in Viral Infectious Diseases Using Stem-Cell-Derived Systems and CRISPR/Cas9 Technology

Affiliations
Review

Modeling Host-Virus Interactions in Viral Infectious Diseases Using Stem-Cell-Derived Systems and CRISPR/Cas9 Technology

Jihoon Kim et al. Viruses. .

Abstract

Pathologies induced by viral infections have undergone extensive study, with traditional model systems such as two-dimensional (2D) cell cultures and in vivo mouse models contributing greatly to our understanding of host-virus interactions. However, the technical limitations inherent in these systems have constrained efforts to more fully understand such interactions, leading to a search for alternative in vitro systems that accurately recreate in vivo physiology in order to advance the study of viral pathogenesis. Over the last decade, there have been significant technological advances that have allowed researchers to more accurately model the host environment when modeling viral pathogenesis in vitro, including induced pluripotent stem cells (iPSCs), adult stem-cell-derived organoid culture systems and CRISPR/Cas9-mediated genome editing. Such technological breakthroughs have ushered in a new era in the field of viral pathogenesis, where previously challenging questions have begun to be tackled. These include genome-wide analysis of host-virus crosstalk, identification of host factors critical for viral pathogenesis, and the study of viral pathogens that previously lacked a suitable platform, e.g., noroviruses, rotaviruses, enteroviruses, adenoviruses, and Zika virus. In this review, we will discuss recent advances in the study of viral pathogenesis and host-virus crosstalk arising from the use of iPSC, organoid, and CRISPR/Cas9 technologies.

Keywords: CRISPR/Cas9 genome editing; adult stem cell; host-virus interactions; induced pluripotent stem cell; modeling of viral pathogenesis; organoid.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Applications of organoids on virus-mediated diseases. Potential applications of iPSC-derived and adult stem-cell-derived organoid systems for the viral pathogen outbreak are illustrated. Established organoids from different organs can serve as a proper virus culture platform for many purposes such as vaccine generation, OMICS analysis, CRISPR/Cas9-mediated screening, and drug screening for personalized medicine.

Similar articles

Cited by

References

    1. Mogensen T.H. Pathogen recognition and inflammatory signaling in innate immune defenses. Clin. Microbiol. Rev. 2009;22:240–273. doi: 10.1128/CMR.00046-08. - DOI - PMC - PubMed
    1. Zur Wiesch P.A., Kouyos R., Engelstadter J., Regoes R.R., Bonhoeffer S. Population biological principles of drug-resistance evolution in infectious diseases. Lancet Infect. Dis. 2011;11:236–247. doi: 10.1016/S1473-3099(10)70264-4. - DOI - PubMed
    1. Shaw T., Bartholomeusz A., Locarnini S. HBV drug resistance: Mechanisms, detection and interpretation. J. Hepatol. 2006;44:593–606. doi: 10.1016/j.jhep.2006.01.001. - DOI - PubMed
    1. Sarrazin C., Kieffer T.L., Bartels D., Hanzelka B., Muh U., Welker M., Wincheringer D., Zhou Y., Chu H.M., Lin C., et al. Dynamic hepatitis c virus genotypic and phenotypic changes in patients treated with the protease inhibitor telaprevir. Gastroenterology. 2007;132:1767–1777. doi: 10.1053/j.gastro.2007.02.037. - DOI - PubMed
    1. Cairns R.A., Harris I.S., Mak T.W. Regulation of cancer cell metabolism. Nat. Rev. Cancer. 2011;11:85–95. doi: 10.1038/nrc2981. - DOI - PubMed

Publication types