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Review
. 2020 Mar;11(3):519-525.
doi: 10.1111/1759-7714.13344. Epub 2020 Feb 4.

Alteration of cell junctions during viral infection

Affiliations
Review

Alteration of cell junctions during viral infection

Dan Dong et al. Thorac Cancer. 2020 Mar.

Abstract

Cell junctions serve as a protective barrier for cells and provide an important channel for information transmission between cells and the surrounding environment. Viruses are parasites that invade and commandeer components of host cells in order to survive and replicate, and they have evolved various mechanisms to alter cell junctions to facilitate viral infection. In this review, we examined the current state of knowledge on the action of viruses on host cell junctions. The existing evidence suggests that targeting the molecules involved in the virus-cell junction interaction can prevent the spread of viral diseases.

Keywords: Adherens junction; gap junction; infection; tight junction; virus.

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Figures

Figure 1
Figure 1
Different viruses invade host cells through specific cell junctions. Rotavirus and Hepatitis C virus disrupt the structure and function of tight junction. Human papilloma virus‐induced changes in the organization of adherens junction proteins. Human immunodeficiency virus spread damaged signals to the adjacent cells through gap junction.
Figure 2
Figure 2
HIV hijack gap junction to spread toxic factors and damaged signals to the adjacent uninfected cells. In pericytes, although HIV only infects a small number of cells, the damage is amplified by the spread of viral factors to adjacent uninfected cells via the gap junction channel. (formula imageThe purple cell) HIV infected cell, (The green cellsformula image) Uninfected cell, (formula imageThe yellow gap junctions) Normal gap junction, and (formula imageThe purple gap junctions) HIV “Hijacked” gap junction.

References

    1. Wang HM, Hou PL, Zhao GM, Yu L, Gao YW, He HB. Development and evaluation of serotype‐specific recombinase polymerase amplification combined with lateral flow dipstick assays for the diagnosis of foot‐and‐mouth disease virus serotype A, O and Asia1. BMC Vet Res 2018; 14: 11. - PMC - PubMed
    1. He CQ, Liu YX, Wang HM, Hou PL, He HB, Ding NZ. New genetic mechanism, origin and population dynamic of bovine ephemeral fever virus. Vet Microbiol 2016; 182: 50–6. - PubMed
    1. Zhao GM, Hou PL, Huan YJ, He CQ, Wang HM, He HB. Development of a recombinase polymerase amplification combined with a lateral flow dipstick assay for rapid detection of the Mycoplasma bovis. BMC Vet Res 2018; 14: 10. - PMC - PubMed
    1. Dimitrov DS. Virus entry: Molecular mechanisms and biomedical applications. Nat Rev Microbiol 2004; 2: 109–22. - PMC - PubMed
    1. Du X, Zhou J. Application of biosensors to detection of epidemic diseases in animals. Res Vet Sci 2018; 118: 444–8. - PubMed

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